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Dog (Canine) Polyclonal ITPR3 Primary Antibody für ELISA - ABIN547586
Futatsugi, Nakamura, Yamada, Ebisui, Nakamura, Uchida, Kitaguchi, Takahashi-Iwanaga, Noda, Aruga, Mikoshiba: IP3 receptor types 2 and 3 mediate exocrine secretion underlying energy metabolism. in Science (New York, N.Y.) 2005
Cow (Bovine) Polyclonal ITPR3 Primary Antibody für ELISA - ABIN250972
Sundivakkam, Kwiatek, Sharma, Minshall, Malik, Tiruppathi: Caveolin-1 scaffold domain interacts with TRPC1 and IP3R3 to regulate Ca2+ store release-induced Ca2+ entry in endothelial cells. in American journal of physiology. Cell physiology 2009
Show all 2 Pubmed References
Human Polyclonal ITPR3 Primary Antibody für IF (p), IHC (p) - ABIN1387432
Velázquez, Enos, Carson, Cranford, Bader, Sougiannis, Pritchett, Fan, Carson, Murphy: miR155 deficiency aggravates high-fat diet-induced adipose tissue fibrosis in male mice. in Physiological reports 2017
TOM70, but not TOM20, clusters in distinct OMM foci, frequently overlapping with sites in which the endoplasmic reticulum (ER) contacts mitochondria. Functionally, TOM70 depletion specifically impairs inositol trisphosphates (IP3)-linked ER to mitochondria Ca(2+) transfer. This phenomenon is dependent on the capacity of TOM70 to interact with IP3-receptors and favor their functional recruitment close to mitochondria.
InsP3R3 is dispensable for primary chemoelectrical transduction in mouse VNO. We conclude that InsP3R3 is not required for gating of Trpc2 in VSNs.
Inositol 1,4,5-trisphosphate receptors (IP3Rs) are required for the hematopoietic and cardiac fate divergence of mouse embryonic stem cells. Deletion of IP3Rs (IP3R-tKO) reduced Flk1+/PDGFRalpha- hematopoietic mesoderm, c-Kit+/CD41+ hematopoietic progenitor cell population, and the colony-forming unit activity, but increased cardiac progenitor markers as well as cardiomyocytes.
study demonstrated that IP3R-mediated Ca(2+) release plays an essential role in regulating B cell development, proliferation, Ab production, and B cell regulatory function in vivo
The results suggest that IP3R1 and IP3R3 are required for extra-embryonic vascularization in the placenta, allantois, and yolk sac.
the IP3R3-Ca(2+) pathway is required for nitric oxide-induced cardiomyocyte differentiation of embryonic stem cells.
a spontaneous mutation of Itpr3 in a progenitor of the BTBR strain produces a heretofore unrecognized dysfunction of GPCR-mediated taste transduction
IP3R3 expressing microvillous cells are actively responsive to injury and promote recovery
KRAP physically interacts with IP3R1 receptors in the kidney and IP3R3 receptors in the stomach.
IP(3)receptor-mediated activation of potassium channels provides a mechanism for glutamatergic and cholinergic inputs to selectively suppress striatal output neuron activity.
The data suggested that that hair shedding is actively controlled by the IP3R3/NFAT-dependent signaling pathway, possibly through the regulation of cytokeratin filaments in keratinocytes.
IP3R1 and 3 are genetically redundant and essential for cardiovascular development; redundant roles of IP3R1 and 3 may be implicated in regulation of cell death and the Mef2c-Smyd1 transcriptional cascade during development of the second heart field
InsP3 receptors co-localize with ORAI calcium release-activated calcium modulator 1 (Orai1) channels in pancreatic acinar cells, even in IP3-deficient knockout mice.
analysis of allosteric mechanisms between ryanodine and inositol-1,4,5-trisphosphate receptors
These findings demonstrate that KRAP physically associates with IP(3)R and regulates the proper localization of IP(3)R in the epithelial cells in vivo and cultured cells.
The characterization of IP3R3 microvillous cells as non-neuronal chemoresponsive cells helps to explain the differing descriptions of microvillous cells in the literature.
