Affinage

PRKAR2B

cAMP-dependent protein kinase type II-beta regulatory subunit · UniProt P31323

Round 2 corrected
Length
418 aa
Mass
46.3 kDa
Annotated
2026-04-28
45 papers in source corpus 18 papers cited in narrative 18 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PRKAR2B is the type II-beta regulatory subunit of cAMP-dependent protein kinase (PKA), serving as a key negative regulator of PKA catalytic activity by occupying the substrate-binding site of catalytic subunits until cAMP binding triggers their release (PMID:2165385). PRKAR2B is compartmentalized to specific subcellular signaling domains through A-kinase anchoring proteins (AKAPs) including D-AKAP2, mAKAP (at the sarcoplasmic reticulum/ryanodine receptor RyR2 complex), and yotiao (at KCNQ1 ion channels), enabling spatially restricted PKA signaling that controls cardiac excitation-contraction coupling and ion channel modulation (PMID:9326583, PMID:10830164, PMID:11799244). PRKAR2B expression is regulated transcriptionally by HIF-1α, XBP1, HHEX, and FOXG1, and post-transcriptionally by multiple miRNAs (miR-200b/c, miR-34c-3p, miR-127, miR-3147) and MAPKAPK2-mediated mRNA stabilization; in cancer contexts, PRKAR2B promotes aerobic glycolysis through a HIF-1α positive feedback loop and an HHEX–PKA–HK2 axis, and drives metastasis via Wnt/β-catenin-induced epithelial-mesenchymal transition (PMID:33025691, PMID:41704777, PMID:29761841, PMID:36817960). In oocytes, PRKAR2B is required for normal meiotic spindle assembly and progression through metaphase I (PMID:29518769).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1990 High

    Establishing the core mechanism by which PRKAR2B inhibits PKA: the autoinhibitory domain of RIIβ occupies the catalytic subunit's substrate-binding site, and cAMP binding releases this inhibition, providing the foundational biochemical framework for all subsequent studies of PRKAR2B function.

    Evidence Biochemical reconstitution with recombinant proteins, peptide-binding assays, and mutagenesis

    PMID:2165385

    Open questions at the time
    • Structural details of the RIIβ–catalytic subunit interface at atomic resolution were not resolved
    • Isoform-specific differences between RIIβ and RIIα in autoinhibition kinetics were not addressed
  2. 1997 High

    Discovery that AKAPs provide subcellular targeting of PRKAR2B: D-AKAP2 was identified as a dual-specificity anchoring protein binding the N-terminal dimerization domain of both RI and RII subunits, establishing the principle that PRKAR2B is compartmentalized through protein–protein interactions.

    Evidence Yeast two-hybrid screen and coprecipitation assays with D-AKAP2 and PKA regulatory subunits

    PMID:9326583

    Open questions at the time
    • Endogenous tissue localization of D-AKAP2–PRKAR2B complexes was not demonstrated
    • Functional consequences of disrupting D-AKAP2–PRKAR2B interaction in vivo were not tested
  3. 2002 High

    PRKAR2B-containing PKA was shown to be tethered to specific ion channels and cardiac receptors via distinct AKAPs (mAKAP at RyR2, yotiao at KCNQ1), demonstrating that AKAP-mediated compartmentalization of PKA enables spatially restricted phosphorylation of cardiac substrates with direct physiological and disease consequences.

    Evidence Cosedimentation, coimmunoprecipitation, functional channel recordings (RyR2), and mutagenesis of yotiao–KCNQ1 interaction including an LQTS-associated mutation

    PMID:10830164 PMID:11799244

    Open questions at the time
    • Whether PRKAR2B specifically (versus RIIα) is the dominant regulatory subunit at these cardiac complexes was not resolved
    • Direct structural characterization of AKAP–RIIβ–catalytic subunit ternary complexes was lacking
  4. 2014 Medium

    PRKAR2B depletion in adrenocortical carcinoma cells revealed that loss of RIIβ activates PKA and cross-activates MEK/ERK and NF-κB pathways, accelerates cell cycle progression, and induces compensatory upregulation of PRKAR1A, establishing PRKAR2B as a context-dependent tumor suppressive brake on proliferative signaling.

