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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. dans Journal of neuroinflammation 2010
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 (Montrer FGFR3 Protéines)).
Cone-specific gene deletion of the inositol-1,4,5-trisphosphate receptor type I (IP3R1) also significantly increased cone density in the CNG (Montrer CNGA1 Protéines)-channel-deficient mice, suggesting that IP3R1 signaling contributes to Ca(2 (Montrer CA2 Protéines)+) 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 (Montrer AHCYL1 Protéines) (inositol triphosphate receptor binding protein) domain.
The results suggest that IP3R1 and IP3R3 (Montrer ITPR3 Protéines) are required for extra-embryonic vascularization in the placenta, allantois, and yolk sac (Montrer ADCY10 Protéines).
The results show that phosphorylations by Cdk1 (Montrer CDK1 Protéines) and MAPK (Montrer MAPK1 Protéines) enhance the activity of IP3R1, which is consistent with its maximal activity observed at the time of fertilization and the role of Ca(2 (Montrer CA2 Protéines)+) release in egg activation.
data indicate that PTPalpha (Montrer PTPRA Protéines) and FAK (Montrer PTK2 Protéines), which are enriched in FAs (Montrer FAS Protéines), interact with IP3R1 at adjacent ER sites to spatially sequester IL-1 (Montrer IL1A Protéines)-induced Ca(2 (Montrer CA2 Protéines)+) signalling
IGF-1 (Montrer IGF1 Protéines) strengthens the interaction between NCS-1 (Montrer NCS1 Protéines) and IP3R in the process of regulation of nuclear Ca2 (Montrer CA2 Protéines)+ signaling in cardiomyocytes.
Car8 (Montrer CA8 Protéines) regulates inflammatory pain by inhibiting the ITPR1-cytosolic free calcium pathway.
cGMP/protein kinase (Montrer CDK7 Protéines) G signaling suppresses Itpr1 phosphorylation and promotes endoplasmic reticulum stress in photoreceptors of Cnga3 (Montrer CNGA3 Protéines)-deficient mice.
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 (Montrer MCU Protéines) channels by regulating threshold and gain of MICU1 (Montrer MICU1 Protéines)-mediated inhibition and activation of MCU (Montrer MCU Protéines).
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 (Montrer CA2 Protéines)+ release due to alterations in the Ca2 (Montrer CA2 Protéines)+ 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 (Montrer SLC8A1 Protéines)-TRPC3 (Montrer TRPC3 Protéines)-IP3R1 complexes and maintained calcium homeostasis in cells treated with TNF-alpha (Montrer TNF Protéines).
wogonoside promotes the expression of PLSCR1 (Montrer PLSCR1 Protéines) and enhances its nuclear translocation and binding to the 1, 4, 5-trisphosphate receptor 1 (IP3R1) promoter in AML (Montrer RUNX1 Protéines) patient-derived primary cells. Wogonoside activates IP3R1, in turn, promotes release of Ca(2 (Montrer CA2 Protéines)+) 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 (Montrer P2RY1 Protéines) receptors in human embryonic stem cells and a transition of P2Y (Montrer P2RY1 Protéines)-IP3R coupling in derived cardiovascular progenitor cells are responsible for the differential Ca(2 (Montrer CA2 Protéines)+) 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.
STIM1 (Montrer STIM1 Protéines) and STIM2 (Montrer Stim2 Protéines) 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 (Montrer C9orf3 Protéines)-CaM (Montrer KRIT1 Protéines) and the stepwise binding of the N lobe (Montrer LTF Protéines) of CaM (Montrer KRIT1 Protéines) to the suppressor domain are important elements of calcium/CaM (Montrer KRIT1 Protéines) 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 (Montrer CA2 Protéines)+ channel is regulated by chromogranin B (Montrer CHGB Protéines)
the redox potential and Ca(2 (Montrer CA2 Protéines)+) can regulate IP(3)R through totally different mechanisms: Ca(2 (Montrer CA2 Protéines)+) 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