Robert, V.; Triffaux, E.; Savignac, M.; Pelletier, L. [Calcium signaling in T lymphocytes] Journal Article In: Med Sci (Paris), vol. 28, no. 8-9, pp. 773-9, 2012, ISSN: 0767-0974 (Print)
0767-0974 (Linking). @article{RN13b,
title = {[Calcium signaling in T lymphocytes]},
author = {Robert, V. and Triffaux, E. and Savignac, M. and Pelletier, L.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/22920880},
doi = {10.1051/medsci/2012288020},
issn = {0767-0974 (Print)
0767-0974 (Linking)},
year = {2012},
date = {2012-01-01},
journal = {Med Sci (Paris)},
volume = {28},
number = {8-9},
pages = {773-9},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Seillet, C.; Laffont, S.; Tremollieres, F.; Rouquie, N.; Ribot, C.; Arnal, J. F.; Douin-Echinard, V.; Gourdy, P.; Guery, J. C. The TLR-mediated response of plasmacytoid dendritic cells is positively regulated by estradiol in vivo through cell-intrinsic estrogen receptor alpha signaling Journal Article In: Blood, vol. 119, no. 2, pp. 454-64, 2012, ISSN: 1528-0020 (Electronic)
0006-4971 (Linking). @article{RN9,
title = {The TLR-mediated response of plasmacytoid dendritic cells is positively regulated by estradiol in vivo through cell-intrinsic estrogen receptor alpha signaling},
author = {Seillet, C. and Laffont, S. and Tremollieres, F. and Rouquie, N. and Ribot, C. and Arnal, J. F. and Douin-Echinard, V. and Gourdy, P. and Guery, J. C.},
url = {http://www.ncbi.nlm.nih.gov/pubmed/22096248
http://www.bloodjournal.org/content/bloodjournal/119/2/454.full.pdf},
doi = {10.1182/blood-2011-08-371831},
issn = {1528-0020 (Electronic)
0006-4971 (Linking)},
year = {2012},
date = {2012-01-01},
journal = {Blood},
volume = {119},
number = {2},
pages = {454-64},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Menard, S.; Morlais, I.; Tahar, R.; Sayang, C.; Mayengue, P. I.; Iriart, X.; Benoit-Vical, F.; Lemen, B.; Magnaval, J. F.; Awono-Ambene, P.; Basco, L. K.; Berry, A. Molecular monitoring of plasmodium falciparum drug susceptibility at the time of the introduction of artemisinin-based combination therapy in Yaounde, Cameroon: implications for the future Journal Article In: Malaria journal, vol. 11, pp. 113, 2012, (Menard, Sandie
Morlais, Isabelle
Tahar, Rachida
Sayang, Collins
Mayengue, Pembe Issamou
Iriart, Xavier
Benoit-Vical, Francoise
Lemen, Brigitte
Magnaval, Jean-Francois
Awono-Ambene, Parfait
Basco, Leonardo K
Berry, Antoine
England
Malar J. 2012 Apr 12;11:113.). @article{b,
title = {Molecular monitoring of plasmodium falciparum drug susceptibility at the time of the introduction of artemisinin-based combination therapy in Yaounde, Cameroon: implications for the future},
author = {Menard, S. and Morlais, I. and Tahar, R. and Sayang, C. and Mayengue, P. I. and Iriart, X. and Benoit-Vical, F. and Lemen, B. and Magnaval, J. F. and Awono-Ambene, P. and Basco, L. K. and Berry, A.},
year = {2012},
date = {2012-01-01},
journal = {Malaria journal},
volume = {11},
pages = {113},
abstract = {BACKGROUND: Regular monitoring of the levels of anti-malarial resistance of Plasmodium falciparum is an essential policy to adapt therapy and improve malaria control. This monitoring can be facilitated by using molecular tools, which are easier to implement than the classical determination of the resistance phenotype. In Cameroon, chloroquine (CQ), previously the first-line therapy for uncomplicated malaria was officially withdrawn in 2002 and replaced initially by amodiaquine (AQ) monotherapy. Then, artemisinin-based combination therapy (ACT), notably artesunate-amodiaquine (AS-AQ) or artemether-lumefantrine (AL), was gradually introduced in 2004. This situation raised the question of the evolution of P. falciparum resistance molecular markers in Yaounde, a highly urbanized Cameroonian city. METHODS: The genotype of pfcrt 72 and 76 and pfmdr1 86 alleles and pfmdr1 copy number were determined using real-time PCR in 447 P. falciparum samples collected between 2005 and 2009. RESULTS: This study showed a high prevalence of parasites with mutant pfcrt 76 (83%) and pfmdr1 86 (93%) codons. On the contrary, no mutations in the pfcrt 72 codon and no samples with duplication of the pfmdr1 gene were observed. CONCLUSION: The high prevalence of mutant pfcrt 76T and pfmdr1 86Y alleles might be due to the choice of alternative drugs (AQ and AS-AQ) known to select such genotypes. Mutant pfcrt 72 codon was not detected despite the prolonged use of AQ either as monotherapy or combined with artesunate. The absence of pfmdr1 multicopies suggests that AL would still remain efficient. The limited use of mefloquine or the predominance of mutant pfmdr1 86Y codon could explain the lack of pfmdr1 amplification. Indeed, this mutant codon is rarely associated with duplication of pfmdr1 gene. In Cameroon, the changes of therapeutic strategies and the simultaneous use of several formulations of ACT or other anti-malarials that are not officially recommended result in a complex selective pressure, rendering the prediction of the evolution of P. falciparum resistance difficult. This public health problem should lead to increased vigilance and regular monitoring.},
note = {Menard, Sandie
Morlais, Isabelle
Tahar, Rachida
Sayang, Collins
Mayengue, Pembe Issamou
Iriart, Xavier
Benoit-Vical, Francoise
Lemen, Brigitte
Magnaval, Jean-Francois
Awono-Ambene, Parfait
Basco, Leonardo K
Berry, Antoine
England
Malar J. 2012 Apr 12;11:113.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
BACKGROUND: Regular monitoring of the levels of anti-malarial resistance of Plasmodium falciparum is an essential policy to adapt therapy and improve malaria control. This monitoring can be facilitated by using molecular tools, which are easier to implement than the classical determination of the resistance phenotype. In Cameroon, chloroquine (CQ), previously the first-line therapy for uncomplicated malaria was officially withdrawn in 2002 and replaced initially by amodiaquine (AQ) monotherapy. Then, artemisinin-based combination therapy (ACT), notably artesunate-amodiaquine (AS-AQ) or artemether-lumefantrine (AL), was gradually introduced in 2004. This situation raised the question of the evolution of P. falciparum resistance molecular markers in Yaounde, a highly urbanized Cameroonian city. METHODS: The genotype of pfcrt 72 and 76 and pfmdr1 86 alleles and pfmdr1 copy number were determined using real-time PCR in 447 P. falciparum samples collected between 2005 and 2009. RESULTS: This study showed a high prevalence of parasites with mutant pfcrt 76 (83%) and pfmdr1 86 (93%) codons. On the contrary, no mutations in the pfcrt 72 codon and no samples with duplication of the pfmdr1 gene were observed. CONCLUSION: The high prevalence of mutant pfcrt 76T and pfmdr1 86Y alleles might be due to the choice of alternative drugs (AQ and AS-AQ) known to select such genotypes. Mutant pfcrt 72 codon was not detected despite the prolonged use of AQ either as monotherapy or combined with artesunate. The absence of pfmdr1 multicopies suggests that AL would still remain efficient. The limited use of mefloquine or the predominance of mutant pfmdr1 86Y codon could explain the lack of pfmdr1 amplification. Indeed, this mutant codon is rarely associated with duplication of pfmdr1 gene. In Cameroon, the changes of therapeutic strategies and the simultaneous use of several formulations of ACT or other anti-malarials that are not officially recommended result in a complex selective pressure, rendering the prediction of the evolution of P. falciparum resistance difficult. This public health problem should lead to increased vigilance and regular monitoring. |