    Evidence siRNA knockdown in H295R cells with Western blotting, flow cytometry, and signaling pathway analysis

    PMID:25268545

    Open questions at the time
    • Mechanisms underlying compensatory PRKAR1A upregulation upon PRKAR2B loss were not elucidated
    • In vivo relevance of these findings was not tested
    • Whether NF-κB activation is a direct or indirect consequence of PKA derepression was unclear
  5. 2018 Medium

    In prostate cancer, PRKAR2B was shown to promote tumor metastasis through activation of Wnt/β-catenin signaling and consequent EMT, and its expression is regulated by the FOXG1–miR-200 axis in neural cells, revealing that PRKAR2B functions as a pro-oncogenic and context-specific signaling node whose abundance is tightly controlled by miRNA-mediated repression.

    Evidence Gain/loss-of-function with Wnt inhibitor rescue and in vivo metastasis model (prostate cancer); multi-omics (small RNA-Seq, proteomics, Co-IP of FOXG1–DDX5–DROSHA) in neural cells

    PMID:28008150 PMID:29761841 PMID:30539330

    Open questions at the time
    • The molecular mechanism by which PRKAR2B activates Wnt/β-catenin signaling is unknown
    • Whether FOXG1-mediated miR-200 regulation of PRKAR2B operates in cancer contexts was not tested
    • Direct physical interaction between PRKAR2B and Wnt pathway components was not demonstrated
  6. 2018 Medium

    PRKAR2B was established as essential for meiotic progression in oocytes: knockdown caused MI arrest with abnormal spindle formation and chromosome aggregation, linking PKA regulation to cell division machinery beyond mitosis.

    Evidence RNAi microinjection in mouse oocytes with immunofluorescence, time-lapse microscopy, and qRT-PCR

    PMID:29518769

    Open questions at the time
    • Whether the spindle defect results from PKA hyperactivation or loss of a non-catalytic scaffolding role of PRKAR2B was not distinguished
    • Downstream PKA substrates mediating spindle assembly in oocytes were not identified
  7. 2020 Medium

    A HIF-1α–PRKAR2B positive feedback loop was demonstrated in prostate cancer: PRKAR2B stabilizes HIF-1α protein, which transcriptionally induces PRKAR2B, driving aerobic glycolysis; simultaneously, XBP1 was identified as a direct transcriptional activator of PRKAR2B, and miR-200b/c as direct repressors, revealing multilayered transcriptional and post-transcriptional control of PRKAR2B abundance in cancer metabolism.

    Evidence ChIP, luciferase reporters, metabolic flux measurements (glucose consumption, ECAR), in vivo tumor growth with glycolysis inhibitor rescue; miRNA target validation and rescue assays

    PMID:31986411 PMID:33025691

    Open questions at the time
    • The mechanism by which PRKAR2B stabilizes HIF-1α protein is unknown
    • Whether the HIF-1α–PRKAR2B loop operates independently of canonical PKA catalytic activity was not resolved
    • Relative contributions of XBP1 versus HIF-1α to PRKAR2B transcription in different tumor types were not compared
  8. 2022 Medium

    Parasite-induced miR-34c-3p was shown to repress PRKAR2B in infected leukocytes, providing cAMP-independent PKA activation that enhances dissemination — demonstrating that host PRKAR2B levels are exploited by intracellular pathogens to hijack PKA signaling.

    Evidence Luciferase reporter validation, miR-34c-3p overexpression/inhibition, PKA activity assays, functional invasion assays in Theileria-infected bovine macrophages

    PMID:36847534

    Open questions at the time
    • Whether PRKAR2B repression alone is sufficient to explain cAMP-independent PKA activation was not formally shown
    • Applicability to human infections beyond Theileria and Plasmodium was not tested
  9. 2023 Medium

    MAPKAPK2 (MK2) was identified as a post-transcriptional regulator of PRKAR2B mRNA stability via its 3′-UTR in head and neck cancer, adding a kinase-mediated mRNA stabilization layer to the regulatory circuitry controlling PRKAR2B abundance.