Data demonstrate that a single aromatic residue in the suppressor domain (Tyr-167 in IP(3)R1 and Trp-168 in IP(3)R3) plays a critical role in the coupling between ligand binding and channel gating.
Results strongly suggest that the Tyr-167 in IP(3)R1 and Trp-168 in IP(3)R3 is critical for the functional coupling between IP(3) binding and channel gating.
Knockdown of IP(3)R3 by small interfering RNA increased apoptosis in differentiating cells but not in undifferentiated ES cells.
Measurements of intracellular calcium changes show that both Itpr3 and ryanodine receptors are involved in a calcium-induced calcium release mechanism, which amplifies the initial Ca2+ influx through plasma membrane T-type calcium channels.
Expression of the type 3 InsP3 receptor is a final common event in the development of hepatocellular carcinoma.
Data demonstrated that IP3R3 is able to modulate intracellular Ca(2+) availability and to coordinate the remodeling of profilin cytoskeleton organization through the ARHGAP18/RhoA/mDia1/FAK pathway.
Suggest that AT haplotype in the ITPR3 gene may serve as a potential marker for genetic susceptibility to cervical squamous cell carcinoma risk in Taiwanese women.
PTEN counteracts FBXL2 to promote IP3R3- and Ca(2+)-mediated apoptosis limiting tumour growth
BAP1 regulates IP3R3-mediated Ca(2+) flux to mitochondria suppressing cell transformation
Studies indicate that the ryanodine receptors (RyRs: RyR1, RyR2, RyR3) and inositol 1,4,5-trisphosphate receptors (IP3Rs: IP3R1, IP3R2, IP3R3) are the major Ca(2+) release channels (CRCs) on the endo/sarcoplasmic reticulum (ER/SR).
the ability to generate tetramers with defined wild type and mutant subunits will be useful in probing fundamental questions relating to IP3Rs (R1, R2, R3) structure and function.
The transcription factor NRF2 binds to the promoter of ITPR3 to inhibit its expression in cholangiocytes, leading to reduced calcium signaling and bile duct secretion.
miR-506 is a regulator of InsP3R3 expression and InsP3R3-mediated Ca2+ signaling and secretion.
It mediate calcium release from intracellular calcium stores such as the ER into the cytoplasm. (review)
Physiologically relevant reactive oxygen species controls cytoplasmic and mitochondrial calcium transport through IP3 receptors.
The Galphaq-protein/coupled receptor/IP3R axis modulates the electromechanical properties of the human myocardium and its propensity to develop arrhythmias.
A molecular and functional link between BKCa channel and IP3R3 in cancer cells as an important mechanism for tumor cell proliferation.
in human pulmonary fibroblasts, PDGF acts through IP3-induced Ca(2+)-release to trigger Ca(2+) waves, which in turn modulate gene expression of several matrix proteins.
Studies indicate that three subtypes of inositol 1,4,5-trisphosphate (IP3) receptors (IP3R1, -2, and -3) are assembled to form homo- and heterotetrameric channels that mediate Ca(2+) release from intracellular stores.
The presence of isoform III of inositol 1,4,5-trisphosphate receptor is the key point of Akt activity on calcium-mediated apoptosis.
Ins(1,4,5)P3R-mediated Ca2+ signaling was critical for starvation-induced autophagy stimulation.
The study provides biochemical evidence of the interaction between FKBP12 and RYR1, RYR3 and IP3R.
the critical region of KRAP protein for the regulation of IP(3)R was determined.
role in cillary movement, coupled with chromogranin A
This gene encodes a receptor for inositol 1,4,5-trisphosphate, a second messenger that mediates the release of intracellular calcium. The receptor contains a calcium channel at the C-terminus and the ligand-binding site at the N-terminus. Knockout studies in mice suggest that type 2 and type 3 inositol 1,4,5-trisphosphate receptors play a key role in exocrine secretion underlying energy metabolism and growth.
, IP3R 3
, inositol 1,4,5-trisphosphate receptor type 3
, type 3 InsP3 receptor
, type 3 inositol 1,4,5-trisphosphate receptor
, inositol 1,4,5-triphosphate receptor, type 3
, inositol 1,4,5-triphosphate receptor 3