Menard, S.; Morlais, I.; Tahar, R.; Sayang, C.; Mayengue, P. I.; Iriart, X.; Benoit-Vical, F.; Lemen, B.; Magnaval, J. F.; Awono-Ambene, P.; Basco, L. K.; Berry, A. Molecular monitoring of plasmodium falciparum drug susceptibility at the time of the introduction of artemisinin-based combination therapy in Yaounde, Cameroon: implications for the future Journal Article In: Malaria journal, vol. 11, pp. 113, 2012, (Apr 12;11:113.). @article{b,
title = {Molecular monitoring of plasmodium falciparum drug susceptibility at the time of the introduction of artemisinin-based combination therapy in Yaounde, Cameroon: implications for the future},
author = {Menard, S. and Morlais, I. and Tahar, R. and Sayang, C. and Mayengue, P. I. and Iriart, X. and Benoit-Vical, F. and Lemen, B. and Magnaval, J. F. and Awono-Ambene, P. and Basco, L. K. and Berry, A.},
year = {2012},
date = {2012-01-01},
journal = {Malaria journal},
volume = {11},
pages = {113},
abstract = {BACKGROUND: Regular monitoring of the levels of anti-malarial resistance of Plasmodium falciparum is an essential policy to adapt therapy and improve malaria control. This monitoring can be facilitated by using molecular tools, which are easier to implement than the classical determination of the resistance phenotype. In Cameroon, chloroquine (CQ), previously the first-line therapy for uncomplicated malaria was officially withdrawn in 2002 and replaced initially by amodiaquine (AQ) monotherapy. Then, artemisinin-based combination therapy (ACT), notably artesunate-amodiaquine (AS-AQ) or artemether-lumefantrine (AL), was gradually introduced in 2004. This situation raised the question of the evolution of P. falciparum resistance molecular markers in Yaounde, a highly urbanized Cameroonian city. METHODS: The genotype of pfcrt 72 and 76 and pfmdr1 86 alleles and pfmdr1 copy number were determined using real-time PCR in 447 P. falciparum samples collected between 2005 and 2009. RESULTS: This study showed a high prevalence of parasites with mutant pfcrt 76 (83%) and pfmdr1 86 (93%) codons. On the contrary, no mutations in the pfcrt 72 codon and no samples with duplication of the pfmdr1 gene were observed. CONCLUSION: The high prevalence of mutant pfcrt 76T and pfmdr1 86Y alleles might be due to the choice of alternative drugs (AQ and AS-AQ) known to select such genotypes. Mutant pfcrt 72 codon was not detected despite the prolonged use of AQ either as monotherapy or combined with artesunate. The absence of pfmdr1 multicopies suggests that AL would still remain efficient. The limited use of mefloquine or the predominance of mutant pfmdr1 86Y codon could explain the lack of pfmdr1 amplification. Indeed, this mutant codon is rarely associated with duplication of pfmdr1 gene. In Cameroon, the changes of therapeutic strategies and the simultaneous use of several formulations of ACT or other anti-malarials that are not officially recommended result in a complex selective pressure, rendering the prediction of the evolution of P. falciparum resistance difficult. This public health problem should lead to increased vigilance and regular monitoring.},
note = {Apr 12;11:113.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
BACKGROUND: Regular monitoring of the levels of anti-malarial resistance of Plasmodium falciparum is an essential policy to adapt therapy and improve malaria control. This monitoring can be facilitated by using molecular tools, which are easier to implement than the classical determination of the resistance phenotype. In Cameroon, chloroquine (CQ), previously the first-line therapy for uncomplicated malaria was officially withdrawn in 2002 and replaced initially by amodiaquine (AQ) monotherapy. Then, artemisinin-based combination therapy (ACT), notably artesunate-amodiaquine (AS-AQ) or artemether-lumefantrine (AL), was gradually introduced in 2004. This situation raised the question of the evolution of P. falciparum resistance molecular markers in Yaounde, a highly urbanized Cameroonian city. METHODS: The genotype of pfcrt 72 and 76 and pfmdr1 86 alleles and pfmdr1 copy number were determined using real-time PCR in 447 P. falciparum samples collected between 2005 and 2009. RESULTS: This study showed a high prevalence of parasites with mutant pfcrt 76 (83%) and pfmdr1 86 (93%) codons. On the contrary, no mutations in the pfcrt 72 codon and no samples with duplication of the pfmdr1 gene were observed. CONCLUSION: The high prevalence of mutant pfcrt 76T and pfmdr1 86Y alleles might be due to the choice of alternative drugs (AQ and AS-AQ) known to select such genotypes. Mutant pfcrt 72 codon was not detected despite the prolonged use of AQ either as monotherapy or combined with artesunate. The absence of pfmdr1 multicopies suggests that AL would still remain efficient. The limited use of mefloquine or the predominance of mutant pfmdr1 86Y codon could explain the lack of pfmdr1 amplification. Indeed, this mutant codon is rarely associated with duplication of pfmdr1 gene. In Cameroon, the changes of therapeutic strategies and the simultaneous use of several formulations of ACT or other anti-malarials that are not officially recommended result in a complex selective pressure, rendering the prediction of the evolution of P. falciparum resistance difficult. This public health problem should lead to increased vigilance and regular monitoring. |
Henry, Julie; Toulza, Eve; Hsu, Chiung-Yueh; Pellerin, Laurence; Balica, Stefana; Mazereeuw-Hautier, Juliette; Paul, Carle; Serre, Guy; Jonca, Nathalie; Simon, Michel Update on the epidermal differentiation complex. Journal Article In: Frontiers in bioscience (Landmark edition), vol. 17, pp. 1517–1532, 2012, ISSN: 1093-4715 (Electronic). @article{Henry2012,
