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anti-Human PRKACB Anticorps:
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analysis of the mechanism underlying synergistic up-regulation of PDE4B2 via a cross-talk between PKA-Cbeta and p65 (Montrer GORASP1 Anticorps)
The gene polymorphism loci rs12132032 in PRKACB maybe a potential risk factor for anencephaly in Chinese population from Shanxi, while gender susceptibility may influence the correlation.
The previously unknown small molecule inhibitor-dependent interaction of Cbeta1 with the cell cycle and apoptosis regulatory protein-1 (Montrer CCAR1 Anticorps) was verified.
PGE (Montrer LIPF Anticorps)(2)-induced CYP1B1 (Montrer CYP1B1 Anticorps) expression is mediated by ligand-independent activation of the ERalpha (Montrer ESR1 Anticorps) pathway as a result of the activation of ERK (Montrer EPHB2 Anticorps), Akt (Montrer AKT1 Anticorps), and PKA in breast cancer cells.
Data show that PI3K activation and PIP3 production lead to recruitment of the PKB/beta-arrestin/PDE4 complex to the membrane via the PKB PH domain, resulting in degradation of the TCR-induced cAMP pool and allowing full T-cell activation to proceed.
Results suggest that PKA can negatively regulate ERalpha (Montrer ESR1 Anticorps), at least in part, through FoxH1 (Montrer FOXH1 Anticorps).
c-MYC (Montrer MYC Anticorps) induces the activity of protein kinase A by inducing the transcription of the gene encoding the PKA catalytic subunit beta in multiple tissues, independent of cell proliferation by direct binding of c-MYC (Montrer MYC Anticorps) to promoter sequences.
Data describe the identification of a variant of the beta catalytic subunit of cyclic AMP (Montrer APRT Anticorps)-dependent protein kinase (Montrer CDK7 Anticorps) (PKACbeta) as a p75 neurotrophin receptor (Montrer NGFR Anticorps)(NTR)-interacting protein, which phosphorylates p75(NTR (Montrer NGFR Anticorps)) at Ser304.
there are abnormalities in [3H]cAMP binding and catalytic activity kinase A in brain of depressed suicide victims, which could be due to reduced expression of RIIbeta (Montrer PRKAR2B Anticorps) and Cbeta.
there is a PKA-Cbeta-mediated inhibitory mechanism of p73 (Montrer TP73 Anticorps) function
critically involved in mediating the phosphorylation of AMP (Montrer TMPRSS5 Anticorps) kinase promoted by hydrogen peroxide in endothelial cells.
We suggest a role of the PRKACB gene splice variant Cbeta2 in regulating innate as well as adaptive immune sensitivity in vivo.
Gli2 (Montrer GLI2 Anticorps) and Gli3 (Montrer GLI3 Anticorps) are dephosphorylated and activated in cilia and that impaired Gli2 (Montrer GLI2 Anticorps) and Gli3 (Montrer GLI3 Anticorps) processing in Ta3 (Montrer HSP90B1 Anticorps) mutant is at least in part due to a decrease in Gli2 (Montrer GLI2 Anticorps) and Gli3 (Montrer GLI3 Anticorps) phosphorylation.
Data indicate that TRPV4 activity and TRPV4 trafficking are under discrete but synergistic control of PKC- and PKA-dependent pathways.
Studies identified three novel alternatively spliced transcript variants of the mouse protein kinase A catalytic beta subunit (Montrer POLG Anticorps) (Cbeta) gene designated Cbeta5, Cbeta6 and Cbeta7.
These data suggest that both developmental and tumor phenotypes caused by Prkar1a (Montrer PRKAR1A Anticorps) mutation result from excess PKA activity due to PKA-Ca.
crystal structure of the catalytic subunit in complex with ADP, aluminum fluoride, Mg2 (Montrer MCOLN1 Anticorps)+ ions and a substrate peptide was determined at 2.0 A resolution
glucose and glucagon (Montrer GCG Anticorps)-like polypeptide-1 (Montrer CYP Anticorps) caused translocation of Calpha (Montrer PRKACA Anticorps) to the nucleus and of Cbeta to the plasma membrane and the nucleus, but did not affect the distribution of Cgamma in pancreatic beta-cells
Protein kinase A, C beta subunit (Montrer POLG Anticorps) is not essential for neuronal development or function but may play a more subtle role in memory that is modulated by strain-specific genetic modifiers.
cAMP is a signaling molecule important for a variety of cellular functions. cAMP exerts its effects by activating the cAMP-dependent protein kinase, which transduces the signal through phosphorylation of different target proteins. The inactive kinase holoenzyme is a tetramer composed of two regulatory and two catalytic subunits. cAMP causes the dissociation of the inactive holoenzyme into a dimer of regulatory subunits bound to four cAMP and two free monomeric catalytic subunits. Four different regulatory subunits and three catalytic subunits have been identified in humans. The protein encoded by this gene is a member of the Ser/Thr protein kinase family and is a catalytic subunit of cAMP-dependent protein kinase. Several alternatively spliced transcript variants encoding distinct isoforms have been observed.
, cAMP-dependent protein kinase catalytic beta subunit isoform 4ab
, cAMP-dependent protein kinase catalytic subunit beta
, protein kinase A catalytic subunit beta
, p70 S6 kinase
, protein kinase, cAMP-dependent, catalytic, beta a
, C-beta subunit
, protein kinase, cAMP-dependent, catalytic, beta
, cAMP-dependent protein kinase C beta