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anti-Mouse (Murine) ITPR1 Antibodies:
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Human Polyclonal ITPR1 Primary Antibody for ICC, IF - ABIN4227715
Cabral, Ishikawa, Garten, Makareeva, Sargent, Weis, Barnes, Webb, Shaw, Ala-Kokko, Lacbawan, Högler, Leikin, Blank, Zimmerberg, Eyre, Yamada, Marini: Absence of the ER Cation Channel TMEM38B/TRIC-B Disrupts Intracellular Calcium Homeostasis and Dysregulates Collagen Synthesis in Recessive Osteogenesis Imperfecta. in PLoS genetics 2016
Show all 3 Pubmed References
Human Polyclonal ITPR1 Primary Antibody for ICC, IF - ABIN439358
Wang, Li, Goode, Paz, Ouyang, Screaton, Fischer, Chen, Tabas, Montminy: Inositol-1,4,5-trisphosphate receptor regulates hepatic gluconeogenesis in fasting and diabetes. in Nature 2012
Human Monoclonal ITPR1 Primary Antibody for ELISA - ABIN561567
Olson, Sandison, Chalmers, McCarron: Microdomains of muscarinic acetylcholine and Ins(1,4,5)P? receptors create 'Ins(1,4,5)P? junctions' and sites of Ca²+ wave initiation in smooth muscle. in Journal of cell science 2013
Human Polyclonal ITPR1 Primary Antibody for IHC, IHC (p) - ABIN4327442
Klar, Hisatsune, Baig, Tariq, Johansson, Rasool, Malik, Ameur, Sugiura, Feuk, Mikoshiba, Dahl: Abolished InsP3R2 function inhibits sweat secretion in both humans and mice. in The Journal of clinical investigation 2014
Data show that endothelial cells (ECs)-specific type 1 1,4,5-trisphosphate receptor knockout (IP3R1(-/-)) mice are hypertensive and display blunted vasodilation in response to acetylcholine (ACh (show FGFR3 Antibodies)).
Cone-specific gene deletion of the inositol-1,4,5-trisphosphate receptor type I (IP3R1) also significantly increased cone density in the CNG (show CNGA1 Antibodies)-channel-deficient mice, suggesting that IP3R1 signaling contributes to Ca(2 (show CA2 Antibodies)+) homeostasis and cone survival.
Pathological mutations of ITPR1 (inositol 1,4,5-trisphosphate receptor, type 1) were found in seven patients from four families all localized in the IRBIT (show AHCYL1 Antibodies) (inositol triphosphate receptor binding protein) domain.
The results suggest that IP3R1 and IP3R3 (show ITPR3 Antibodies) are required for extra-embryonic vascularization in the placenta, allantois, and yolk sac (show ADCY10 Antibodies).
The results show that phosphorylations by Cdk1 (show CDK1 Antibodies) and MAPK (show MAPK1 Antibodies) enhance the activity of IP3R1, which is consistent with its maximal activity observed at the time of fertilization and the role of Ca(2 (show CA2 Antibodies)+) release in egg activation.
data indicate that PTPalpha (show PTPRA Antibodies) and FAK (show PTK2 Antibodies), which are enriched in FAs (show FAS Antibodies), interact with IP3R1 at adjacent ER sites to spatially sequester IL-1 (show IL1A Antibodies)-induced Ca(2 (show CA2 Antibodies)+) signalling
IGF-1 (show IGF1 Antibodies) strengthens the interaction between NCS-1 (show NCS1 Antibodies) and IP3R in the process of regulation of nuclear Ca2 (show CA2 Antibodies)+ signaling in cardiomyocytes.
Car8 (show CA8 Antibodies) regulates inflammatory pain by inhibiting the ITPR1-cytosolic free calcium pathway.
cGMP/protein kinase (show CDK7 Antibodies) G signaling suppresses Itpr1 phosphorylation and promotes endoplasmic reticulum stress in photoreceptors of Cnga3 (show CNGA3 Antibodies)-deficient mice.