title = {Update on the epidermal differentiation complex.},
author = {Henry, Julie and Toulza, Eve and Hsu, Chiung-Yueh and Pellerin, Laurence and Balica, Stefana and Mazereeuw-Hautier, Juliette and Paul, Carle and Serre, Guy and Jonca, Nathalie and Simon, Michel},
doi = {10.2741/4001},
issn = {1093-4715 (Electronic)},
year = {2012},
date = {2012-01-01},
journal = {Frontiers in bioscience (Landmark edition)},
volume = {17},
pages = {1517--1532},
abstract = {On human chromosome 1q21, a 2-Mb region called the epidermal differentiation complex comprises many genes encoding structural and regulatory proteins that are of crucial importance for keratinocyte differentiation and stratum corneum properties. Apart from those for involucrin and loricrin, most of the genes are organized in four families: the genes encoding EF-hand calcium-binding proteins of the S100A family, the genes encoding the small proline rich proteins (SPRRs) and the late cornified envelope (LCE) proteins, two families of cornified cell envelope components, and the genes encoding the S100-fused type proteins (SFTPs). This review focuses on the SPRRs, LCE proteins and SFTPs. It describes their structures, their specific functions and, when known, the mechanisms involved in the regulation of their expression. It also highlights their possible involvement in skin diseases.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
On human chromosome 1q21, a 2-Mb region called the epidermal differentiation complex comprises many genes encoding structural and regulatory proteins that are of crucial importance for keratinocyte differentiation and stratum corneum properties. Apart from those for involucrin and loricrin, most of the genes are organized in four families: the genes encoding EF-hand calcium-binding proteins of the S100A family, the genes encoding the small proline rich proteins (SPRRs) and the late cornified envelope (LCE) proteins, two families of cornified cell envelope components, and the genes encoding the S100-fused type proteins (SFTPs). This review focuses on the SPRRs, LCE proteins and SFTPs. It describes their structures, their specific functions and, when known, the mechanisms involved in the regulation of their expression. It also highlights their possible involvement in skin diseases. |
Chevalier, Grégoire; Suberbielle, Elsa; Monnet, Céline; Duplan, Valérie; Martin-Blondel, Guillaume; Farrugia, Fanny; Masson, Gwendal Le; Liblau, Roland; Gonzalez-Dunia, Daniel Neurons are MHC Class I-Dependent Targets for CD8 T Cells upon Neurotropic Viral Infection Journal Article In: PLoS Pathog, vol. 7, no. 11, 2011, ISSN: 1553-7374. @article{Chevalier2011,
title = {Neurons are MHC Class I-Dependent Targets for CD8 T Cells upon Neurotropic Viral Infection},
author = {Grégoire Chevalier and Elsa Suberbielle and Céline Monnet and Valérie Duplan and Guillaume Martin-Blondel and Fanny Farrugia and Gwendal Le Masson and Roland Liblau and Daniel Gonzalez-Dunia},
editor = {Glenn F. Rall},
doi = {10.1371/journal.ppat.1002393},
issn = {1553-7374},
year = {2011},
date = {2011-11-17},
urldate = {2011-11-17},
journal = {PLoS Pathog},
volume = {7},
number = {11},
publisher = {Public Library of Science (PLoS)},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Mazereeuw-Hautier, J; Leclerc, E A; Simon, M; Serre, G; Jonca, N A novel mutation in CDSN causes peeling skin disease in a patient from Morocco. Journal Article In: British journal of dermatology, vol. 165, no. 5, pp. 1152–1155, 2011, ISSN: 1365-2133 (Electronic). @article{Mazereeuw-Hautier2011,
title = {A novel mutation in CDSN causes peeling skin disease in a patient from Morocco.},
author = {Mazereeuw-Hautier, J and Leclerc, E A and Simon, M and Serre, G and Jonca, N},
doi = {10.1111/j.1365-2133.2011.10529.x},
issn = {1365-2133 (Electronic)},
year = {2011},
date = {2011-11-01},
booktitle = {The British journal of dermatology},
journal = {British journal of dermatology},
volume = {165},
number = {5},
pages = {1152--1155},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Bodemer, C; Bourrat, E; Mazereeuw-Hautier, J; Boralevi, F; Barbarot, S; Bessis, D; Blanchet-Bardon, C; Bourdon-Lanoy, E; Stalder, J-F; Ribet, V; Guerrero, D; Sibaud, V Short- and medium-term efficacy of specific hydrotherapy in inherited ichthyosis. Journal Article In: The British journal of dermatology, vol. 165, no. 5, pp. 1087–1094, 2011, ISSN: 1365-2133 (Electronic). @article{Bodemer2011,
title = {Short- and medium-term efficacy of specific hydrotherapy in inherited ichthyosis.},
author = {Bodemer, C and Bourrat, E and Mazereeuw-Hautier, J and Boralevi, F and Barbarot, S and Bessis, D and Blanchet-Bardon, C and Bourdon-Lanoy, E and Stalder, J-F and Ribet, V and Guerrero, D and Sibaud, V},
doi = {10.1111/j.1365-2133.2011.10510.x},
issn = {1365-2133 (Electronic)},
year = {2011},
date = {2011-11-01},
journal = {The British journal of dermatology},
volume = {165},
number = {5},
pages = {1087--1094},
abstract = {BACKGROUND: Management of inherited ichthyoses is symptomatic. Despite treatment, skin symptoms have a major impact on patients' quality of life (QoL). OBJECTIVES: To assess the short- and medium-term efficacy of hydrotherapy on QoL and clinical symptoms of patients with inherited ichthyosis. METHODS: In this 9-month prospective, open-label, multicentre study, 20 children and 24 adults with ichthyosis were enrolled in several French reference and competence centres, 2 months before undergoing a 3-week treatment with specific hydrotherapeutic management at Avène Hydrotherapy Centre. At baseline (2 months before hydrotherapy), beginning (D0) and end of hydrotherapy (D18), and 3 and 6 months later at the reference and competence centres, patients self-assessed QoL using the Dermatology Life Quality Index (DLQI) or its paediatric version (Children's DLQI), and investigators evaluated ichthyosis severity using a specific clinical ichthyosis score. RESULTS: The DLQI scores were significantly improved not only at the end of the hydrotherapy treatment (-56% vs. baseline; mean ± SD 3textperiodcentered59 ± 4textperiodcentered30 at D18 vs. 8textperiodcentered35 ± 5textperiodcentered71 at D0; P textless 0textperiodcentered0001), but also at 3 months (-28% vs. baseline; P = 0textperiodcentered01) and 6 months after hydrotherapy (-26% vs. baseline; mean ± SD 5textperiodcentered21 ± 5textperiodcentered11 vs. 6textperiodcentered89 ± 5textperiodcentered38; P = 0textperiodcentered03) (primary criterion). Clinical symptoms were also significantly improved at all post-treatment visits, with a decrease of the mean clinical ichthyosis score by -38% between D0 and D18, by -30% at 3 months and by -31% at 6 months vs. baseline. CONCLUSIONS: A 3-week treatment at Avène Hydrotherapy Centre provided significant and persisting improvement of QoL and clinical symptoms in patients with inherited ichthyoses.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