    Evidence MK2 knockdown, transcript turnover assays, 3′-UTR analysis, nCounter gene expression assay in HNSCC cells

    PMID:36817960

    Open questions at the time
    • The RNA-binding protein intermediary between MK2 and PRKAR2B 3′-UTR was not identified
    • Whether MK2-mediated PRKAR2B stabilization affects PKA activity in HNSCC was not measured
  10. 2025 Medium

    The HHEX–PRKAR2B–PKA–HK2 axis was delineated in pancreatic cancer: HHEX transcriptionally represses PRKAR2B, relieving PKA catalytic inhibition; under high glucose, elevated cAMP further activates PKA, which upregulates hexokinase 2 to drive glycolysis and metastasis, establishing a metabolic signaling cascade centered on PRKAR2B.

    Evidence ChIP, gain/loss-of-function of HHEX and PRKAR2B, PKA activity assays, in vivo high-glucose and glycolysis inhibition experiments in PDAC models

    PMID:41704777

    Open questions at the time
    • Whether PKA directly phosphorylates HK2 or regulates it transcriptionally was not determined
    • The generalizability of the HHEX–PRKAR2B axis beyond PDAC is unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key open questions remain: (1) the structural basis for isoform-specific (RIIβ versus RIIα) AKAP selectivity and catalytic subunit regulation; (2) the molecular mechanism by which PRKAR2B influences Wnt/β-catenin and HIF-1α signaling independently of canonical PKA kinase activity; (3) direct identification of PKA substrates downstream of PRKAR2B in oocyte meiosis and spindle assembly.
  • No high-resolution structure of full-length RIIβ in complex with AKAPs and catalytic subunits
  • Non-canonical (kinase-independent) functions of PRKAR2B remain poorly characterized
  • Genetic models (knockout mice) for PRKAR2B have not been extensively phenotyped across tissues in the timeline

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4
Localization
GO:0005829 cytosol 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-162582 Signal Transduction 7 R-HSA-1640170 Cell Cycle 3 R-HSA-1430728 Metabolism 2
Partners
AKAP10AKAP6AKAP9DDX5HHEXHIF1APRKACAXBP1
Complex memberships
PKA holoenzyme (type II)mAKAP-RyR2 macromolecular complexyotiao-KCNQ1 signaling complex

