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PRKAR1A is a potent tumor suppressor that inhibits the ERK (显示 EPHB2 蛋白)/Snail (显示 SNAI1 蛋白)/E-cadherin (显示 CDH1 蛋白) pathway in lung adenocarcinoma
t-Darpp phosphorylation at T39 seems to be crucial for t-Darpp-mediated PKA activation and this activation appears to occur through an association with RI and sequestering of RI away from PKAc. The t-Darpp-RI interaction could be a druggable target to reduce PKA activity in drug-resistant cancer.
the T allele of SNP rs60684937 located at 67,419,130 bp on chromosome 17 was associated with increased plasma EPO (显示 EPO 蛋白) and a relatively increased expression of a non-coding transcript of PRKAR1A in sickle cell disease patients
In this study we demonstrate a new role of MRAP2 in the regulation of the orexin receptor 1 (OX1R (显示 HCRTR1 蛋白)) and identify the specific regions of MRAP2 required for the regulation of OX1R (显示 HCRTR1 蛋白) and PKR1 (显示 PROKR1 蛋白). Importantly, like MC4R (显示 MC4R 蛋白) and PKRs, OX1R (显示 HCRTR1 蛋白) is predominately expressed in the brain where it regulates food intake
Screening of PRKAR1A and PDE4D (显示 PDE4D 蛋白) in a Large Italian Series of Patients Clinically Diagnosed With Albright Hereditary Osteodystrophy and/or Pseudohypoparathyroidism
Found evidence for kidney and liver cystic phenotypes in the Carney complex, a tumoral syndrome caused by mut (显示 PKD1 蛋白)ations in PRKAR1A.
Data suggest that introduction of cGMP-specific (显示 PDE6A 蛋白) residues using site-directed mutagenesis reduces selectivity of cyclic nucleotide-binding domain (CNBD) of PRKAR1A; combination of two mutations (G316R/A336T) results in a cGMP-selective binding site in the C-terminal CNBD; introduction of corresponding mutations (T192R/A212T) into the N-terminal CNBD results in a highly cGMP-selective binding site.
Data show that ELOVL7, SOCS3 (显示 SOCS3 蛋白), ACSL4 (显示 ACSL4 蛋白) and CLU (显示 CLU 蛋白) were upregulated while PRKAR1A and ABCG1 (显示 ABCG1 蛋白) were downregulated in the phlegm-dampness group.
Electrostatic interactions are mediators in the allosteric activation of protein kinase A RIalpha.
the present study reported for the first time an intronic splice site mutation in the PRKAR1A gene of a Chinese family with Carney complex, which probably caused skin pigmentation observed in affected family members.
This mouse knockout model supports the role of prkar1a as a tumor suppressor gene in the pancreas and points to the PKA pathway as a possible therapeutic target for these lesions.
This model, the first describing the germline expression of a PRKAR1A mutation causing dominant repression of cAMP-dependent PKA, reproduced the main features of acrodysostosis 1 in humans.
This study demonstrated that loss of one Prkar1a allele was associated with a significant increase in PKA activity in the basolateral (BLA (显示 LACTB 蛋白)) and central (CeA (显示 CEA 蛋白)) amygdala and ventromedial hypothalamus (VMH) in both Prkar1a(+/-) and Prkar1a(+/-)/Prkaca (显示 PRKACA 蛋白)(+/-) mice.
Kidney-specific loss of Prkar1a induced renal cystic disease and markedly aggravated cystogenesis in the Pkd1 (显示 PKD1 蛋白)(RC) models.
data demonstrate that haploinsufficiency for either one of the type-II regulatory subunits improved the bone phenotype of mice haploinsufficient for Prkar1a
PRKAR1A gene and its locus are altered in mixed odontogenic tumors. Expression is decreased in a subset of tumors, and Prkar1a(+) (/) (-) mice do not show abnormalities, which indicates that additional genes play a role in this tumor's pathogenesis.