BACKGROUND: Management of inherited ichthyoses is symptomatic. Despite treatment, skin symptoms have a major impact on patients' quality of life (QoL). OBJECTIVES: To assess the short- and medium-term efficacy of hydrotherapy on QoL and clinical symptoms of patients with inherited ichthyosis. METHODS: In this 9-month prospective, open-label, multicentre study, 20 children and 24 adults with ichthyosis were enrolled in several French reference and competence centres, 2 months before undergoing a 3-week treatment with specific hydrotherapeutic management at Avène Hydrotherapy Centre. At baseline (2 months before hydrotherapy), beginning (D0) and end of hydrotherapy (D18), and 3 and 6 months later at the reference and competence centres, patients self-assessed QoL using the Dermatology Life Quality Index (DLQI) or its paediatric version (Children's DLQI), and investigators evaluated ichthyosis severity using a specific clinical ichthyosis score. RESULTS: The DLQI scores were significantly improved not only at the end of the hydrotherapy treatment (-56% vs. baseline; mean ± SD 3textperiodcentered59 ± 4textperiodcentered30 at D18 vs. 8textperiodcentered35 ± 5textperiodcentered71 at D0; P textless 0textperiodcentered0001), but also at 3 months (-28% vs. baseline; P = 0textperiodcentered01) and 6 months after hydrotherapy (-26% vs. baseline; mean ± SD 5textperiodcentered21 ± 5textperiodcentered11 vs. 6textperiodcentered89 ± 5textperiodcentered38; P = 0textperiodcentered03) (primary criterion). Clinical symptoms were also significantly improved at all post-treatment visits, with a decrease of the mean clinical ichthyosis score by -38% between D0 and D18, by -30% at 3 months and by -31% at 6 months vs. baseline. CONCLUSIONS: A 3-week treatment at Avène Hydrotherapy Centre provided significant and persisting improvement of QoL and clinical symptoms in patients with inherited ichthyoses. |
Lyoumi, Saïd; Abitbol, Marie; Rainteau, Dominique; Karim, Zoubida; Bernex, Florence; Oustric, Vincent; Millot, Sarah; Lettéron, Philippe; Heming, Nicholas; Guillmot, Laurent; Montagutelli, Xavier; Berdeaux, Gilles; Gouya, Laurent; Poupon, Raoul; Deybach, Jean-Charles; Beaumont, Carole; Puy, Hervé Protoporphyrin retention in hepatocytes and Kupffer cells prevents sclerosing cholangitis in erythropoietic protoporphyria mouse model Journal Article In: Gastroenterology, vol. 141, no. 4, pp. 1509–1519, 1519.e1–3, 2011, ISSN: 1528-0012. @article{lyoumi_protoporphyrin_2011,
title = {Protoporphyrin retention in hepatocytes and Kupffer cells prevents sclerosing cholangitis in erythropoietic protoporphyria mouse model},
author = {Lyoumi, Saïd and Abitbol, Marie and Rainteau, Dominique and Karim, Zoubida and Bernex, Florence and Oustric, Vincent and Millot, Sarah and Lettéron, Philippe and Heming, Nicholas and Guillmot, Laurent and Montagutelli, Xavier and Berdeaux, Gilles and Gouya, Laurent and Poupon, Raoul and Deybach, Jean-Charles and Beaumont, Carole and Puy, Hervé},
doi = {10.1053/j.gastro.2011.06.078},
issn = {1528-0012},
year = {2011},
date = {2011-10-01},
journal = {Gastroenterology},
volume = {141},
number = {4},
pages = {1509--1519, 1519.e1--3},
abstract = {BACKGROUND & AIMS: Chronic, progressive hepatobiliary disease is the most severe complication of erythropoietic protoporphyria (EPP) and can require liver transplantation, although the mechanisms that lead to liver failure are unknown. We characterized protoporphyrin-IX (PPIX)-linked hepatobiliary disease in BALB/c and C57BL/6 (Fechm1Pas) mice with mutations in ferrochelatase as models for EPP.
METHODS: Fechm1Pas and wild-type (control) mice were studied at 12-14 weeks of age. PPIX was quantified; its distribution in the liver, serum levels of lipoprotein-X, liver histology, contents of bile salt and cholesterol phospholipids, and expression of genes were compared in mice of the BALB/c and C57BL/6 backgrounds. The in vitro binding affinity of PPIX for bile components was determined.
RESULTS: Compared with mice of the C57BL/6 background, BALB/c Fechm1Pas mice had a more severe pattern of cholestasis, fibrosis with portoportal bridging, bile acid regurgitation, sclerosing cholangitis, and hepatolithiasis. In C57BL/6 Fechm1Pas mice, PPIX was sequestrated mainly in the cytosol of hepatocytes and Kupffer cells, whereas, in BALB/c Fechm1Pas mice, PPIX was localized within enlarged bile canaliculi. Livers of C57BL/6 Fechm1Pas mice were protected through a combination of lower efflux of PPIX and reduced synthesis and export of bile acid.
CONCLUSIONS: PPIX binds to bile components and disrupts the physiologic equilibrium of phospholipids, bile acids, and cholesterol in bile. This process might be involved in pathogenesis of sclerosing cholangitis from EPP; a better understanding might improve diagnosis and development of reagents to treat or prevent liver failure in patients with EPP.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
BACKGROUND & AIMS: Chronic, progressive hepatobiliary disease is the most severe complication of erythropoietic protoporphyria (EPP) and can require liver transplantation, although the mechanisms that lead to liver failure are unknown. We characterized protoporphyrin-IX (PPIX)-linked hepatobiliary disease in BALB/c and C57BL/6 (Fechm1Pas) mice with mutations in ferrochelatase as models for EPP.
METHODS: Fechm1Pas and wild-type (control) mice were studied at 12-14 weeks of age. PPIX was quantified; its distribution in the liver, serum levels of lipoprotein-X, liver histology, contents of bile salt and cholesterol phospholipids, and expression of genes were compared in mice of the BALB/c and C57BL/6 backgrounds. The in vitro binding affinity of PPIX for bile components was determined.
RESULTS: Compared with mice of the C57BL/6 background, BALB/c Fechm1Pas mice had a more severe pattern of cholestasis, fibrosis with portoportal bridging, bile acid regurgitation, sclerosing cholangitis, and hepatolithiasis. In C57BL/6 Fechm1Pas mice, PPIX was sequestrated mainly in the cytosol of hepatocytes and Kupffer cells, whereas, in BALB/c Fechm1Pas mice, PPIX was localized within enlarged bile canaliculi. Livers of C57BL/6 Fechm1Pas mice were protected through a combination of lower efflux of PPIX and reduced synthesis and export of bile acid.