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1990 PRKAR2B (RIIβ), as a type II regulatory subunit of cAMP-dependent protein kinase A (PKA), contains an autoinhibitory region that occupies the peptide-binding site of the catalytic subunit, thereby preventing substrate access; cAMP binding to the regulatory subunit relieves this inhibition and activates catalytic subunits. Biochemical reconstitution, recombinant protein expression, peptide binding assays, and protein chemistry Annual review of biochemistry High 2165385
1997 D-AKAP2, a dual-specificity A-kinase anchoring protein, physically interacts with both type I (RIα) and type II (RIIα, RIIβ/PRKAR2B) regulatory subunits of PKA via a C-terminal R-binding domain (residues 333–372), and this binding involves the N-terminal dimerization domain of the regulatory subunits; D-AKAP2 also contains a putative RGS domain, suggesting a link between G-protein signaling and PKA compartmentalization. Yeast two-hybrid screen, coprecipitation assays, cDNA cloning Proceedings of the National Academy of Sciences of the United States of America High 9326583
2000 PKA (whose activity is regulated by regulatory subunits including PRKAR2B) is assembled into a macromolecular complex at the ryanodine receptor RyR2 on the sarcoplasmic reticulum via the anchoring protein mAKAP; PKA phosphorylation of RyR2 dissociates FKBP12.6 and increases channel open probability, and in failing human hearts RyR2 is PKA-hyperphosphorylated, causing defective channel regulation. Cosedimentation, coimmunoprecipitation, functional channel recordings Cell High 10830164
2002 Beta-adrenergic receptor modulation of the IKs potassium channel (KCNQ1-KCNE1) requires assembly of a macromolecular signaling complex including PKA (regulatory subunits) and protein phosphatase 1 (PP1) anchored to hKCNQ1 via the scaffold protein yotiao through a leucine zipper motif; an LQTS mutation (hKCNQ1-G589D) disrupts this interaction. Coimmunoprecipitation, functional reconstitution in heterologous cells, mutagenesis Science (New York, N.Y.) High 11799244
2014 In adrenocortical carcinoma cells (H295R), siRNA-mediated depletion of PRKAR2B activates both PKA and MEK/ERK signaling pathways and NF-κB pathway (via reduced IκB expression), promotes cell cycle progression with accumulation of cyclins A, B, cdk1, cdc2, and p21Cip, and induces anti-apoptotic Bcl-xL expression; notably, PRKAR2B depletion is compensated by upregulation of PRKAR1A protein, whereas PRKAR1A depletion does not affect PRKAR2B levels. siRNA knockdown, Western blotting, flow cytometry (cell cycle), apoptosis assays, signaling pathway analysis Hormone and metabolic research Medium 25268545
2017 PRKAR2B promotes castration-resistant prostate cancer (CRPC) cell proliferation and invasion and inhibits apoptosis; whole-genome transcriptome and GO analysis of PRKAR2B knockdown revealed that PRKAR2B accelerates cell cycle progression by modulating cell cycle genes including CCNB1, MCM2, PLK1, and AURKB. siRNA knockdown, whole-genome transcriptome analysis, GO enrichment, functional proliferation/invasion/apoptosis assays Oncotarget Medium 28008150
2018 PRKAR2B promotes prostate cancer cell invasion and tumor metastasis in vivo by activating Wnt/β-catenin signaling, which in turn induces epithelial-mesenchymal transition (EMT) as evidenced by decreased E-cadherin and increased Vimentin, N-cadherin, and Fibronectin; pharmacological inhibition of Wnt/β-catenin attenuates PRKAR2B-induced EMT and invasion. Gain- and loss-of-function (overexpression and siRNA), in vitro invasion assays, in vivo metastasis model, Western blotting, Wnt pathway inhibitor rescue Journal of cellular biochemistry Medium 29761841
2018 In neural cells, FOXG1 regulates PRKAR2B expression both transcriptionally and posttranscriptionally: FOXG1 affects biogenesis of miR-200b/a/429 by interacting with the RNA helicase DDX5/p68 and recruiting it to the DROSHA microprocessor complex; elevated miR-200 represses PRKAR2B mRNA, and increased PRKAR2B protein attenuates PKA activity at postsynaptic sites, potentially contributing to neuronal dysfunction in FOXG1 syndrome. Genome-wide small RNA sequencing, quantitative proteomics, RNA-Seq, coimmunoprecipitation (FOXG1-DDX5-DROSHA), miR-200 overexpression in N2a cells Molecular neurobiology Medium 30539330
