Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Haouaria Balghi"'
Autor:
Maziar Divangahi, Haouaria Balghi, Gawiyou Danialou, Alain S Comtois, Alexandre Demoule, Sheila Ernest, Christina Haston, Renaud Robert, John W Hanrahan, Danuta Radzioch, Basil J Petrof
Publikováno v:
PLoS Genetics, Vol 5, Iss 7, p e1000586 (2009)
Cystic fibrosis (CF) patients often have reduced mass and strength of skeletal muscles, including the diaphragm, the primary muscle of respiration. Here we show that lack of the CF transmembrane conductance regulator (CFTR) plays an intrinsic role in
Externí odkaz:
https://doaj.org/article/922b93df895c415bad69e05d3490893f
Publikováno v:
Journal of Biological Chemistry. 288:21815-21823
Cystic fibrosis transmembrane conductance regulator (CFTR) is a chloride (Cl−) channel, which plays an important role in physiological anion and fluid secretion, and is defective in several diseases. Although its activation by PKA and PKC has been
Autor:
Xuexin Zhang, Philippe Romeo, Julie Goepp, Mohamed Trebak, Benjamin Rappaz, Adeline Wohlhuter-Haddad, Paul W. Wiseman, David Y. Thomas, Pasquale Ferraro, Renaud Robert, John W. Hanrahan, Haouaria Balghi, Yishan Luo, Alexandra Evagelidis
Publikováno v:
FASEB journal : official publication of the Federation of American Societies for Experimental Biolog
Cystic fibrosis (CF) is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR). The most common mutation, ΔF508, causes retention of CFTR in the endoplasmic reticulum (ER). Some CF abnormalities can be explained b
Autor:
Ludivine Mondin, Stéphane Sebille, Guy Raymond, Haouaria Balghi, Anne Cantereau, Bruno Constantin, Christian Cognard
Publikováno v:
The Journal of General Physiology
Journal of General Physiology
Journal of General Physiology, Rockefeller University Press, 2006, 128 (2), pp.219-30. ⟨10.1085/jgp.200609559⟩
Journal of General Physiology, Rockefeller University Press, 2006, 128 (2), pp.219-230. ⟨10.1085/jgp.200609559⟩
Journal of General Physiology
Journal of General Physiology, Rockefeller University Press, 2006, 128 (2), pp.219-30. ⟨10.1085/jgp.200609559⟩
Journal of General Physiology, Rockefeller University Press, 2006, 128 (2), pp.219-230. ⟨10.1085/jgp.200609559⟩
International audience; We present here evidence for the enhancement, at rest, of an inositol 1,4,5-trisphosphate (IP3)-mediated calcium signaling pathway in myotubes from dystrophin-deficient cell lines (SolC1(-)) as compared to a cell line from the
Autor:
Vincent Thoreau, Bruno Constantin, Sylvie Patri, Elise Mok, Haouaria Balghi, Ludivine Mondin, Stéphane Sebille, Guy Raymond, Alain Kitzis, Christian Cognard
Publikováno v:
Journal of General Physiology
Journal of General Physiology, Rockefeller University Press, 2006, 127 (2), pp.171-82. ⟨10.1085/jgp.200509456⟩
The Journal of General Physiology
Journal of General Physiology, Rockefeller University Press, 2006, 127 (2), pp.171-82. ⟨10.1085/jgp.200509456⟩
The Journal of General Physiology
International audience; We present here evidence for the enhancement of an inositol 1,4,5-trisphosphate (IP3) mediated calcium signaling pathway in myotubes from dystrophin-deficient cell lines (SolC1(-)) as compared to a cell line from the same orig
Autor:
Haouaria Balghi, David Y. Thomas, Leanna Y. Chen, Pekka Määttänen, Kalle Gehring, Leslie A. Scarffe, Kurt Dejgaard, Babette Schade, Alexey Yu. Denisov, Gregor Jansen, William J. Muller
Chaperones and foldases in the endoplasmic reticulum (ER) ensure correct protein folding. Extensive protein-protein interaction maps have defined the organization and function of many cellular complexes, but ER complexes are under-represented. Conseq
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d032adb6289d572fee1858c25fc46104
https://europepmc.org/articles/PMC3434782/
https://europepmc.org/articles/PMC3434782/
Autor:
Donglei Zhang, Jie Liao, Graeme W. Carlile, Pierre Lesimple, Heidi M. Sampson, Haouaria Balghi, Daniel D Waller, David Y. Thomas, Romeo Phillipe, Suzana M. Anjos, Françoise Dantzer, Julie Goepp, Pasquale Ferraro, Renaud Robert, Fabiana Ciciriello, John W. Hanrahan
Publikováno v:
Frontiers in Pharmacology, Vol 3 (2012)
Frontiers in Pharmacology
Frontiers in Pharmacology
Most cystic fibrosis is caused by mutations in CFTR that prevent its trafficking from the ER to the plasma membrane and is associated with exaggerated inflammation, altered metabolism, and diminished responses to oxidative stress. PARP-1 is activated
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b7ddc7e0be07ea010971b8615f5c6f40
http://journal.frontiersin.org/article/10.3389/fphar.2012.00165/abstract
http://journal.frontiersin.org/article/10.3389/fphar.2012.00165/abstract
Publikováno v:
Biophysical Journal. 100(3)
Calcium signaling regulates many cellular processes and is upregulated in cystic fibrosis (CF) epithelial cells. Agonists stimulate Ca2+ release from ER stores and trigger the formation of a complex between the plasma membrane (PM) Ca2+ channel Orai1
Autor:
Hugo R. de Jonge, Pierre Lesimple, Bart Kus, Haouaria Balghi, Na Liu, Graeme W. Carlile, Bob J. Scholte, David Y. Thomas, John W. Hanrahan, Renaud Robert, Daniela Rotin, Jie Liao, Martina Wilke
Publikováno v:
Molecular Pharmacology, 77(6), 922-930. American Society for Pharmacology and Experimental Therapeutics
Cystic fibrosis (CF) is caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, which encodes a cAMP-activated anion channel expressed in epithelial cells. The most common mutation Delta Phe508 leads to protein misfolding, rete
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6f88ad9d5c0dcd3f00b675ef3401e5c2
https://pure.eur.nl/en/publications/d83290f0-b0c8-4175-9ce9-6da88e4d1025
https://pure.eur.nl/en/publications/d83290f0-b0c8-4175-9ce9-6da88e4d1025
Publikováno v:
American Journal of Physiology-Cell Physiology
American Journal of Physiology-Cell Physiology, American Physiological Society, 2009, 297 (5), pp.C1133-45. ⟨10.1152/ajpcell.00048.2009⟩
American Journal of Physiology-Cell Physiology, American Physiological Society, 2009, 297 (5), pp.C1133-C1145. ⟨10.1152/ajpcell.00048.2009⟩
American Journal of Physiology-Cell Physiology, American Physiological Society, 2009, 297 (5), pp.C1133-45. ⟨10.1152/ajpcell.00048.2009⟩
American Journal of Physiology-Cell Physiology, American Physiological Society, 2009, 297 (5), pp.C1133-C1145. ⟨10.1152/ajpcell.00048.2009⟩
Evidence for a modulatory effect of cyclosporin A (CsA) on calcium signaling and cell survival in dystrophin-deficient cells is presented. Our previous works strongly supported the hypothesis of an overactivation of Ca2+release via inositol 1,4,5-tri
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c7b3b329932c9bc3bd2e8553971e69df
https://hal.archives-ouvertes.fr/hal-02880242
https://hal.archives-ouvertes.fr/hal-02880242