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anti-Mouse (Murine) ITPR1 Antibodies:
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Human Monoclonal ITPR1 Primary Antibody for ISt, IHC - ABIN1304717
Fos, Becart, Canonigo Balancio, Boehning, Altman: Association of the EF-hand and PH domains of the guanine nucleotide exchange factor SLAT with IP₃ receptor 1 promotes Ca²⁺ signaling in T cells. in Science signaling 2014
Show all 17 Pubmed References
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 IHC (p), WB - ABIN3043862
Yu, Chen, Wang, Kuang, Liu, Zhang, Du: Neuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of NF-?B and STAT3 in transient focal stroke. in PLoS ONE 2013
Human Polyclonal ITPR1 Primary Antibody for IHC, WB - ABIN1742253
Morciano, Beckhaus, Karas, Zimmermann, Volknandt: The proteome of the presynaptic active zone: from docked synaptic vesicles to adhesion molecules and maxi-channels. in Journal of neurochemistry 2009
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
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
The results of first study associating IP3R1 activity with changes in autophagy, mitochondrial Ca2+ levels, mitochondrial membrane potential, mitochondrial dynamics, and mitophagy in adult mouse skeletal muscle suggest that increased IP3R activity in mdx fibers plays an important role in the pathophysiology of Duchenne muscular dystrophy.
Tespa1 functions in T cell development and the regulation of TCR-induced Ca(2+) signalling through IP3R1
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.
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).
Cone-specific gene deletion of the inositol-1,4,5-trisphosphate receptor type I (IP3R1) also significantly increased cone density in the CNG-channel-deficient mice, suggesting that IP3R1 signaling contributes to Ca(2+) 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 (inositol triphosphate receptor binding protein) domain.
The results suggest that IP3R1 and IP3R3 are required for extra-embryonic vascularization in the placenta, allantois, and yolk sac.
The results show that phosphorylations by Cdk1 and MAPK enhance the activity of IP3R1, which is consistent with its maximal activity observed at the time of fertilization and the role of Ca(2+) release in egg activation.
data indicate that PTPalpha and FAK, which are enriched in FAs, interact with IP3R1 at adjacent ER sites to spatially sequester IL-1-induced Ca(2+) signalling
IGF-1 strengthens the interaction between NCS-1 and IP3R in the process of regulation of nuclear Ca2+ signaling in cardiomyocytes.
Car8 regulates inflammatory pain by inhibiting the ITPR1-cytosolic free calcium pathway.
cGMP/protein kinase G signaling suppresses Itpr1 phosphorylation and promotes endoplasmic reticulum stress in photoreceptors of Cnga3-deficient mice.
Association of SLAT with IP receptor 1 promotes Ca(2) signaling in T cells.
IP3R-mediated Ca2+ signaling reinforces Tcf-1 activity to both ensure normal development and to prevent thymocyte neoplasia.
reduced retinal DA metabolism/turnover may be associated with increased susceptibility to myopia in mice with ON pathway defect mutations.
These results demonstrated, for the first time, that IP3R physically interacts with Cx43 and participates in the regulation of Cx43 phosphorylation on S279/282, thereby affecting GJ intercellular communication in ventricular myocytes
DISC1 binds ITPR1 mRNA with HZF, thereby regulating its dendritic transport for synaptic plasticity.
Ca(2+)-mediated cell death signaling between the IRE1alpha-InsP3R pathway in the endoplasmic reticulum, is reported.
By upholding myosin II activity, constitutive calcium release from the endoplasmic reticulum through IPR1 maintains dendritic cell polarity during migration.
IP3R palmitoylation is a critical regulator of Ca(2+) flux in immune cells and a previously unidentified DHHC/Selk complex is responsible for this process.
Data show that native IP3 receptors (IP3Rs) are scaffolded into small clusters within endoplasmic reticulum (ER) membranes.
ITPR1 homozygous pathogenic variant is associated with Gillespie syndrome presenting a cardiac defect (pulmonary valve stenosis) and a genitourinary malformation.
MICU2 restricts spatial crosstalk between InsP3R and MCU channels by regulating threshold and gain of MICU1-mediated inhibition and activation of MCU.
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+ release due to alterations in the Ca2+ 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-TRPC3-IP3R1 complexes and maintained calcium homeostasis in cells treated with TNF-alpha.
wogonoside promotes the expression of PLSCR1 and enhances its nuclear translocation and binding to the 1, 4, 5-trisphosphate receptor 1 (IP3R1) promoter in AML patient-derived primary cells. Wogonoside activates IP3R1, in turn, promotes release of Ca(2+) 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 receptors in human embryonic stem cells and a transition of P2Y-IP3R coupling in derived cardiovascular progenitor cells are responsible for the differential Ca(2+) 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-M146L leads to the opening of permeability transition pore in high conductance state.
Data suggest that ADRB2 (beta2 adrenergic receptor) activation (as illustrated by epinephrine and nor epinephrine) leads to robust calcium ion mobilization from intracellular stores in endoplasmic reticulum via activation of phosphoinositide phospholipase C (PLC) and opening of inositol trisphosphate receptor (IP3R).
Data indicate that unlike ryanodine receptor RyRs, inositol 145-trisphosphate receptor IP3Rs are present and continually functional at early stages of cardiomyocyte differentiation.
ITPR1 is the SCA15 causative gene.
results demonstrate biallelic and monoallelic ITPR1 mutations as the underlying genetic defects for Gillespie syndrome, further extending the spectrum of ITPR1-related diseases
Dominant De Novo ITPR1 Mutations Cause Gillespie Syndrome.
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+ signals.
STIM1 and STIM2 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-CaM and the stepwise binding of the N lobe of CaM to the suppressor domain are important elements of calcium/CaM 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+ channel is regulated by chromogranin B
the redox potential and Ca(2+) can regulate IP(3)R through totally different mechanisms: Ca(2+) 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