CONCLUSIONS: PPIX binds to bile components and disrupts the physiologic equilibrium of phospholipids, bile acids, and cholesterol in bile. This process might be involved in pathogenesis of sclerosing cholangitis from EPP; a better understanding might improve diagnosis and development of reagents to treat or prevent liver failure in patients with EPP. |
Hsu, Chiung-Yueh; Henry, Julie; Raymond, Anne-Aurélie; Méchin, Marie-Claire; Pendaries, Valérie; Nassar, Dany; Hansmann, Britta; Balica, Stéfana; Burlet-Schiltz, Odile; Schmitt, Anne-Marie; Takahara, Hidenari; Paul, Carle; Serre, Guy; Simon, Michel Deimination of human filaggrin-2 promotes its proteolysis by calpain 1. Journal Article In: The Journal of biological chemistry, vol. 286, no. 26, pp. 23222–23233, 2011, ISSN: 1083-351X (Electronic). @article{Hsu2011,
title = {Deimination of human filaggrin-2 promotes its proteolysis by calpain 1.},
author = {Hsu, Chiung-Yueh and Henry, Julie and Raymond, Anne-Aurélie and Méchin, Marie-Claire and Pendaries, Valérie and Nassar, Dany and Hansmann, Britta and Balica, Stéfana and Burlet-Schiltz, Odile and Schmitt, Anne-Marie and Takahara, Hidenari and Paul, Carle and Serre, Guy and Simon, Michel},
doi = {10.1074/jbc.M110.197400},
issn = {1083-351X (Electronic)},
year = {2011},
date = {2011-07-01},
journal = {The Journal of biological chemistry},
volume = {286},
number = {26},
pages = {23222--23233},
abstract = {Filaggrin-2 (FLG2), a member of the S100-fused type protein family, shares numerous features with filaggrin (FLG), a key protein implicated in the epidermal barrier functions. Both display a related structural organization, an identical pattern of expression and localization in human epidermis, and proteolytic processing of a large precursor. Here, we tested whether FLG2 was a substrate of calpain 1, a calcium-dependent protease directly involved in FLG catabolism. In addition, deimination being critical for FLG degradation, we analyzed whether FLG2 deimination interfered with its proteolytic processing. With this aim, we first produced a recombinant form of FLG2 corresponding to subunits B7 to B10 fused to a COOH-terminal His tag. Incubation with calpain 1 in the presence of calcium induced a rapid degradation of the recombinant protein and the production of several peptides, as shown by Coomassie Blue-stained gels and Western blotting with anti-FLG2 or anti-His antibodies. MALDI-TOF mass spectrometry confirmed this result and further evidenced the production of non-immunoreactive smaller peptides. The degradation was not observed when a calpain 1-specific inhibitor was added. The calpain cleavage sites identified by Edman degradation were regularly present in the B-type repeats of FLG2. Moreover, immunohistochemical analysis of normal human skin revealed colocalization of FLG2 and calpain 1 in the upper epidermis. Finally, the FLG2 deiminated by human peptidylarginine deiminases was shown to be more susceptible to calpain 1 than the unmodified protein. Altogether, these data demonstrate that calpain 1 is essential for the proteolytic processing of FLG2 and that deimination accelerates this process.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Filaggrin-2 (FLG2), a member of the S100-fused type protein family, shares numerous features with filaggrin (FLG), a key protein implicated in the epidermal barrier functions. Both display a related structural organization, an identical pattern of expression and localization in human epidermis, and proteolytic processing of a large precursor. Here, we tested whether FLG2 was a substrate of calpain 1, a calcium-dependent protease directly involved in FLG catabolism. In addition, deimination being critical for FLG degradation, we analyzed whether FLG2 deimination interfered with its proteolytic processing. With this aim, we first produced a recombinant form of FLG2 corresponding to subunits B7 to B10 fused to a COOH-terminal His tag. Incubation with calpain 1 in the presence of calcium induced a rapid degradation of the recombinant protein and the production of several peptides, as shown by Coomassie Blue-stained gels and Western blotting with anti-FLG2 or anti-His antibodies. MALDI-TOF mass spectrometry confirmed this result and further evidenced the production of non-immunoreactive smaller peptides. The degradation was not observed when a calpain 1-specific inhibitor was added. The calpain cleavage sites identified by Edman degradation were regularly present in the B-type repeats of FLG2. Moreover, immunohistochemical analysis of normal human skin revealed colocalization of FLG2 and calpain 1 in the upper epidermis. Finally, the FLG2 deiminated by human peptidylarginine deiminases was shown to be more susceptible to calpain 1 than the unmodified protein. Altogether, these data demonstrate that calpain 1 is essential for the proteolytic processing of FLG2 and that deimination accelerates this process. |
Jonca, Nathalie; Caubet, Cécile; Leclerc, Emilie A; Guerrin, Marina; Simon, Michel; Serre, Guy Protease sensitivity of corneodesmosin variants encoded by the six more common CDSN haplotypes. Journal Article In: The journal of investigative dermatology, vol. 131, no. 6, pp. 1381–1384, 2011, ISSN: 1523-1747 (Electronic). @article{Jonca2011,
title = {Protease sensitivity of corneodesmosin variants encoded by the six more common CDSN haplotypes.},
author = {Jonca, Nathalie and Caubet, Cécile and Leclerc, Emilie A and Guerrin, Marina and Simon, Michel and Serre, Guy},
doi = {10.1038/jid.2011.7},
issn = {1523-1747 (Electronic)},
year = {2011},
date = {2011-06-01},
booktitle = {The Journal of investigative dermatology},
journal = {The journal of investigative dermatology},
volume = {131},
number = {6},
pages = {1381--1384},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Viret, C.; Leung-Theung-Long, S.; Serre, L.; C.and Vignali Lamare, D. A. and Malissen; Carrier, A.; Guerder, S. Thymus-specific serine protease controls autoreactive CD4 T cell development and autoimmune diabetes in mice. Journal Article In: J Clin Invest , vol. 121, no. 5, pp. 1810-1821, 2011. @article{Viret2011,
title = { Thymus-specific serine protease controls autoreactive CD4 T cell development and autoimmune diabetes in mice.},
author = {Viret, C. and Leung-Theung-Long, S. and Serre, L. and Lamare, C.and Vignali, D.A.and Malissen, B. and Carrier, A. and Guerder, S. },
url = {https://www.ncbi.nlm.nih.gov/pubmed/?term=Thymus-specific+serine+protease+controls+autoreactive+CD4+T+cell+development+and+autoimmune+diabetes+in+mice.},
doi = { 10.1172/JCI43314},
year = {2011},
date = {2011-05-01},
journal = {J Clin Invest },
volume = {121},
number = {5},
pages = {1810-1821},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Henry, Julie; Hsu, Chiung-Yueh; Haftek, Marek; Nachat, Rachida; de Koning, Heleen D; Gardinal-Galera, Isabelle; Hitomi, Kiyotaka; Balica, Stéfana; Jean-Decoster, Catherine; Schmitt, Anne-Marie; Paul, Carle; Serre, Guy; Simon, Michel Hornerin is a component of the epidermal cornified cell envelopes. Journal Article In: FASEB journal : official publication of the Federation of American Societies for Experimental Biology, vol. 25, no. 5, pp. 1567–1576, 2011, ISSN: 1530-6860 (Electronic). @article{Henry2011,
title = {Hornerin is a component of the epidermal cornified cell envelopes.},
author = {Henry, Julie and Hsu, Chiung-Yueh and Haftek, Marek and Nachat, Rachida and de Koning, Heleen D and Gardinal-Galera, Isabelle and Hitomi, Kiyotaka and Balica, Stéfana and Jean-Decoster, Catherine and Schmitt, Anne-Marie and Paul, Carle and Serre, Guy and Simon, Michel},
doi = {10.1096/fj.10-168658},
issn = {1530-6860 (Electronic)},
year = {2011},
date = {2011-05-01},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {25},
number = {5},
pages = {1567--1576},
