scholarly journals Characterization of a Cytosolic and a Luminal Ca2+Binding Site in the Type I Inositol 1,4,5-Trisphosphate Receptor

1996 ◽  
Vol 271 (43) ◽  
pp. 27005-27012 ◽  
Author(s):  
Ilse Sienaert ◽  
Humbert De Smedt ◽  
Jan B. Parys ◽  
Ludwig Missiaen ◽  
Sara Vanlingen ◽  
...  
Keyword(s):  
Binding Site ◽  
Type I ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor

scholarly journals Cloning and Characterization of the Type I Inositol 1,4,5-Trisphosphate Receptor Gene Promoter

1997 ◽  
Vol 272 (36) ◽  
pp. 22425-22431 ◽  
Author(s):  
Keith L. Kirkwood ◽  
Kristen Homick ◽  
Marc B. Dragon ◽  
Peter G. Bradford
Keyword(s):  
Receptor Gene ◽  
Gene Promoter ◽  
Type I ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor

scholarly journals Polycystin 2 Interacts with Type I Inositol 1,4,5-Trisphosphate Receptor to Modulate Intracellular Ca2+Signaling

2005 ◽  
Vol 280 (50) ◽  
pp. 41298-41306 ◽  
Author(s):  
Yun Li ◽  
Jerry M. Wright ◽  
Feng Qian ◽  
Gregory G. Germino ◽  
William B. Guggino
Keyword(s):  
Type I ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor

Molecular basis for calcium signaling in hepatic stellate cells

2007 ◽  
Vol 292 (4) ◽  
pp. G975-G982 ◽  
Author(s):  
Emma A. Kruglov ◽  
Paulo R. A. V. Correa ◽  
Gaurav Arora ◽  
Jin Yu ◽  
Michael H. Nathanson ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
P2y Receptors ◽  
Type I ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor ◽  
Healthy Liver ◽  
Organ Fibrosis ◽  
Injured Liver

Progressive liver fibrosis (with the resultant cirrhosis) is the primary cause of chronic liver failure. Hepatic stellate cells (HSCs) are critically important mediators of liver fibrosis. In the healthy liver, HSCs are quiescent lipid-storing cells limited to the perisinusoidal endothelium. However, in the injured liver, HSCs undergo myofibroblastic transdifferentiation (activation), which is a critical step in the development of organ fibrosis. HSCs express P2Y receptors linking extracellular ATP to inositol (1,4,5)-trisphosphate-mediated cytosolic Ca2+ signals. Here, we report that HSCs express only the type I inositol (1,4,5)-trisphosphate receptor and that the receptor shifts into the nucleus and cell extensions upon activation. These cell extensions, furthermore, express sufficient machinery to enable local application of ATP to evoke highly localized Ca2+ signals that induce localized contractions. These autonomous units of subcellular signaling and response reveal a new level of subcellular organization, which, in turn, establishes a novel paradigm for the local control of fibrogenesis in the liver.

scholarly journals Defining the minimal structural requirements for partial agonism at the type I myo -inositol 1,4,5-trisphosphate receptor

FEBS Letters ◽  
1997 ◽  
Vol 402 (2-3) ◽  
pp. 241-245 ◽  
Author(s):  
Robert A. Wilcox ◽  
Abdul Fauq ◽  
Alan P. Kozikowski ◽  
Stefan R. Nahorski
Keyword(s):  
Type I ◽  
Partial Agonism ◽  
Structural Requirements ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor
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