PRKCBProtein Kinase C, Beta1
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(2017) Genomewide association studies identify PRKCB as genetic susceptibility locus for primary biliary cirrhosis in the Japanese population.
In addition, the Hif1an, Inppl1, Runx1, Nr4a2, Creb3l1, Fzd1, Prkcb, Cbx6, Eif2c2, Ncor2, Tnrc6b, Carm1, Sf1 and Ppap2b in all of potential target genes of miR-184 were enriched in 5 GO terms related to cellular biosynthetic process (P less than 0.01) such as regulation of cellular macromolecule biosynthetic process, regulation of macromolecule biosynthetic process, regulation of cellular biosynthetic process, regulation of biosynthetic process and regulation of gene expression (Table 2, Figure 4).
In particular, miR-129 has 16 predicted target genes [platelet-derived growth factor receptor, alpha polypeptide (PDGFRA); platelet-derived growth factor receptor, beta polypeptide (PDGFRB); epidermal growth factor receptor (EGFR); phospholipase C, gamma 1 (PLCG1), SHC (Src homology 2 domain containing) transforming protein 4 (SHC4); protein kinase C, alpha (PRKCA); protein kinase C, beta (PRKCB); protein kinase C, delta (PRKCD) protein kinase C, epsilon (PRKCE); protein kinase C, iota (PRKCI); growth factor receptor-bound protein 2 (GRB2); son of sevenless homolog 1 (SOS1); SOS2; v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS); death-associated protein kinase 1 (DAPK1); DAPK2; DAPK3; and ribosomal protein S6 kinase, 90kDa, polypeptide 5 (RPS6KA5) (also known as MSK1)].
Moreover, protein kinase C-[beta] (PRKCB) activation is directly regulated by the chimeric oncogene EWSR1-FLI1.
During the postmyocardial infarction period, we showed that nondiabetic hearts responded with altered levels for transcripts representing markers of inflammation (upregulation of Il10, Tnf, Il1b, and Il6 expressions), apoptosis (upregulation of Tp53, Bax, and caspase 3 expressions), antioxidant defense (downregulation of Gpx3, Gpx4, Gstk1, Txnrd2, Sod3, and catalase expressions), and the prosurvival PI3K/Akt pathway (upregulation of Rps6k, Btk, Pik3cg, and Prkcb and down regulation of pdk2 and Prkcz expressions).
Six highly ranked genes (DENND1B, LYN, MRPL30, POC1B, PRKCB, and RP4-655J12.3) were identified as candidates for T2DM (Table 1).