abstract = {A single-nucleotide polymorphism within the gene encoding hornerin (HRNR) has recently been linked with atopic dermatitis (AD) susceptibility. HRNR shares features with filaggrin, a key protein for keratinocyte differentiation, but conflicting reports have been published concerning its expression in the epidermis, and its role is still unknown. To analyze HRNR expression and function in the epidermis, anti-HRNR antibodies were produced and used in Western blot analysis and immunohistochemical, confocal, and immunoelectron microscopy analyses of human skin and of cornified cell envelopes purified from plantar stratum corneum. We also tested whether HRNR was a substrate of transglutaminases. In the epidermis, HRNR was detected at the periphery of keratohyalin granules in the upper granular layer and at the corneocyte periphery in the whole cornified layer. Detected in Western blot analysis as numerous bands, HRNR was relatively insoluble and only extracted from epidermis with urea and/or reducing agents. The presence of HRNR in the purified envelopes was confirmed by immunoelectron microscopy and by Western blot analysis after V8-protease digestion. HRNR was shown to be a substrate of transglutaminase 3. These data demonstrate that HRNR is a component of cornified cell envelopes of human epidermis. Its reduced expression in AD may contribute to the epidermal barrier defect observed in the disease.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
A single-nucleotide polymorphism within the gene encoding hornerin (HRNR) has recently been linked with atopic dermatitis (AD) susceptibility. HRNR shares features with filaggrin, a key protein for keratinocyte differentiation, but conflicting reports have been published concerning its expression in the epidermis, and its role is still unknown. To analyze HRNR expression and function in the epidermis, anti-HRNR antibodies were produced and used in Western blot analysis and immunohistochemical, confocal, and immunoelectron microscopy analyses of human skin and of cornified cell envelopes purified from plantar stratum corneum. We also tested whether HRNR was a substrate of transglutaminases. In the epidermis, HRNR was detected at the periphery of keratohyalin granules in the upper granular layer and at the corneocyte periphery in the whole cornified layer. Detected in Western blot analysis as numerous bands, HRNR was relatively insoluble and only extracted from epidermis with urea and/or reducing agents. The presence of HRNR in the purified envelopes was confirmed by immunoelectron microscopy and by Western blot analysis after V8-protease digestion. HRNR was shown to be a substrate of transglutaminase 3. These data demonstrate that HRNR is a component of cornified cell envelopes of human epidermis. Its reduced expression in AD may contribute to the epidermal barrier defect observed in the disease. |
Jonca, Nathalie; Leclerc, Emilie A; Caubet, Cécile; Simon, Michel; Guerrin, Marina; Serre, Guy Corneodesmosomes and corneodesmosin: from the stratum corneum cohesion to the pathophysiology of genodermatoses. Journal Article In: European journal of dermatology : EJD, vol. 21 Suppl 2, pp. 35–42, 2011, ISSN: 1167-1122 (Print). @article{Jonca2011b,
title = {Corneodesmosomes and corneodesmosin: from the stratum corneum cohesion to the pathophysiology of genodermatoses.},
author = {Jonca, Nathalie and Leclerc, Emilie A and Caubet, Cécile and Simon, Michel and Guerrin, Marina and Serre, Guy},
doi = {10.1684/ejd.2011.1264},
issn = {1167-1122 (Print)},
year = {2011},
date = {2011-05-01},
journal = {European journal of dermatology : EJD},
volume = {21 Suppl 2},
pages = {35--42},
abstract = {Corneodesmosin (CDSN) was identified 20 years ago by raising monoclonal antibodies against human plantar stratum corneum. The protein is specific to corneodesmosomes, cell-junction structures that, in humans, are found in the epidermis, the hard palate epithelium, and the inner root sheath of the hair follicles. Synthesized by the granular keratinocytes and secreted via the lamellar bodies, CDSN is incorporated into the desmoglea of the desmosomes, shortly before their transformation into corneodesmosomes during cornification. CDSN displays adhesive properties, mostly attributable to its N-terminal glycine-rich domain, and is sequentially proteolyzed as corneocytes migrate towards the skin surface prior to desquamation. The recent inactivation of Cdsn in mice induced a lethal epidermal barrier disruption and hair follicle degeneration, related to corneodesmosome dysfunction. That confirmed the essential role of the protein in maintaining integrity of the epidermis and the hair follicle. The CDSN gene is located in PSORS1, the major psoriasis susceptibility locus on the chromosome 6, but to date its involvement in the disease pathophysiology is not clear. By contrast, two different monogenic diseases associated with nonsense mutations in CDSN, were recently identified. First, hypotrichosis simplex of the scalp in which mutated CDSN accumulates in the dermis and forms amyloid deposits; then, peeling skin disease in which the genetic defect induces dyscohesion of the stratum corneum, responsible for abnormal desquamation and increased skin penetration of allergens.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Corneodesmosin (CDSN) was identified 20 years ago by raising monoclonal antibodies against human plantar stratum corneum. The protein is specific to corneodesmosomes, cell-junction structures that, in humans, are found in the epidermis, the hard palate epithelium, and the inner root sheath of the hair follicles. Synthesized by the granular keratinocytes and secreted via the lamellar bodies, CDSN is incorporated into the desmoglea of the desmosomes, shortly before their transformation into corneodesmosomes during cornification. CDSN displays adhesive properties, mostly attributable to its N-terminal glycine-rich domain, and is sequentially proteolyzed as corneocytes migrate towards the skin surface prior to desquamation. The recent inactivation of Cdsn in mice induced a lethal epidermal barrier disruption and hair follicle degeneration, related to corneodesmosome dysfunction. That confirmed the essential role of the protein in maintaining integrity of the epidermis and the hair follicle. The CDSN gene is located in PSORS1, the major psoriasis susceptibility locus on the chromosome 6, but to date its involvement in the disease pathophysiology is not clear. By contrast, two different monogenic diseases associated with nonsense mutations in CDSN, were recently identified. First, hypotrichosis simplex of the scalp in which mutated CDSN accumulates in the dermis and forms amyloid deposits; then, peeling skin disease in which the genetic defect induces dyscohesion of the stratum corneum, responsible for abnormal desquamation and increased skin penetration of allergens. |
Brasse-Lagnel, Carole; Karim, Zoubida; Letteron, Philippe; Bekri, Soumeya; Bado, André; Beaumont, Carole Intestinal DMT1 cotransporter is down-regulated by hepcidin via proteasome internalization and degradation Journal Article In: Gastroenterology, vol. 140, no. 4, pp. 1261–1271.e1, 2011, ISSN: 1528-0012. @article{brasse-lagnel_intestinal_2011,
title = {Intestinal DMT1 cotransporter is down-regulated by hepcidin via proteasome internalization and degradation},
author = {Brasse-Lagnel, Carole and Karim, Zoubida and Letteron, Philippe and Bekri, Soumeya and Bado, André and Beaumont, Carole},
doi = {10.1053/j.gastro.2010.12.037},
issn = {1528-0012},
year = {2011},
date = {2011-04-01},
journal = {Gastroenterology},
volume = {140},
number = {4},
pages = {1261--1271.e1},
abstract = {BACKGROUNDS & AIMS: The mechanism by which hepcidin regulates iron export from macrophages has been well established and is believed to involve degradation of ferroportin. However, in the small intestine, hepcidin's mechanisms of action are not known. We studied human polarized intestinal (Caco-2/TC7) cells and mouse duodenal segments, ex vivo, to investigate the molecular mechanisms by which hepcidin down-regulates intestinal transepithelial iron transport.
