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anti-Mouse (Murine) ITPR1 Antibodies:
anti-Rat (Rattus) ITPR1 Antibodies:
anti-Human ITPR1 Antibodies:
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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 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
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.
IP3R-mediated Ca2 (show CA2 Antibodies)+ signaling reinforces Tcf-1 (show HNF1A Antibodies) activity to both ensure normal development and to prevent thymocyte neoplasia.
These results demonstrated, for the first time, that IP3R physically interacts with Cx43 (show GJA1 Antibodies) and participates in the regulation of Cx43 (show GJA1 Antibodies) phosphorylation on S279/282, thereby affecting GJ intercellular communication in ventricular myocytes
DISC1 (show DISC1 Antibodies) binds ITPR1 mRNA with HZF (show ZNF385A Antibodies), thereby regulating its dendritic transport for synaptic plasticity.
Ca(2 (show CA2 Antibodies)+)-mediated cell death signaling between the IRE1alpha (show ERN1 Antibodies)-InsP3R pathway in the endoplasmic reticulum, is reported.
Studies indicate that four IP3-binding sites within the tetrameric inositol 1,4,5-trisphosphate receptors (IP3Rs) must bind inositol 145-trisphosphate (IP3) before the channel can open for intracellular Ca2 (show CA2 Antibodies)+ signals.
Data show that inositol 145-trisphosphate receptor type 1 (IP3R1) -with a single inositol 145-trisphosphate (IP3) binding-deficient subunit lack activity.
SNPs in ITPR1 and CNTN4 (show CNTN4 Antibodies) are involved in the regulation of serum uric acid concentrations in Mexican Americans
concluded that the HERPUD1 (show HERPUD1 Antibodies)-mediated cytoprotective effect against oxidative stress depends on the ITPR and Ca(2 (show CA2 Antibodies)+) transfer from the endoplasmic reticulum to mitochondria
Studies indicate that the ryanodine receptors (RyRs: RyR1 (show RYR1 Antibodies), RyR2 (show RYR2 Antibodies), RyR3 (show RYR3 Antibodies)) and inositol 1,4,5-trisphosphate receptors (IP3Rs: IP3R1, IP3R2 (show ITPR2 Antibodies), IP3R3 (show ITPR3 Antibodies)) are the major Ca(2 (show CA2 Antibodies)+) release channels (CRCs) on the endo/sarcoplasmic reticulum (ER/SR).
ITPR1 missense mutations cause infantile-onset cerebellar ataxia (show USP14 Antibodies).
cAMP is delivered directly and at saturating concentrations to its targets, mediate sensitization of IP3R and a more slowly developing inhibition of IP3 accumulation.
ITPR1 has a role in the pathogenesis of autoimmune cerebellitis in cerebellar ataxia (show USP14 Antibodies).
we identified two in our cohort with a diagnosis of ataxic cerebral palsy who were found to have a de novo mutation in ITPR1
Ca(2 (show CA2 Antibodies)+) release mediated by IP3R1 is an essential mechanism during the early steps of myoblast differentiation.
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