| Hypoxia and the hypoxia inducible factor 1alpha activate protein kinase A by repressing RII beta subunit transcription. | Hypoxia and the hypoxia inducible factor 1α activate protein kinase A by repressing RII beta subunit transcription.
Lucia K, Wu Y, Garcia JM, Barlier A, Buchfelder M, Saeger W, Renner U, Stalla GK, Theodoropoulou M., Free PMC Article | 11/28/2020 |
| PRKAR2B-HIF-1alpha loop promotes aerobic glycolysis and tumour growth in prostate cancer. | PRKAR2B-HIF-1α loop promotes aerobic glycolysis and tumour growth in prostate cancer.
Xia L, Sun J, Xie S, Chi C, Zhu Y, Pan J, Dong B, Huang Y, Xia W, Sha J, Xue W., Free PMC Article | 11/21/2020 |
| Transcriptional regulation of PRKAR2B by miR-200b-3p/200c-3p and XBP1 in human prostate cancer. | Transcriptional regulation of PRKAR2B by miR-200b-3p/200c-3p and XBP1 in human prostate cancer.
Xia L, Han Q, Chi C, Zhu Y, Pan J, Dong B, Huang Y, Xia W, Xue W, Sha J. | 11/21/2020 |
| Biochemical studies demonstrate how the removal of ATP primes the holoenzyme for cAMP-mediated activation. The opposing competition between ATP/cAMP is unique to RIalpha..Comparisons to the RIIb holoenzyme demonstrate isoform-specific holoenzyme interfaces and highlights distinct allosteric mechanisms for activation in addition to the structural diversity of the isoforms | Two PKA RIα holoenzyme states define ATP as an isoform-specific orthosteric inhibitor that competes with the allosteric activator, cAMP.
Lu TW, Wu J, Aoto PC, Weng JH, Ahuja LG, Sun N, Cheng CY, Zhang P, Taylor SS., Free PMC Article | 03/28/2020 |
| PRKAR2B induces epithelial-mesenchymal transition and promotes castration-resistant prostate cancers metastasis by activating the Wnt/beta-catenin signaling. PRKAR2B might be served as a potential target for castration-resistant prostate cancers therapy. | PRKAR2B promotes prostate cancer metastasis by activating Wnt/β-catenin and inducing epithelial-mesenchymal transition.
Sha J, Han Q, Chi C, Zhu Y, Pan J, Dong B, Huang Y, Xia W, Xue W. | 10/26/2019 |
| 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. | Differential expression of the protein kinase A subunits in normal adrenal glands and adrenocortical adenomas.
Weigand I, Ronchi CL, Rizk-Rabin M, Dalmazi GD, Wild V, Bathon K, Rubin B, Calebiro D, Beuschlein F, Bertherat J, Fassnacht M, Sbiera S., Free PMC Article | 07/14/2018 |
| 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. | PRKAR2B plays an oncogenic role in the castration-resistant prostate cancer.
Sha J, Xue W, Dong B, Pan J, Wu X, Li D, Liu D, Huang Y., Free PMC Article | 02/24/2018 |
| 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. | Single Turnover Autophosphorylation Cycle of the PKA RIIβ Holoenzyme.
Zhang P, Knape MJ, Ahuja LG, Keshwani MM, King CC, Sastri M, Herberg FW, Taylor SS., Free PMC Article | 04/16/2016 |
| Leu206Arg and Leu199_Cys200insTrp mutations in PRKACA impair its association with PRKAR2B and PRKAR1A. | PKA catalytic subunit mutations in adrenocortical Cushing's adenoma impair association with the regulatory subunit.
Calebiro D, Hannawacker A, Lyga S, Bathon K, Zabel U, Ronchi C, Beuschlein F, Reincke M, Lorenz K, Allolio B, Kisker C, Fassnacht M, Lohse MJ. | 10/17/2015 |
| 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. | Comparison of the effects of PRKAR1A and PRKAR2B depletion on signaling pathways, cell growth, and cell cycle control of adrenocortical cells.
Basso F, Rocchetti F, Rodriguez S, Nesterova M, Cormier F, Stratakis CA, Ragazzon B, Bertherat J, Rizk-Rabin M., Free PMC Article | 07/25/2015 |
| Because of limited power, PRKAR2B's role in antipsychotic-induced weight gain is unclear, but biological evidence suggests that PRKAR2B may be involved | Protein kinase cAMP-dependent regulatory type II beta (PRKAR2B) gene variants in antipsychotic-induced weight gain.
Gagliano SA, Tiwari AK, Freeman N, Lieberman JA, Meltzer HY, Kennedy JL, Knight J, Müller DJ. | 03/21/2015 |
| Meta-analysis and genome-wide association study of gene-disease association. (HuGE Navigator) | Meta-analysis of genome-wide association studies confirms a susceptibility locus for knee osteoarthritis on chromosome 7q22.