METHODS: Iron transport was analyzed using ⁵⁵FeNTA. Expression of Divalent Metal Transporter 1 (DMT1) and ferroportin was evaluated by reverse-transcription quantitative polymerase chain reaction and immunoblotting. Videomicroscopy analysis was performed on live cells that expressed either DMT1 or ferroportin fused to green fluorescent protein.
RESULTS: In Caco-2/TC7 cells, physiologic doses of hepcidin (50-1000 nmol/L) inhibited transport of ⁵⁵Fe in a dose-dependent manner; a half-maximum effect was observed at 75-100 nmol/L. However, 200 nmol/L hepcidin induced a significant decrease in DMT1 protein expression but no change in ferroportin protein levels, unlike macrophages. This result was confirmed ex vivo in isolated duodenal segments: 200 nmol/L hepcidin induced a significant reduction in iron transport and DMT1 protein levels but no change in ferroportin levels. In Caco-2/TC7 cells, the effect of hepcidin on the DMT1 protein level was completely abolished in the presence of a proteasome inhibitor (MG-132); DMT1 ubiquitination was induced by the addition of hepcidin.
CONCLUSIONS: An acute increase in hepcidin concentration reduces intestinal iron absorption through ubiquitin-dependent proteasome degradation of DMT1.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
BACKGROUNDS & AIMS: The mechanism by which hepcidin regulates iron export from macrophages has been well established and is believed to involve degradation of ferroportin. However, in the small intestine, hepcidin's mechanisms of action are not known. We studied human polarized intestinal (Caco-2/TC7) cells and mouse duodenal segments, ex vivo, to investigate the molecular mechanisms by which hepcidin down-regulates intestinal transepithelial iron transport.
METHODS: Iron transport was analyzed using ⁵⁵FeNTA. Expression of Divalent Metal Transporter 1 (DMT1) and ferroportin was evaluated by reverse-transcription quantitative polymerase chain reaction and immunoblotting. Videomicroscopy analysis was performed on live cells that expressed either DMT1 or ferroportin fused to green fluorescent protein.
RESULTS: In Caco-2/TC7 cells, physiologic doses of hepcidin (50-1000 nmol/L) inhibited transport of ⁵⁵Fe in a dose-dependent manner; a half-maximum effect was observed at 75-100 nmol/L. However, 200 nmol/L hepcidin induced a significant decrease in DMT1 protein expression but no change in ferroportin protein levels, unlike macrophages. This result was confirmed ex vivo in isolated duodenal segments: 200 nmol/L hepcidin induced a significant reduction in iron transport and DMT1 protein levels but no change in ferroportin levels. In Caco-2/TC7 cells, the effect of hepcidin on the DMT1 protein level was completely abolished in the presence of a proteasome inhibitor (MG-132); DMT1 ubiquitination was induced by the addition of hepcidin.
CONCLUSIONS: An acute increase in hepcidin concentration reduces intestinal iron absorption through ubiquitin-dependent proteasome degradation of DMT1. |
Leclerc, Emilie A; Gazeilles, Leila; Serre, Guy; Guerrin, Marina; Jonca, Nathalie The ubiquitous dermokine delta activates Rab5 function in the early endocytic pathway. Journal Article In: PloS one, vol. 6, no. 3, pp. e17816, 2011, ISSN: 1932-6203 (Electronic). @article{Leclerc2011,
title = {The ubiquitous dermokine delta activates Rab5 function in the early endocytic pathway.},
author = {Leclerc, Emilie A and Gazeilles, Leila and Serre, Guy and Guerrin, Marina and Jonca, Nathalie},
doi = {10.1371/journal.pone.0017816},
issn = {1932-6203 (Electronic)},
year = {2011},
date = {2011-03-01},
journal = {PloS one},
volume = {6},
number = {3},
pages = {e17816},
abstract = {The expression of the recently identified dermokine (Dmkn) gene leads to four families of proteins with as yet unknown functions. The secreted $alpha$, $beta$ and $gamma$ isoforms share an epidermis-restricted expression pattern, whereas the $delta$ isoform is intracellular and ubiquitous. To get an insight into Dmkn$delta$ function, we performed yeast two-hybrid screening and identified the small GTPases Rab5 as partners for Dmkn$delta$. The Rab5 proteins are known to regulate membrane docking and fusion in the early endocytic pathway. GST pull-down assays confirmed the direct interaction between Rab5 and Dmkn$delta$. Transient expression of Dmkn$delta$ in HeLa cells led to the formation of punctate structures colocalized with endogenous Rab5 and clathrin, indicating Dmkn$delta$ involvement in the early steps of endocytosis. Dmkn$delta$ indeed colocalized with transferrin at early stages of endocytosis, but did not modulate its endocytosis or recycling kinetics. We also showed that Dmkn$delta$ was able to bind both inactive (GDP-bound) and active (GTP-bound) forms of Rab5 in vitro but preferentially targeted GDP-bound form in HeLa cells. Interestingly, Dmkn$delta$ expression rescued the Rab5S34N-mediated inhibition of endosome fusion. Moreover, Dmkn$delta$ caused the enlargement of vesicles positive for Rab5 by promoting GTP loading onto the small GTPase. Together our data reveal that Dmkn$delta$ activates Rab5 function and thus is involved in the early endosomal trafficking.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The expression of the recently identified dermokine (Dmkn) gene leads to four families of proteins with as yet unknown functions. The secreted $alpha$, $beta$ and $gamma$ isoforms share an epidermis-restricted expression pattern, whereas the $delta$ isoform is intracellular and ubiquitous. To get an insight into Dmkn$delta$ function, we performed yeast two-hybrid screening and identified the small GTPases Rab5 as partners for Dmkn$delta$. The Rab5 proteins are known to regulate membrane docking and fusion in the early endocytic pathway. GST pull-down assays confirmed the direct interaction between Rab5 and Dmkn$delta$. Transient expression of Dmkn$delta$ in HeLa cells led to the formation of punctate structures colocalized with endogenous Rab5 and clathrin, indicating Dmkn$delta$ involvement in the early steps of endocytosis. Dmkn$delta$ indeed colocalized with transferrin at early stages of endocytosis, but did not modulate its endocytosis or recycling kinetics. We also showed that Dmkn$delta$ was able to bind both inactive (GDP-bound) and active (GTP-bound) forms of Rab5 in vitro but preferentially targeted GDP-bound form in HeLa cells. Interestingly, Dmkn$delta$ expression rescued the Rab5S34N-mediated inhibition of endosome fusion. Moreover, Dmkn$delta$ caused the enlargement of vesicles positive for Rab5 by promoting GTP loading onto the small GTPase. Together our data reveal that Dmkn$delta$ activates Rab5 function and thus is involved in the early endosomal trafficking. |
