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Human ITPR1 Protein expressed in Wheat germ - ABIN1308255
Jarius, Wandinger, Horn, Heuer, Wildemann: A new Purkinje cell antibody (anti-Ca) associated with subacute cerebellar ataxia: immunological characterization. in Journal of neuroinflammation 2010
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 Proteins)-channel-deficient mice, suggesting that IP3R1 signaling contributes to Ca(2 (show CA2 Proteins)+) 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 Proteins) (inositol triphosphate receptor binding protein) domain.
The results suggest that IP3R1 and IP3R3 (show ITPR3 Proteins) are required for extra-embryonic vascularization in the placenta, allantois, and yolk sac (show ADCY10 Proteins).
The results show that phosphorylations by Cdk1 (show CDK1 Proteins) and MAPK (show MAPK1 Proteins) 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 Proteins)+) release in egg activation.
data indicate that PTPalpha (show PTPRA Proteins) and FAK (show PTK2 Proteins), which are enriched in FAs (show FAS Proteins), interact with IP3R1 at adjacent ER sites to spatially sequester IL-1 (show IL1A Proteins)-induced Ca(2 (show CA2 Proteins)+) signalling
IGF-1 (show IGF1 Proteins) strengthens the interaction between NCS-1 (show NCS1 Proteins) and IP3R in the process of regulation of nuclear Ca2 (show CA2 Proteins)+ signaling in cardiomyocytes.
Car8 (show CA8 Proteins) regulates inflammatory pain by inhibiting the ITPR1-cytosolic free calcium pathway.
cGMP/protein kinase (show CDK7 Proteins) G signaling suppresses Itpr1 phosphorylation and promotes endoplasmic reticulum stress in photoreceptors of Cnga3 (show CNGA3 Proteins)-deficient mice.
Association of SLAT (show DEF6 Proteins) with IP receptor 1 promotes Ca(2 (show CA2 Proteins)) signaling in T cells.
IP3R-mediated Ca2 (show CA2 Proteins)+ signaling reinforces Tcf-1 (show HNF1A Proteins) activity to both ensure normal development and to prevent thymocyte neoplasia.
predominant role of P2Y1 (show P2RY1 Proteins) receptors in human embryonic stem cells and a transition of P2Y (show P2RY1 Proteins)-IP3R coupling in derived cardiovascular progenitor cells are responsible for the differential Ca(2 (show CA2 Proteins)+) 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 Proteins)-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 (show CA2 Proteins)+ signals.
STIM1 (show STIM1 Proteins) and STIM2 (show Stim2 Proteins) 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 Proteins)-CaM (show KRIT1 Proteins) and the stepwise binding of the N lobe (show LTF Proteins) of CaM (show KRIT1 Proteins) to the suppressor domain are important elements of calcium/CaM (show KRIT1 Proteins) 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 Proteins)+ channel is regulated by chromogranin B (show CHGB Proteins)
the redox potential and Ca(2 (show CA2 Proteins)+) can regulate IP(3)R through totally different mechanisms: Ca(2 (show CA2 Proteins)+) 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