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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. Additionally we are shipping ITPKB Antibodies (56) and ITPKB Proteins (7) and many more products for this protein.
Thus, non-canonical phosphoinositide 3-kinase-antagonism by Itpkb restricts pre-T cell receptor (show PTCRA ELISA Kits) induced metabolic activation to enforce coincidence-detection of pre-T cell receptor (show PTCRA ELISA Kits) expression and Notch (show NOTCH1 ELISA Kits)-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.
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 (show MCOLN1 ELISA Kits)+) 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 (show ITPKA ELISA Kits), Itpkb, Itpkc (show ITPKC ELISA Kits)]
Itpkb and inositol tetrakisphosphate mediate a survival signal in B cells.
B cells from Itpkb(-/-) Ig hen (show RPS6 ELISA Kits) egg lysozyme (show LYZ ELISA Kits) mice possess an anergic phenotype, hypoproliferate in response to cognate Ag, and yet they exhibit enhanced Ag-induced calcium signaling
The authors confirm downregulation of miR (show MLXIP ELISA Kits)-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 (show ITPKA ELISA Kits) and B (ITPKA (show ITPKA ELISA Kits) and ITPKB) was observed upon hESCs spontaneous differentiation.
IP3KB not only regulates cytoplasmic Ca(2 (show CA2 ELISA Kits)+) signals by phosphorylation of subplasmalemmal and cytoplasmic Ins (show INS ELISA Kits)(1,4,5)P(3) but may also be involved in modulating nuclear Ca(2 (show CA2 ELISA Kits)+) 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 (show CA2 ELISA Kits)+ responses to extracellular signals
We aim to summarize the existing information about functionally uncoupled IP(3)R (show ITPR1 ELISA Kits) and RyR (show RYR1 ELISA Kits) channels, and to discuss the concept that those channels can participate in Ca(2 (show CA2 ELISA Kits)+)-leak pathways.
In each of the three isoforms a nuclear export signal has evolved in the catalytic domain either de novo (IP3K-A (show ITPKA ELISA Kits)) or as a substitute for an earlier evolved corresponding N-terminal signal (IP3K-B and IP3K-C (show ITPKC ELISA Kits)).
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