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    GENE:

    PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)

    i
    Other names: PRKAR2B, Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta, Protein Kinase, CAMP-Dependent, Regulatory Subunit Type II Beta, CAMP-Dependent Protein Kinase Type II-Beta Regulatory Subunit, Protein Kinase, CAMP-Dependent, Regulatory, Type II, Beta, PRKAR2, CAMP-Dependent Protein Kinase Type II-Beta Regulatory Chain, WUGSC:H_RG363E19.2, H_RG363E19.2, RII-BETA
    Associations

    News

    Trials
    6d
    HHEX-PRKAR2B axis-mediated PKA activation drives glucose metabolism-dependent progression of pancreatic ductal adenocarcinoma. (PubMed, iScience)
    In vivo, high glucose synergized with PKA activation to promote metastasis, whereas glycolysis inhibition blocked new metastases. Thus, HHEX-PRKAR2B-mediated PKA activation is a critical hub for PDAC progression, modulated by glucose and reinforcing glycolysis via HK2, revealing novel therapeutic targets for metabolic intervention.
    Journal
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    HK2 (Hexokinase 2) • PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)
    3ms
    Glioma angiogenesis phosphoproteome landscape and biomarker sets identified with phenome-centered multiomics toward 3P medical approaches. (PubMed, EPMA J)
    These findings provide concrete molecular targets for antiangiogenic therapy and establish clinically actionable biomarkers for glioma patient stratification in the 3PM framework. The online version contains supplementary material available at 10.1007/s13167-025-00428-1.
    Journal
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    HIF1A (Hypoxia inducible factor 1, alpha subunit) • CAMK2D (Calcium/Calmodulin Dependent Protein Kinase II Delta) • HSPB1 (Heat shock 27kDa protein 1) • L1CAM (L1 cell adhesion molecule) • PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • MYLK (Myosin Light Chain Kinase) • PDHA1 (Pyruvate Dehydrogenase E1 Subunit Alpha 1) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)
    over1year
    Development and Validation of a Predictive Model for Resistance to Platinum-Based Chemotherapy in Patients with Ovarian Cancer through Proteomic Analysis. (PubMed, J Proteome Res)
    The model also performed well in predicting PFS and OS at various time points. Based on these proteins, our predictive model can precisely predict platinum response and survival outcomes in HGSOC patients, which can assist clinicians in promptly identifying potentially platinum-resistant individuals.
    Journal • Predictive model
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    PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)
    over1year
    Machine learning-based screening and validation of liver metastasis-specific genes in colorectal cancer. (PubMed, Sci Rep)
    In vitro experiments indicated that SPP1 may act as a cancer-promoting factor. The hub CRLM-specific gene SPP1 can help determine the diagnosis, prognosis, and immune infiltration of patients with CRLM.
    Journal • Machine learning
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    SPP1 (Secreted Phosphoprotein 1) • PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)
    2years
    Transcriptomic and machine learning analyses identify hub genes of metabolism and host immune response that are associated with the progression of breast capsular contracture. (PubMed, Genes Dis)
    Potential molecular mechanisms were identified based on the expression levels in the high and low PRKAR2B groups. Our findings indicate that PRKAR2B is a novel diagnostic biomarker for breast capsular contracture and might also influence the grade and progression of capsular contracture.
    Journal • Machine learning
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    PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)
    2years
    Single-Cell RNA Sequencing Uncovers Abnormal Differentiation of Neutrophil and Megakaryocyte Might Mediated Ruxolitinib Resistance for Patinets with PMF (ASH 2023)
    In Rux resistant group, Up-regulation of inflammatory and tumor-related signaling pathways promotes the occurrence of PMF inflammation and amplification of malignant clones; Up-regulation of LGALS9 in neutrophil band to receptor TIM3 mediates T cell depletion; the regulation of platelets-platelets in PMF is mediated by CD40L-CD40 ligand receptors; MIF-CD74 might be the relationship between PMF-HSC and PMF-PLT in the context of primary myelofibrosis.
    IO biomarker