Evangelou E, Valdes AM, Kerkhof HJ, Styrkarsdottir U, Zhu Y, Meulenbelt I, Lories RJ, Karassa FB, Tylzanowski P, Bos SD, arcOGEN Consortium, Akune T, Arden NK, Carr A, Chapman K, Cupples LA, Dai J, Deloukas P, Doherty M, Doherty S, Engstrom G, Gonzalez A, Halldorsson BV, Hammond CL, Hart DJ, Helgadottir H, Hofman A, Ikegawa S, Ingvarsson T, Jiang Q, Jonsson H, Kaprio J, Kawaguchi H, Kisand K, Kloppenburg M, Kujala UM, Lohmander LS, Loughlin J, Luyten FP, Mabuchi A, McCaskie A, Nakajima M, Nilsson PM, Nishida N, Ollier WE, Panoutsopoulou K, van de Putte T, Ralston SH, Rivadeneira F, Saarela J, Schulte-Merker S, Shi D, Slagboom PE, Sudo A, Tamm A, Tamm A, Thorleifsson G, Thorsteinsdottir U, Tsezou A, Wallis GA, Wilkinson JM, Yoshimura N, Zeggini E, Zhai G, Zhang F, Jonsdottir I, Uitterlinden AG, Felson DT, van Meurs JB, Stefansson K, Ioannidis JP, Spector TD, Translation Research in Europe Applied Technologies for Osteoarthritis (TreatOA)., Free PMC Article | 12/5/2010 |
| Observational study and genome-wide association study of gene-disease association and gene-environment interaction. (HuGE Navigator) | Biological pathway-based genome-wide association analysis identified the vasoactive intestinal peptide (VIP) pathway important for obesity.
Liu YJ, Guo YF, Zhang LS, Pei YF, Yu N, Yu P, Papasian CJ, Deng HW., Free PMC Article | 06/30/2010 |
| Clinical trial and genome-wide association study of gene-disease association. (HuGE Navigator) | Genomewide pharmacogenomic study of metabolic side effects to antipsychotic drugs.
Adkins DE, Aberg K, McClay JL, Bukszár J, Zhao Z, Jia P, Stroup TS, Perkins D, McEvoy JP, Lieberman JA, Sullivan PF, van den Oord EJ., Free PMC Article | 04/7/2010 |
| 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 | cAMP-dependent protein kinase A (PKA) signaling induces TNFR1 exosome-like vesicle release via anchoring of PKA regulatory subunit RIIbeta to BIG2.
Islam A, Jones H, Hiroi T, Lam J, Zhang J, Moss J, Vaughan M, Levine SJ., Free PMC Article | 01/21/2010 |
| PKA RII(beta) is responsible for increased glucocorticoid sensitivity, critical for cAMP-mediated synergistic cell killing in CEM cells | Protein kinase A (PKA) isoform RIIbeta mediates the synergistic killing effect of cAMP and glucocorticoid in acute lymphoblastic leukemia cells.
Ji Z, Mei FC, Miller AL, Thompson EB, Cheng X., Free PMC Article | 01/21/2010 |
| Loss of PRKAR2B protein due to a post-transcriptional mechanism in ACA-S is a new mechanism of cAMP pathway dysregulation in adrenocortical tumorigenesis. | Identification of a clinically homogenous subgroup of benign cortisol-secreting adrenocortical tumors characterized by alterations of the protein kinase A (PKA) subunits and high PKA activity.
Vincent-Dejean C, Cazabat L, Groussin L, Perlemoine K, Fumey G, Tissier F, Bertagna X, Bertherat J. | 01/21/2010 |
| 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. | Different expression of protein kinase A (PKA) regulatory subunits in cortisol-secreting adrenocortical tumors: relationship with cell proliferation.
Mantovani G, Lania AG, Bondioni S, Peverelli E, Pedroni C, Ferrero S, Pellegrini C, Vicentini L, Arnaldi G, Bosari S, Beck-Peccoz P, Spada A. | 01/21/2010 |
| 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 | Protein kinase A in postmortem brain of depressed suicide victims: altered expression of specific regulatory and catalytic subunits.
Dwivedi Y, Rizavi HS, Shukla PK, Lyons J, Faludi G, Palkovits M, Sarosi A, Conley RR, Roberts RC, Tamminga CA, Pandey GN. | 01/21/2010 |
| serine 114 phosphorylation and nuclear localization of RIIbeta controls the regulation of IL-2 gene expression in T cells. | Down-regulation of IL-2 production in T lymphocytes by phosphorylated protein kinase A-RIIbeta.
Elliott MR, Shanks RA, Khan IU, Brooks JW, Burkett PJ, Nelson BJ, Kyttaris V, Juang YT, Tsokos GC, Kammer GM. | 01/21/2010 |
| 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. | Protein kinase A regulatory subunit type II beta directly interacts with and suppresses CREB transcriptional activity in activated T cells.
Elliott MR, Tolnay M, Tsokos GC, Kammer GM. | 01/21/2010 |
| 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 | Mechanisms behind lipolytic catecholamine resistance of subcutaneous fat cells in the polycystic ovarian syndrome.
Faulds G, Rydén M, Ek I, Wahrenberg H, Arner P. | 01/21/2010 |