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The protein encoded by this protein regulates inositol phosphate metabolism by phosphorylation of second messenger inositol 1,4,5-trisphosphate to Ins(1,3,4,5)P4. Zusätzlich bieten wir Ihnen ITPKB Antikörper (56) und und viele weitere Produktgruppen zu diesem Protein an.
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Thus, non-canonical phosphoinositide 3-kinase-antagonism by Itpkb restricts pre-T cell receptor induced metabolic activation to enforce coincidence-detection of pre-T cell receptor expression and Notch-engagement.
These data identify Itpkb as an essential mediator of T cell activation and suggest Itpkb inhibition as a novel approach to treat autoimmune disease.
Itpkb controls hematopoietic stem cell homeostasis and prevent death from severe anemia in mice.
Itpkb controls survival, proliferation and cytokine production in mouse peripheral T cells.
controls survival and prevents anergy in B cells
Data present the structure of the complete catalytic domain of inositol 1,4,5-trisphophate 3-kinase B, including the CaM binding domain in complex with Mg(2+) and ATP.
These data show that the absence of expression of the three isoenzymes of Itpk does not prevent the formation of IP5 and IP6, at least in mouse embryonic fibroblasts.[Itpka, Itpkb, Itpkc]
Itpkb and inositol tetrakisphosphate mediate a survival signal in B cells.
InsP3KB is also a physiological modulator of myelopoiesis.
B cells from Itpkb(-/-) Ig hen egg lysozyme mice possess an anergic phenotype, hypoproliferate in response to cognate Ag, and yet they exhibit enhanced Ag-induced calcium signaling
ITPKB does not affect the cellular actin structure and does not suppress dissemination of human lung cancer cells in mice.
miR-140-5p regulates this context-specific autophagy through its target, inositol 1,4,5-trisphosphate kinase 2 (IP3k2). Therefore, the results of the present study demonstrated that miR-140-5p mediated drug-resistance in osteosarcoma cells by inducing autophagy.
The authors confirm downregulation of miR-132 and upregulation of ITPKB in three distinct human Alzheimer's disease patient cohorts.
ITPKB is increased in Alzheimer's brain three-fold in the cerebral cortex of most patients with Alzheimer's disease compared with control subjects and accumulates in dystrophic neurites associated with amyloid plaques.
a specific increase in inositol 1,4,5-trisphosphate 3-kinase A and B (ITPKA and ITPKB) was observed upon hESCs spontaneous differentiation.
IP3KB not only regulates cytoplasmic Ca(2+) signals by phosphorylation of subplasmalemmal and cytoplasmic Ins(1,4,5)P(3) but may also be involved in modulating nuclear Ca(2+) signals generated from these nuclear envelope invaginations.
results highlight the potential role of the three isoforms of InsP3 3-kinase as direct InsP3 metabolizing enzymes and direct regulators of Ca2+ responses to extracellular signals
We aim to summarize the existing information about functionally uncoupled IP(3)R and RyR channels, and to discuss the concept that those channels can participate in Ca(2+)-leak pathways.
In each of the three isoforms a nuclear export signal has evolved in the catalytic domain either de novo (IP3K-A) or as a substitute for an earlier evolved corresponding N-terminal signal (IP3K-B and IP3K-C).
The protein encoded by this protein regulates inositol phosphate metabolism by phosphorylation of second messenger inositol 1,4,5-trisphosphate to Ins(1,3,4,5)P4. The activity of this encoded protein is responsible for regulating the levels of a large number of inositol polyphosphates that are important in cellular signaling. Both calcium/calmodulin and protein phosphorylation mechanisms control its activity.
inositol-trisphosphate 3-kinase B
, inositol 1,4,5-trisphosphate 3-kinase B
, 1D-myo-inositol-trisphosphate 3-kinase B
, inositol-trisphosphate 3-kinase B-like
, IP3 3-kinase B
, IP3K B
, insP 3-kinase B
, proliferation-inducing protein 37