2018 In mouse oocytes, PRKAR2B is most highly expressed at metaphase I (MI) and is required for normal oocyte maturation; RNAi-mediated knockdown of Prkar2b causes MI-stage arrest with abnormal spindle formation and chromosome aggregation, and reduces expression of other PKA family members (except Prkaca) and the majority of pentose phosphate pathway (PPP) factors. RNAi microinjection, immunofluorescence, time-lapse video microscopy, qRT-PCR, immunohistochemistry Cellular physiology and biochemistry Medium 29518769
2020 PRKAR2B promotes aerobic glycolysis (Warburg effect) in prostate cancer cells by increasing HIF-1α protein levels; HIF-1α in turn transcriptionally induces PRKAR2B expression (as shown by luciferase reporter and chromatin immunoprecipitation), forming a positive feedback loop; PRKAR2B-mediated tumor growth is largely abolished by glycolytic inhibitor 2-DG, galactose replacement, or HIF-1α knockdown. Loss- and gain-of-function, Western blotting, real-time qPCR, luciferase reporter assay, chromatin immunoprecipitation, glucose consumption/lactate/ECAR measurements, in vivo tumor growth Cell proliferation Medium 33025691
2020 miR-200b-3p and miR-200c-3p directly repress PRKAR2B expression in prostate cancer cells and are downregulated in metastatic CRPC; the transcription factor XBP1 directly drives PRKAR2B transcription; rescue experiments show that PRKAR2B mediates the proliferative and anti-apoptotic effects of miR-200b-3p/200c-3p suppression and XBP1 activity. miRNA target validation, luciferase reporter, qPCR, Western blotting, siRNA knockdown rescue assays, ChIP Biomedicine & pharmacotherapy Medium 31986411
2020 SARS-CoV-2 proteins physically associate with PRKAR2B as part of the human protein interaction network; PRKAR2B was identified as a host protein that physically interacts with SARS-CoV-2 proteins by affinity-purification mass spectrometry in human cells. Affinity purification mass spectrometry (AP-MS) in HEK293 cells expressing tagged SARS-CoV-2 proteins Nature Low 32353859
2021 BioPlex 3.0 large-scale AP-MS interaction network identifies protein-protein interactions involving PRKAR2B in HEK293T and HCT116 cells, placing PRKAR2B within defined protein communities consistent with PKA signaling complexes. Affinity purification mass spectrometry (AP-MS) across 10,128 human proteins Cell Low 33961781
2022 In Theileria annulata-infected bovine leukocytes and Plasmodium falciparum-infected red blood cells, infection-induced upregulation of miR-34c-3p represses PRKAR2B expression at the mRNA level, leading to increased PKA catalytic activity independent of cAMP flux; this cAMP-independent PKA activation enhances the tumorigenic, disseminating phenotype of infected macrophages and improves parasite fitness. miRNA target validation (luciferase reporter, qRT-PCR), miR-34c-3p overexpression and inhibition, PKA activity assays, functional invasion/dissemination assays mSphere Medium 36847534
2023 MAPKAPK2 (MK2) regulates PRKAR2B mRNA stability in head and neck squamous cell carcinoma (HNSCC); MK2 knockdown reduces PRKAR2B transcript levels, and transcript turnover studies indicate MK2 controls PRKAR2B mRNA stability via its 3'-UTR. NGS transcriptome profiling, MK2 knockdown, 3'-UTR filtering, nCounter gene expression assay, immunohistochemistry, transcript stability assays Computational and structural biotechnology journal Medium 36817960
2025 In porcine adipocytes, the circular RNA circSAMD4A promotes adipogenic differentiation by competitively binding miR-127, thereby alleviating miR-127-mediated repression of PRKAR2B and enhancing PRKAR2B expression and lipid accumulation. RNA sequencing, circRNA/miRNA functional assays, luciferase reporter, lipid accumulation assays Animal science journal Low 40589305
2025 In diabetic kidney disease (DKD), miR-3147 (upregulated in glomerular mesangial cells under high glucose) targets PRKAR2B mRNA and represses its expression, promoting mesangial cell proliferation and early-stage apoptosis under high glucose conditions. miRNA-Seq, luciferase reporter validation, miR-3147 overexpression in mesangial cells, cell viability and apoptosis assays Renal failure Low 40571682
2026 In pancreatic ductal adenocarcinoma (PDAC), the transcription factor HHEX transcriptionally represses PRKAR2B expression; downregulation of HHEX reduces PRKAR2B, relieving inhibition on PKA catalytic activity; a high-glucose microenvironment further promotes cAMP production to activate PKA, which then upregulates hexokinase 2 (HK2) to enhance glycolysis and metastasis; glycolysis inhibition blocks metastasis driven by this axis. Loss- and gain-of-function (HHEX, PRKAR2B), ChIP/transcription factor binding assays, PKA activity assays, HK2 expression analysis, in vivo high-glucose/glycolysis inhibition experiments iScience Medium 41704777

