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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.
Our results indicate that changes in cell shape changed nuclear morphology and then the gene expression of IP3R1 (show ITPR1 Proteins) and SERCA2 (show ATP2A2 Proteins), which produced different intracellular calcium transient patterns.
The findings of this study show the dependence of LTP (show SCP2 Proteins) and gliotransmission on Ca(2 (show CA2 Proteins)+) release by astrocytic IP3 Rs.
FUNDC1 (show FUNDC1 Proteins) binds to IP3R2 to modulate ER Ca(2 (show CA2 Proteins)+) release into mitochondria and cytosol. Disruption of the FUNDC1 (show FUNDC1 Proteins) and IP3R2 interaction lowers the levels of Ca(2 (show CA2 Proteins)+) in mitochondria and cytosol, both of which instigate aberrant mitochondrial fission, mitochondrial dysfunction, cardiac dysfunction, and heart failure.
InsP3 dependent sarcoplasmic reticulum-Ca2 (show CA2 Proteins)+ flux constitute the main mechanism of functional crosstalk between InsP3R2 and RyR2 resulting in more Ca2 (show CA2 Proteins)+ sensitized RyRs to trigger subsequent Ca2 (show CA2 Proteins)+-induced Ca2 (show CA2 Proteins)+ release activation.
the absence of IP3R2 led to increased innate immunity, which may contribute to the decreased survival of the SOD1(G93A) mice.our data indicate that IP3R2 protects against the negative effects of inflammation, suggesting that the increase in IP3R2 expression in ALS patients is a protective response.
Using inositol 1,4,5-trisphosphate receptor type 2 knockout (Itpr2(-/-)) mice to specifically disturb somatic Ca(2 (show CA2 Proteins)+) signaling in astrocytes, the authors showed that developmental elimination of the ventral posteromedial nucleus relay synapse was impaired.
IP3R2 KO mice had smaller infarction than WT mice in acute and chronic phases of ischemia
Akt2 (show AKT2 Proteins) upregulates dendritic cell migration at least in part by ETS1 (show ETS1 Proteins)-dependent stimulation of IP3R2 transcription.
Disrupting IP3R (show ITPR1 Proteins)/Bcl-2 (show BCL2 Proteins) interaction therefore leads in those cells to increased Ca(2 (show CA2 Proteins)) release and apoptosis. Intriguingly, IP3R2 is not only implicated in apoptosis but also in the induction of senescence, another tumour-suppressive mechanism.
we systematically evaluating RCC (show XRCC1 Proteins) risk-associated SNPs indentified from previous GWAS in a Chinese population, finding that one SNP located in PDZD2 and two SNPs located in ITPR2 were ccRCC-risk associated in Chinese population.
Studies indicate that the ryanodine receptors (RyRs: RyR1 (show RYR1 Proteins), RyR2, RyR3 (show RYR3 Proteins)) and inositol 1,4,5-trisphosphate receptors (IP3Rs: IP3R1 (show ITPR1 Proteins), IP3R2, IP3R3 (show ITPR3 Proteins)) are the major Ca(2 (show CA2 Proteins)+) release channels (CRCs) on the endo/sarcoplasmic reticulum (ER/SR).
Data suggest miR (show MLXIP Proteins)-1290 as the new oncomiR involved in laryngeal squamous cell carcinoma pathogenesis probably through downregulation of its target genes MAF (show MAF Proteins) and ITPR2.
results show a functional role of calcium release by the ITPR2 channel and its subsequent accumulation in the mitochondria
High expression of inositol 1,4,5-trisphosphate receptor, type 2 is associated with acute myeloid leukemia (show BCL11A Proteins).
A genome-wide association study identifies ITPR2 as a susceptibility gene for Kashin-Beck disease in Han Chinese.
Loss of InsP3R2-mediated calcium release causes isolated anhidrosis in humans.
ITPR2 and hypertrophy specific gene expression is regulated, in part, by a positive feedback regulation between InsP3R2 and calcineurin-NFATc (show NFATC1 Proteins) signaling pathways.
The Galphaq (show GNAQ Proteins)-protein/coupled receptor/IP3R (show ITPR1 Proteins) axis modulates the electromechanical properties of the human myocardium and its propensity to develop arrhythmias.
receptor for inositol 1,4,5-triphosphate\; involved in regulating intracellular Ca(2+) concentration
inositol 1,4,5-trisphosphate receptor, type 2
, inositol 1,4,5-triphosphate receptor, type 2
, IP3 receptor
, IP3R 2
, inositol 1,4,5-triphosphate receptor 5
, inositol 1,4,5-trisphosphate receptor type 2
, inositol 1,4,5-trisphosphate type V receptor
, inositol trisphosphate receptor type 2
, type 2 InsP3 receptor
, type 2 inositol 1,4,5-trisphosphate receptor
, inositol 1,4,5-triphosphate receptor 2
, inositol triphosphate receptor type 2