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The results show that phosphorylations by Cdk1 (show CDK1 ELISA Kits) and MAPK (show MAPK1 ELISA Kits) 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 ELISA Kits)+) release in egg activation.
data indicate that PTPalpha (show PTPRA ELISA Kits) and FAK (show PTK2 ELISA Kits), which are enriched in FAs (show FAS ELISA Kits), interact with IP3R1 at adjacent ER sites to spatially sequester IL-1 (show IL1A ELISA Kits)-induced Ca(2 (show CA2 ELISA Kits)+) signalling
IGF-1 (show IGF1 ELISA Kits) strengthens the interaction between NCS-1 (show NCS1 ELISA Kits) and IP3R in the process of regulation of nuclear Ca2 (show CA2 ELISA Kits)+ signaling in cardiomyocytes.
Car8 (show CA8 ELISA Kits) regulates inflammatory pain by inhibiting the ITPR1-cytosolic free calcium pathway.
cGMP/protein kinase (show CDK7 ELISA Kits) G signaling suppresses Itpr1 phosphorylation and promotes endoplasmic reticulum stress in photoreceptors of Cnga3 (show CNGA3 ELISA Kits)-deficient mice.
Association of SLAT (show DEF6 ELISA Kits) with IP receptor 1 promotes Ca(2 (show CA2 ELISA Kits)) signaling in T cells.
IP3R-mediated Ca2 (show CA2 ELISA Kits)+ signaling reinforces Tcf-1 (show HNF1A ELISA Kits) 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 ELISA Kits) and participates in the regulation of Cx43 (show GJA1 ELISA Kits) phosphorylation on S279/282, thereby affecting GJ intercellular communication in ventricular myocytes
DISC1 (show DISC1 ELISA Kits) binds ITPR1 mRNA with HZF, thereby regulating its dendritic transport for synaptic plasticity.
Ca(2 (show CA2 ELISA Kits)+)-mediated cell death signaling between the IRE1alpha (show ERN1 ELISA Kits)-InsP3R pathway in the endoplasmic reticulum, is reported.
Studies indicate that the ryanodine receptors (RyRs: RyR1 (show RYR1 ELISA Kits), RyR2 (show RYR2 ELISA Kits), RyR3 (show RYR3 ELISA Kits)) and inositol 1,4,5-trisphosphate receptors (IP3Rs: IP3R1, IP3R2 (show ITPR2 ELISA Kits), IP3R3 (show ITPR3 ELISA Kits)) are the major Ca(2 (show CA2 ELISA Kits)+) release channels (CRCs) on the endo/sarcoplasmic reticulum (ER/SR).
ITPR1 missense mutations cause infantile-onset cerebellar ataxia (show USP14 ELISA Kits).
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 ELISA Kits).
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 ELISA Kits)+) release mediated by IP3R1 is an essential mechanism during the early steps of myoblast differentiation.
IP3R palmitoylation is a critical regulator of Ca(2 (show CA2 ELISA Kits)+) flux in immune cells and a previously unidentified DHHC/Selk (show HSP ELISA Kits) complex is responsible for this process.
a pleiotropic enzyme transglutaminase type 2 targets the allosteric coupling domain of IP3R type 1 (IP3R1) and negatively regulates IP3R1-mediated calcium signaling and autophagy by locking the subunit configurations.
Both ITPR1 and Beclin-1 (show BECN1 ELISA Kits) silencing in 786-0 cells inhibited NK-induced autophagy.
These data indicate that imiquimod triggers IP3 receptor-dependent Ca(2 (show CA2 ELISA Kits)+) signaling independently of TLR7 (show TLR7 ELISA Kits).
STIM1 (show STIM1 ELISA Kits) and STIM2 (show Stim2 ELISA Kits) 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 ELISA Kits)-CaM (show KRIT1 ELISA Kits) and the stepwise binding of the N lobe (show LTF ELISA Kits) of CaM (show KRIT1 ELISA Kits) to the suppressor domain are important elements of calcium/CaM (show KRIT1 ELISA Kits) 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 ELISA Kits)+ channel is regulated by chromogranin B (show CHGB ELISA Kits)
the redox potential and Ca(2 (show CA2 ELISA Kits)+) can regulate IP(3)R through totally different mechanisms: Ca(2 (show CA2 ELISA Kits)+) 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