Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher tous les synonymes
Sélectionnez vos espèces d'intérêt
analysis of the mechanism underlying synergistic up-regulation of PDE4B2 via a cross-talk between PKA-Cbeta and p65 (Montrer GORASP1 Protéines)
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 was verified.
PGE (Montrer LIPF Protéines)(2)-induced CYP1B1 (Montrer CYP1B1 Protéines) expression is mediated by ligand-independent activation of the ERalpha (Montrer ESR1 Protéines) pathway as a result of the activation of ERK (Montrer EPHB2 Protéines), Akt (Montrer AKT1 Protéines), 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 Protéines), at least in part, through FoxH1 (Montrer FOXH1 Protéines).
c-MYC (Montrer MYC Protéines) 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 Protéines) to promoter sequences.
Data describe the identification of a variant of the beta catalytic subunit of cyclic AMP (Montrer APRT Protéines)-dependent protein kinase (Montrer CDK7 Protéines) (PKACbeta) as a p75 neurotrophin receptor (Montrer NGFR Protéines)(NTR)-interacting protein, which phosphorylates p75(NTR (Montrer NGFR Protéines)) 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 Protéines) and Cbeta.
there is a PKA-Cbeta-mediated inhibitory mechanism of p73 (Montrer TP73 Protéines) function
critically involved in mediating the phosphorylation of AMP (Montrer TMPRSS5 Protéines) kinase promoted by hydrogen peroxide in endothelial cells.
Protein kinase A signaling explains vasopressin (Montrer AVP Protéines)-mediated regulation of membrane trafficking and gene transcription.
We suggest a role of the PRKACB gene splice variant Cbeta2 in regulating innate as well as adaptive immune sensitivity in vivo.
Gli2 and Gli3 (Montrer GLI3 Protéines) are dephosphorylated and activated in cilia and that impaired Gli2 and Gli3 (Montrer GLI3 Protéines) processing in Ta3 (Montrer HSP90B1 Protéines) mutant is at least in part due to a decrease in Gli2 and Gli3 (Montrer GLI3 Protéines) 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 Protéines) (Cbeta) gene designated Cbeta5, Cbeta6 and Cbeta7.
These data suggest that both developmental and tumor phenotypes caused by Prkar1a (Montrer PRKAR1A Protéines) 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 Protéines)+ ions and a substrate peptide was determined at 2.0 A resolution
glucose and glucagon (Montrer GCG Protéines)-like polypeptide-1 caused translocation of Calpha (Montrer PRKACA Protéines) 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 Protéines) 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