scholarly journals Unraveling the role of polycystin-2/inositol 1,4,5-trisphosphate receptor interaction in Ca2+signaling

2010 ◽  
Vol 3 (6) ◽  
pp. 530-532 ◽  
Author(s):  
Eva Sammels ◽  
Benoit Devogelaere ◽  
Djalila Mekahli ◽  
Geert Bultyncki ◽  
Ludwig Missiaen ◽  
...  
Keyword(s):  
Receptor Interaction ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor

122 Role of calmodulin on the calcium-dependent regulation of the inositol 1,4,5-trisphosphate receptor

1996 ◽  
Vol 25 ◽  
pp. S24
Author(s):  
Takayuki Michikawa ◽  
Junji Hirota ◽  
Seiko Kawano ◽  
Masayasu Hiraoka ◽  
Teiichi Furuichi ◽  
...  
Keyword(s):  
Calcium Dependent ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor

scholarly journals Astrocytes contribute to synapse elimination via type 2 inositol 1,4,5-trisphosphate receptor-dependent release of ATP

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Junhua Yang ◽  
Hongbin Yang ◽  
Yali Liu ◽  
Xia Li ◽  
Liming Qin ◽  
...  
Keyword(s):  
Purinergic Signaling ◽  
Dependent Manner ◽  
Intracerebroventricular Injection ◽  
Synapse Elimination ◽  
Inositol 1,4,5 Trisphosphate ◽  
Selective Elimination ◽  
Underlying Mechanisms ◽  
Trisphosphate Receptor

Selective elimination of unwanted synapses is vital for the precise formation of neuronal circuits during development, but the underlying mechanisms remain unclear. Using inositol 1,4,5-trisphosphate receptor type 2 knockout (Itpr2−/−) mice to specifically disturb somatic Ca2+ signaling in astrocytes, we showed that developmental elimination of the ventral posteromedial nucleus relay synapse was impaired. Interestingly, intracerebroventricular injection of ATP, but not adenosine, rescued the deficit in synapse elimination in Itpr2−/− mice. Further studies showed that developmental synapse elimination was also impaired in P2ry1−/− mice and was not rescued by ATP, indicating a possible role of purinergic signaling. This hypothesis was confirmed by MRS-2365, a selective P2Y1 agonist, could also rescue the deficient of synapse elimination in Itpr2−/− mice. Our results uncovered a novel mechanism suggesting that astrocytes release ATP in an IP3R2-dependent manner to regulate synapse elimination.

scholarly journals Calcium Signaling in Cholangiocytes: Methods, Mechanisms, and Effects

2018 ◽  
Vol 19 (12) ◽  
pp. 3913 ◽  
Author(s):  
Michele Rodrigues ◽  
Dawidson Gomes ◽  
Michael Nathanson
Keyword(s):  
Calcium Signaling ◽  
Second Messenger ◽  
Experimental Models ◽  
Cell Type ◽  
Release Channel ◽  
Cellular Processes ◽  
Inositol 1,4,5 Trisphosphate ◽  
Regulation Of Secretion ◽  
Trisphosphate Receptor

Calcium (Ca2+) is a versatile second messenger that regulates a number of cellular processes in virtually every type of cell. The inositol 1,4,5-trisphosphate receptor (ITPR) is the only intracellular Ca2+ release channel in cholangiocytes, and is therefore responsible for Ca2+-mediated processes in these cells. This review will discuss the machinery responsible for Ca2+ signals in these cells, as well as experimental models used to investigate cholangiocyte Ca2+ signaling. We will also discuss the role of Ca2+ in the normal and abnormal regulation of secretion and apoptosis in cholangiocytes, two of the best characterized processes mediated by Ca2+ in this cell type.

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