Mattiuzzo, Nicolas R; Toulza, Eve; Jonca, Nathalie; Serre, Guy; Guerrin, Marina A large-scale multi-technique approach identifies forty-nine new players of keratinocyte terminal differentiation in human epidermis. Journal Article In: Experimental dermatology, vol. 20, no. 2, pp. 113–118, 2011, ISSN: 1600-0625 (Electronic). @article{Mattiuzzo2011,
title = {A large-scale multi-technique approach identifies forty-nine new players of keratinocyte terminal differentiation in human epidermis.},
author = {Mattiuzzo, Nicolas R and Toulza, Eve and Jonca, Nathalie and Serre, Guy and Guerrin, Marina},
doi = {10.1111/j.1600-0625.2010.01188.x},
issn = {1600-0625 (Electronic)},
year = {2011},
date = {2011-02-01},
journal = {Experimental dermatology},
volume = {20},
number = {2},
pages = {113--118},
abstract = {At the latest stage of terminal differentiation in the epidermis, granular keratinocytes (GKs) undergo cornification, a programmed cell death required for the establishment of a functional skin barrier. A complex genetic regulatory network orchestrates the underlying biochemical modifications, but very few transcription factors specific to this programme have been identified to date. Here, we describe a large-scale, multi-technique approach performed on cells purified from normal human epidermis, primarily focusing on the identification of regulators. We combined data from microarray analysis of cell fractions enriched in GKs or basal keratinocytes, from an expressed sequence tag (EST) library built from GKs and from an in silico promoter analysis of 52 differentiation-associated genes. Among 3576 genes potentially expressed in GK, 298 candidates were selected, and half were directly profiled for the first time in the different layers of the epidermis by quantitative real-time PCR. Forty-nine genes upregulated during terminal differentiation, associated with numerous function of GK including lipid synthesis and secretion, were identified. Of 94 transcription factors detected, 37 were found to be either positively or negatively regulated, suggesting their involvement as regulators of gene expression in the GKs. These results largely extend the number of genes known as involved in the latest step of the terminal differentiation of human epidermis as well as the number of transcription factors known to control the expression of these genes.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
At the latest stage of terminal differentiation in the epidermis, granular keratinocytes (GKs) undergo cornification, a programmed cell death required for the establishment of a functional skin barrier. A complex genetic regulatory network orchestrates the underlying biochemical modifications, but very few transcription factors specific to this programme have been identified to date. Here, we describe a large-scale, multi-technique approach performed on cells purified from normal human epidermis, primarily focusing on the identification of regulators. We combined data from microarray analysis of cell fractions enriched in GKs or basal keratinocytes, from an expressed sequence tag (EST) library built from GKs and from an in silico promoter analysis of 52 differentiation-associated genes. Among 3576 genes potentially expressed in GK, 298 candidates were selected, and half were directly profiled for the first time in the different layers of the epidermis by quantitative real-time PCR. Forty-nine genes upregulated during terminal differentiation, associated with numerous function of GK including lipid synthesis and secretion, were identified. Of 94 transcription factors detected, 37 were found to be either positively or negatively regulated, suggesting their involvement as regulators of gene expression in the GKs. These results largely extend the number of genes known as involved in the latest step of the terminal differentiation of human epidermis as well as the number of transcription factors known to control the expression of these genes. |
Vasilopoulos, Yiannis; Sharaf, Nazar; di Giovine, Franco; Simon, Michel; Cork, Michael J; Duff, Gordon W; Tazi-Ahnini, Rachid The 3'-UTR AACCins5874 in the stratum corneum chymotryptic enzyme gene (SCCE/KLK7), associated with atopic dermatitis; causes an increased mRNA expression without altering its stability. Journal Article In: Journal of dermatological science, vol. 61, no. 2, pp. 131–133, 2011, ISSN: 1873-569X (Electronic). @article{Vasilopoulos2011,
title = {The 3'-UTR AACCins5874 in the stratum corneum chymotryptic enzyme gene (SCCE/KLK7), associated with atopic dermatitis; causes an increased mRNA expression without altering its stability.},
author = {Vasilopoulos, Yiannis and Sharaf, Nazar and di Giovine, Franco and Simon, Michel and Cork, Michael J and Duff, Gordon W and Tazi-Ahnini, Rachid},
doi = {10.1016/j.jdermsci.2010.11.013},
issn = {1873-569X (Electronic)},
year = {2011},
date = {2011-02-01},
booktitle = {Journal of dermatological science},
journal = {Journal of dermatological science},
volume = {61},
number = {2},
pages = {131--133},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Viret, C.; Lamare, C.; Guiraud, M.; Fazilleau, N.; Bour, A.; Malissen, B.; Carrier, A.; Guerder, S. Thymus-specific serine protease contributes to the diversification of the functional endogenous CD4 T cell receptor repertoire. Journal Article In: J Exp Med., vol. 208, pp. 3-11, 2011. @article{Viret2011b,
title = {Thymus-specific serine protease contributes to the diversification of the functional endogenous CD4 T cell receptor repertoire. },
author = {Viret, C. and Lamare, C. and Guiraud, M. and Fazilleau, N. and Bour, A. and Malissen, B. and Carrier, A. and Guerder, S. },
url = {https://www.ncbi.nlm.nih.gov/pubmed/21173102},
doi = {10.1084/jem.20100027},
year = {2011},
date = {2011-01-17},
journal = {J Exp Med.},
volume = {208},
pages = {3-11},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Gennero, I.; Laurencin-Dalicieux, S.; Conte-Auriol, F.; Briand-Mesange, F.; Laurencin, D.; Rue, J.; Beton, N.; Malet, N.; Mus, M.; Tokumura, A.; Bourin, P.; Vico, L.; Brunel, G.; Oreffo, R. O.; Chun, J.; Salles, J. P. Absence of the lysophosphatidic acid receptor LPA1 results in abnormal bone development and decreased bone mass Journal Article In: Bone, vol. 49, no. 3, pp. 395-403, 2011, ISSN: 1873-2763 (Electronic)
1873-2763 (Linking). @article{RN21b,
title = {Absence of the lysophosphatidic acid receptor LPA1 results in abnormal bone development and decreased bone mass},
author = {Gennero, I. and Laurencin-Dalicieux, S. and Conte-Auriol, F. and Briand-Mesange, F. and Laurencin, D. and Rue, J. and Beton, N. and Malet, N. and Mus, M. and Tokumura, A. and Bourin, P. and Vico, L. and Brunel, G. and Oreffo, R. O. and Chun, J. and Salles, J. P.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/21569876},
doi = {10.1016/j.bone.2011.04.018},
issn = {1873-2763 (Electronic)
1873-2763 (Linking)},
year = {2011},
date = {2011-01-01},
journal = {Bone},
volume = {49},
number = {3},
pages = {395-403},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