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    CD74 (CD74 Molecule) • TNFA (Tumor Necrosis Factor-Alpha) • CXCL8 (Chemokine (C-X-C motif) ligand 8) • HAVCR2 (Hepatitis A Virus Cellular Receptor 2) • GATA1 (GATA Binding Protein 1) • YBX1 (Y-Box Binding Protein 1) • CD40LG (CD40 ligand) • PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • E2F7 (E2F Transcription Factor 7) • E2F8 (E2F Transcription Factor 8) • ITGA2B (Integrin Subunit Alpha 2b) • LGALS9 (Galectin 9) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta) • SUZ12 (SUZ12 Polycomb Repressive Complex 2 Subunit)
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    Jakafi (ruxolitinib)
    over2years
    Analysis of Under-Diagnosed Malignancy during Fine Needle Aspiration Cytology of Lymphadenopathies. (PubMed, Int J Mol Sci)
    These results thus point to candidate genes that could be used as biomarkers to minimize the false-negative rate of FNAC diagnosis. We are currently pursuing the development of a gene chip to improve the diagnosis of lymphadenopathy patients with the ultimate goal of improving their prognosis.
    Journal • Cytology
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    PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)
    over2years
    Brief Report: MET fusions in Non-small cell lung cancer: Clinicopathologic features and response to MET inhibition. (PubMed, J Thorac Oncol)
    MET fusions are very rare oncogenic driver events in NSCLC and predominantly appear in adenocarcinomas. They are heterogeneous in terms of fusion partners and breakpoints. Patients with MET fusion can benefit from MET TKI therapy.
    Journal
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    BRAF (B-raf proto-oncogene) • KIF5B (Kinesin Family Member 5B) • CAPZA2 (Capping Actin Protein Of Muscle Z-Line Subunit Alpha 2) • PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • TRIM4 (Tripartite Motif Containing 4) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)
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    BRAF V600E • BRAF V600 • MET mutation • MET fusion
    almost3years
    Structural variants detected by optical genome mapping in acute lymphoblastic leukemia patient-derived xenografts models (AACR 2023)
    OGM assays were more comprehensive, and novel rare SVs were identified in ALL. Combining the results of gene fusions between different technologies will provide more accurate predictions for ALL classifications. The combination of aberrant SVs may synergize to influence the efficacy of imatinib, which warrants further investigations.
    Clinical
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    ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • KMT2A (Lysine Methyltransferase 2A) • IKZF1 (IKAROS Family Zinc Finger 1) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)
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    BCR-ABL1 fusion • KMT2A rearrangement • MLL rearrangement • IKZF1 deletion • ABL1 deletion
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    imatinib
    almost3years
    MAPKAPK2-centric transcriptome profiling reveals its major role in governing molecular crosstalk of IGFBP2, MUC4, and PRKAR2B during HNSCC pathogenesis. (PubMed, Comput Struct Biotechnol J)
    Conclusively, MK2-regulated candidate genes were identified in this study, and their plausible involvement in HNSCC pathogenesis was elucidated. These genes possess investigative values as targets for diagnosis and therapeutic interventions for HNSCC.
    Journal
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    MUC4 (Mucin 4, Cell Surface Associated) • IGFBP2 (Insulin-like growth factor binding protein 2) • PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)
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    dactinomycin
    3years
    Resistance to MET inhibition in MET-dependent NSCLC and therapeutic activity after switching from type I to type II MET inhibitors. (PubMed, Eur J Cancer)
    Resistance to MET inhibition is heterogeneous with on- and off-target mechanisms occurring regardless of the initial MET aberration. Switching therapy between different types of kinase inhibitors can lead to repeated responses in cases with second-site mutations. Controlled clinical trials in this setting with larger patient numbers are needed, as evidence to date is limited to preclinical data and case series.
    Clinical • Journal
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    HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • KIF5B (Kinesin Family Member 5B) • PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)
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    KRAS mutation • HER-2 amplification • MET amplification • MET exon 14 mutation • KIF5B-MET fusion • MET fusion