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RNAi-mediated Prkar2b suppression resulted in MI-stage arrest during oocyte development, and these oocytes exhibited abnormal spindle formation and chromosome aggregation.
deficiency induces brownlike adipocytes in inguinal white adipose tissue, increases expression of uncoupling protein1 and other thermogenic genes
Data (including data from studies using knockout mice) suggest that S100A1 (S-100 calcium-binding protein A1, alpha chain) is involved in protein kinase A- (RIIalpha and RIIbeta)-dependent signaling resulting in nuclear redistribution/influx of HDAC4 (histone deacetylase 4) in skeletal muscle fibers.
RIIbeta-PKA modulates the duration of leptin receptor signalling and therefore the magnitude of the catabolic response to leptin.
Release of pRIIbeta in the presence of cAMP is reduced by calcium, whereas autophosphorylation at the phosphorylation site inhibits holoenzyme reassociation with the catalytic subunit.
RIIBeta protein kinase A knockout was protective against induced seizure susceptibility.
Deficiency of the RIIbeta subunit of PKA affects locomotor activity and energy homeostasis in distinct neuronal populations.
study describes the 2.3 angstrom structure of full-length tetrameric RIIbeta(2):C(2) holoenzyme
Conditioned taste aversion (CTA) learning was examined in mice with a targeted disruption of a gene for a specific regulatory subunit of PKA (RIIbeta), which is selectively expressed in amygdala. Disruption of PKA signaling interferes with CTA.
RII-PKAII complements TSHR action by stably propagating robust cAMP signals in cell compartments
Here we show that visual cortical plasticity remains intact in AC1/AC8-/- mice, whereas Ocular dominance plasticity and LTD, but not LTP, are absent in RIIbeta-/- mice
Disruption of the RIIbeta regulatory subunit of protein kinase A (PKA) results in mice with a lean phenotype, nocturnal hyperactivity, and increased resting metabolic rate.
An activity-dependent model for barrel map development in brain circuitry is revealed that is mediated by a cAMP/PKA-dependent pathway that relies on PKARIIbeta function.
increased ingestion of ethanol by protein kinase A(PKA) subunit RIIbeta(-/-) mice is likely the result of altered PKA activity within neuronal pathways that control ethanol-consummatory behaviors
the RIIbeta gene mutation alters adiposity and locomotor activity by modifying PKA signaling pathways downstream of the agouti antagonism of MC4R in the hypothalamus
In this study, the authors linked for the first time the loss of RIIbeta protein levels to the PRKACA mutation status and found the down-regulation of RIIbeta to arise post-transcriptionally.
Study identified the overexpression of PRKAR2B in castration-resistant prostate cancer (CRPC) mouse models and patients, and showed it promoted CRPC cell proliferation, invasion and survival by mainly modulates cell cycle gene expression. These results provide evidence that PRKAR2B is a novel oncogenic gene in CRPC.
Leu206Arg and Leu199_Cys200insTrp mutations in PRKACA impair its association with PRKAR2B and PRKAR1A.
Although the depletion of PRKAR1A and PRKAR2B in adrenocortical cells has similar effects on cell proliferation and apoptosis; loss of these PKA subunits differentially affects cyclin expression.
Because of limited power, PRKAR2B's role in antipsychotic-induced weight gain is unclear, but biological evidence suggests that PRKAR2B may be involved
lipolytic catecholamine resistance of sc adipocytes in polycystic ovary syndrome is probably due to a combination of decreased amounts of beta(2)-adrenergic receptors, the regulatory II beta-component of protein kinase A, and hormone-sensitive lipase
Nuclear RII beta can act as a repressor of CREB transcriptional activity in T cells, providing a potential functional significance for aberrant levels of nuclear RII beta in systemic lupus erythematosus T cells.
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 and Cbeta
serine 114 phosphorylation and nuclear localization of RIIbeta controls the regulation of IL-2 gene expression in T cells.
A high R1/R2 ratio favors the proliferation of well differentiated and hormone producing adrenocortical cells, while unbalanced expression of these subunits is not required for malignant transformation.
Loss of PRKAR2B protein due to a post-transcriptional mechanism in ACA-S is a new mechanism of cAMP pathway dysregulation in adrenocortical tumorigenesis.
PKA RII(beta) is responsible for increased glucocorticoid sensitivity, critical for cAMP-mediated synergistic cell killing in CEM cells
both the constitutive and cAMP-induced release of TNFR1 exosome-like vesicles occur via PKA-dependent pathways that are regulated by the anchoring of RIIbeta to BIG2 via AKAP domains B and C
angle X-ray scattering studies indicate that the RIalpha, RIIalpha, and RIIbeta homodimers differ markedly in overall shape, despite extensive sequence homology and similar molecular masses
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 one of the regulatory subunits. This subunit can be phosphorylated by the activated catalytic subunit. This subunit has been shown to interact with and suppress the transcriptional activity of the cAMP responsive element binding protein 1 (CREB1) in activated T cells. Knockout studies in mice suggest that this subunit may play an important role in regulating energy balance and adiposity. The studies also suggest that this subunit may mediate the gene induction and cataleptic behavior induced by haloperidol.
protein kinase, cAMP-dependent, regulatory, type II, beta
, cAMP-dependent protein kinase, regulatory subunit beta 2
, cAMP-dependent protein kinase type II-beta regulatory subunit-like
, protein kinase, cAMP dependent regulatory, type II beta
, cAMP-dependent protein kinase type II-beta regulatory subunit
, Type II beta regulatory subunit of cAMP-dependent protein kinase
, cAMP-dependent protein kinase type II-beta regulatory chain