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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 (54) 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 (zeige PTCRA Proteine) induced metabolic activation to enforce coincidence-detection of pre-T cell receptor (zeige PTCRA Proteine) expression and Notch (zeige NOTCH1 Proteine)-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 (zeige MCOLN1 Proteine)+) 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 (zeige GPRIN2 Proteine), at least in mouse embryonic fibroblasts.[Itpka (zeige ITPKA Proteine), Itpkb, Itpkc (zeige ITPKC Proteine)]
Itpkb and inositol tetrakisphosphate mediate a survival signal in B cells.
B cells from Itpkb(-/-) Ig hen (zeige RPS6 Proteine) egg lysozyme (zeige LYZ Proteine) mice possess an anergic phenotype, hypoproliferate in response to cognate Ag, and yet they exhibit enhanced Ag-induced calcium signaling
miR (zeige MLXIP Proteine)-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 (zeige MLXIP Proteine)-140-5p mediated drug-resistance in osteosarcoma cells by inducing autophagy.
The authors confirm downregulation of miR (zeige MLXIP Proteine)-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 (zeige ITPKA Proteine) and B (ITPKA (zeige ITPKA Proteine) and ITPKB) was observed upon hESCs spontaneous differentiation.
IP3KB not only regulates cytoplasmic Ca(2 (zeige CA2 Proteine)+) signals by phosphorylation of subplasmalemmal and cytoplasmic Ins (zeige INS Proteine)(1,4,5)P(3) but may also be involved in modulating nuclear Ca(2 (zeige CA2 Proteine)+) 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 (zeige CA2 Proteine)+ responses to extracellular signals
We aim to summarize the existing information about functionally uncoupled IP(3)R (zeige ITPR1 Proteine) and RyR (zeige RYR1 Proteine) channels, and to discuss the concept that those channels can participate in Ca(2 (zeige CA2 Proteine)+)-leak pathways.
In each of the three isoforms a nuclear export signal has evolved in the catalytic domain either de novo (IP3K-A (zeige ITPKA Proteine)) or as a substitute for an earlier evolved corresponding N-terminal signal (IP3K-B and IP3K-C (zeige ITPKC Proteine)).
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