Prkar1a activation enhances beta-catenin (显示 CTNNB1 蛋白) transcriptional activity through nuclear localization to PML (显示 PML 蛋白) bodies.
Loss of Prkar1a can only promote tumorigenesis when Prkar1a-mediated apoptosis is somehow countered.
Data show that mammary-specific loss of Prkar1a leads to elevated type-II PKA isozyme activation and this is sufficient to drive breast carcinogenesis.
Results show that mouse Prkar1a and human PRKAR2A (显示 PRKAR2A 蛋白) exhibited a dynamic spatio-temporal expression in tooth development, whereas neither human PRKAR1A nor mouse Prkar2a (显示 PRKAR2A 蛋白) showed their expression in odontogenesis.
ceramide activates plasma membrane Ca2+-ATPase from kidney-promixal tubule cells with protein kinase A as an intermediate
Results demonstrate that PKA activity regulated by Mys is indispensable for negative regulation of the Hh signaling pathway in Hh-responsive cells.
Data suggest that enzyme activation by cAMP involves highly stable conformation of Prkar1a as it binds to Prkaca; glycine residue, G235, appears to function as hinge in B/C helix conserved in Prkar1a; this "Flipback" conformation plays role in cAMP association to A domain of Prkar1a. (Prkar1a = cyclic AMP-dependent protein kinase RIalpha subunit; Prkaca = cyclic AMP-dependent protein kinase catalytic subunit)
Data suggest PRKAR1A contains two structurally homologous cAMP-binding domains that exhibit marked differences in dynamic profiles in activation/inhibition of Prkaca (显示 PRKACA 蛋白); conservation of structure does not necessarily imply conservation of dynamics.
Results describe the structures of the protein kinase A RIalpha subunit D/D domain alone and in complex with D-AKAP2 (显示 AKAP10 蛋白).
Data show that RSK1 (显示 RPS6KA1 蛋白) regulates PKAc activity in a cAMP-independent manner, and PKARIalpha by associating with RSK1 (显示 RPS6KA1 蛋白) regulates its activation and its biological functions.
angle X-ray scattering studies indicate RIalpha, RIIalpha, and RIIbeta (显示 PRKAR2B 蛋白) homodimers differ markedly in overall shape despite extensive sequence homology and similar molecular masses;cAMP binding does not cause large conformational changes(Prkar1a, Prkar2a (显示 PRKAR2A 蛋白))
the PKA RIalpha subunit dynamic C helix mediates isoform-specific domain reorganization upon C subunit binding
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. This gene encodes one of the regulatory subunits. This protein was found to be a tissue-specific extinguisher that down-regulates the expression of seven liver genes in hepatoma x fibroblast hybrids. Mutations in this gene cause Carney complex (CNC). This gene can fuse to the RET protooncogene by gene rearrangement and form the thyroid tumor-specific chimeric oncogene known as PTC2. A nonconventional nuclear localization sequence (NLS) has been found for this protein which suggests a role in DNA replication via the protein serving as a nuclear transport protein for the second subunit of the Replication Factor C (RFC40). Several alternatively spliced transcript variants encoding two different isoforms have been observed.
cAMP-dependent protein kinase regulatory subunit RIalpha
, cAMP-dependent protein kinase type I-alpha regulatory chain
, cAMP-dependent protein kinase type I-alpha regulatory subunit
, protein kinase A type 1a regulatory subunit
, tissue-specific extinguisher 1
, protein kinase, cAMP dependent regulatory, type 1, alpha
, protein kinase, cAMP dependent regulatory, type I, alpha
, cAMP-dependent protein kinase type I regulatory subunit
, protein kinase, cAMP-dependent, regulatory, type I, alpha (tissue specific extinguisher 1)
, cAMP-dependent protein kinase, regulatory subunit alpha 1
, cAMP-dependent protein kinase regulatory subunit alpha 1
, cAMP-dependent protein kinase type I-alpha regulatory subunit-like
, protein kinase, cAMP-dependent, regulatory subunit type I alpha S homeolog