Source papers

Stage 0 corpus · 45 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2020 A SARS-CoV-2 protein interaction map reveals targets for drug repurposing. Nature 3411 32353859
2000 PKA phosphorylation dissociates FKBP12.6 from the calcium release channel (ryanodine receptor): defective regulation in failing hearts. Cell 1641 10830164
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
1990 cAMP-dependent protein kinase: framework for a diverse family of regulatory enzymes. Annual review of biochemistry 1019 2165385
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2014 A proteome-scale map of the human interactome network. Cell 977 25416956
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2000 DNA cloning using in vitro site-specific recombination. Genome research 815 11076863
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2003 Glucagon and regulation of glucose metabolism. American journal of physiology. Endocrinology and metabolism 635 12626323
2002 Requirement of a macromolecular signaling complex for beta adrenergic receptor modulation of the KCNQ1-KCNE1 potassium channel. Science (New York, N.Y.) 591 11799244
2020 Comparative host-coronavirus protein interaction networks reveal pan-viral disease mechanisms. Science (New York, N.Y.) 564 33060197
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
1995 Cell cycle regulation of the activity and subcellular localization of Plk1, a human protein kinase implicated in mitotic spindle function. The Journal of cell biology 427 7790358
2016 Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing. Cell 423 26871637
2021 A proximity-dependent biotinylation map of a human cell. Nature 339 34079125
2011 Novel asymmetrically localizing components of human centrosomes identified by complementary proteomics methods. The EMBO journal 265 21399614
2022 Tau interactome maps synaptic and mitochondrial processes associated with neurodegeneration. Cell 256 35063084
2003 Polo-like kinase 1 regulates Nlp, a centrosome protein involved in microtubule nucleation. Developmental cell 216 12852856
2018 An AP-MS- and BioID-compatible MAC-tag enables comprehensive mapping of protein interactions and subcellular localizations. Nature communications 201 29568061
1997 D-AKAP2, a novel protein kinase A anchoring protein with a putative RGS domain. Proceedings of the National Academy of Sciences of the United States of America 198 9326583
2002 Centrosomal proteins CG-NAP and kendrin provide microtubule nucleation sites by anchoring gamma-tubulin ring complex. Molecular biology of the cell 190 12221128
2003 The DNA sequence of human chromosome 7. Nature 188 12853948
1997 The Tat protein of HIV-1 induces tumor necrosis factor-alpha production. Implications for HIV-1-associated neurological diseases. The Journal of biological chemistry 188 9278385
2000 The centrosomal protein C-Nap1 is required for cell cycle-regulated centrosome cohesion. The Journal of cell biology 187 11076968
2000 Colocalization and coassembly of two human brain M-type potassium channel subunits that are mutated in epilepsy. Proceedings of the National Academy of Sciences of the United States of America 175 10781098
2013 Interlaboratory reproducibility of large-scale human protein-complex analysis by standardized AP-MS. Nature methods 170 23455922
2020 PRKAR2B-HIF-1α loop promotes aerobic glycolysis and tumour growth in prostate cancer. Cell proliferation 44 33025691
2018 PRKAR2B promotes prostate cancer metastasis by activating Wnt/β-catenin and inducing epithelial-mesenchymal transition. Journal of cellular biochemistry 31 29761841
2020 Transcriptional regulation of PRKAR2B by miR-200b-3p/200c-3p and XBP1 in human prostate cancer. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 27 31986411
2018 FOXG1 Regulates PRKAR2B Transcriptionally and Posttranscriptionally via miR200 in the Adult Hippocampus. Molecular neurobiology 18 30539330
2014 Comparison of the effects of PRKAR1A and PRKAR2B depletion on signaling pathways, cell growth, and cell cycle control of adrenocortical cells. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 18 25268545
2017 PRKAR2B plays an oncogenic role in the castration-resistant prostate cancer. Oncotarget 17 28008150
2018 Knockdown of PRKAR2B Results in the Failure of Oocyte Maturation. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 16 29518769
2023 miR-34c-3p Regulates Protein Kinase A Activity Independent of cAMP by Dicing prkar2b Transcripts in Theileria annulata-Infected Leukocytes. mSphere 8 36847534
2014 Protein kinase cAMP-dependent regulatory type II beta (PRKAR2B) gene variants in antipsychotic-induced weight gain. Human psychopharmacology 8 24737441
2023 MAPKAPK2-centric transcriptome profiling reveals its major role in governing molecular crosstalk of IGFBP2, MUC4, and PRKAR2B during HNSCC pathogenesis. Computational and structural biotechnology journal 6 36817960
2022 Long noncoding RNA TDRG1 aggravates doxorubicin-induced cardiomyopathy by binding with miR-873-5p to upregulate PRKAR2. Environmental toxicology 5 35524977
2022 Long non-coding RNA TDRG1 aggravates colorectal cancer stemness by binding with miR-873-5p to upregulate PRKAR2. Environmental toxicology 3 35730470
2025 ceRNA Profiling Reveals circSAMD4A Promoted Porcine Adipocytes Differentiation via Targeting miR-127/PRKAR2B. Animal science journal = Nihon chikusan Gakkaiho 1 40589305
2026 HHEX-PRKAR2B axis-mediated PKA activation drives glucose metabolism-dependent progression of pancreatic ductal adenocarcinoma. iScience 0 41704777
2025 Glomerular mesangial derived extracellular vesicles deteriorate diabetic kidney disease via miR-3147/PRKAR2B axis. Renal failure 0 40571682