Association of SLAT (show DEF6 Antibodies) with IP receptor 1 promotes Ca(2 (show CA2 Antibodies)) signaling in T cells.
Findings show that a pathogenic gain-of-function missense mutation within the suppressor region of ITPR1 causes SCA29 without cerebellar atrophy or other neuroimaging abnormalities; the Arg36Cys variant results in enhanced Ca2 (show CA2 Antibodies)+ release due to alterations in the Ca2 (show CA2 Antibodies)+ signal patterns from transient to sigmoidal, supporting a gain-of-function disease mechanism.
we provide a detailed phenotypic description of a family with a missense mutation in ITPR1
High ITPR1 expression is associated with cervical carcinoma.
We also observed that acetylcholine attenuated the formation of NCX1 (show SLC8A1 Antibodies)-TRPC3 (show TRPC3 Antibodies)-IP3R1 complexes and maintained calcium homeostasis in cells treated with TNF-alpha (show TNF Antibodies).
wogonoside promotes the expression of PLSCR1 (show PLSCR1 Antibodies) and enhances its nuclear translocation and binding to the 1, 4, 5-trisphosphate receptor 1 (IP3R1) promoter in AML (show RUNX1 Antibodies) patient-derived primary cells. Wogonoside activates IP3R1, in turn, promotes release of Ca(2 (show CA2 Antibodies)+) from endoplasmic reticulum, and eventually leads to cell differentiation
study broadens the mutational spectrum of ITPR1 and also emphasizes the importance of considering ITPR1 mutations as a potential cause of inherited cerebellar ataxias
predominant role of P2Y1 (show P2RY1 Antibodies) receptors in human embryonic stem cells and a transition of P2Y (show P2RY1 Antibodies)-IP3R coupling in derived cardiovascular progenitor cells are responsible for the differential Ca(2 (show CA2 Antibodies)+) mobilization between these cells.
we broadened the spectrum of ITPR1-related ataxias by identifying a de novo missense mutations in a patient with very severe hypoplasia of cerebellum and pons, mimicking PCH.
Homozygous ITPR1 missense variant [c.5360T>C; p.(L1787P)] segregated with cerebellar hypoplasia. Heterozygous carriers were asymptomatic.
increased mitochondrial calcium due to the gain-of-function enhancement of IP3R channels in the cells expressing PS1 (show PSEN1 Antibodies)-M146L leads to the opening of permeability transition pore in high conductance state.
STIM1 (show STIM1 Antibodies) and STIM2 (show Stim2 Antibodies) are expressed in bovine aortic endothelial cells and they both interact with IP3R-1.
we propose a model in which the partial unfolding of the suppressor domain by apo (show C9orf3 Antibodies)-CaM (show KRIT1 Antibodies) and the stepwise binding of the N lobe (show LTF Antibodies) of CaM (show KRIT1 Antibodies) to the suppressor domain are important elements of calcium/CaM (show KRIT1 Antibodies) inhibition of IP(3)R
structural mapping of the amino acid sequences to several functional domains is deduced within the structure of the InsP3R1 tetramer
the InsP3R/Ca2 (show CA2 Antibodies)+ channel is regulated by chromogranin B (show CHGB Antibodies)
the redox potential and Ca(2 (show CA2 Antibodies)+) can regulate IP(3)R through totally different mechanisms: Ca(2 (show CA2 Antibodies)+) by the indirect effect and the redox potential by direct action causing conformational changes
This gene encodes an intracellular receptor for inositol 1,4,5-trisphosphate. Upon stimulation by inositol 1,4,5-trisphosphate, this receptor mediates calcium release from the endoplasmic reticulum. Mutations in this gene cause spinocerebellar ataxia type 15, a disease associated with an heterogeneous group of cerebellar disorders. Multiple transcript variants have been identified for this gene.
inositol 1,4,5-triphosphate receptor, type 1
, type I inositol triphosphate receptor
, IP3 receptor
, IP3R 1
, InsP3R type I