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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 ELISA Kits)-channel-deficient mice, suggesting that IP3R1 signaling contributes to Ca(2 (show CA2 ELISA Kits)+) 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 ELISA Kits) (inositol triphosphate receptor binding protein) domain.
The results suggest that IP3R1 and IP3R3 (show ITPR3 ELISA Kits) are required for extra-embryonic vascularization in the placenta, allantois, and yolk sac (show ADCY10 ELISA Kits).
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.
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 ELISA Kits)-M146L leads to the opening of permeability transition pore in high conductance state.
Data suggest that ADRB2 (beta2 adrenergic receptor (show ADRB2 ELISA Kits)) 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 (show PIPLC ELISA Kits)) 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 ELISA Kits)+ signals.
Data show that inositol 145-trisphosphate receptor type 1 (IP3R1) -with a single inositol 145-trisphosphate (IP3) binding-deficient subunit lack activity.
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