General Information of the m6A Target Gene (ID: M6ATAR00621)
Target Name Protein kinase C eta type (PKC-eta)
Synonyms
PKC-L; nPKC-eta
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Gene Name PKC-eta
Chromosomal Location 14q23.1
Family Protein kinase superfamily, AGC Ser/Thr protein kinase family, PKC subfamily
Function
Calcium-independent, phospholipid- and diacylglycerol (DAG)-dependent serine/threonine-protein kinase that is involved in the regulation of cell differentiation in keratinocytes and pre-B cell receptor, mediates regulation of epithelial tight junction integrity and foam cell formation, and is required for glioblastoma proliferation and apoptosis prevention in MCF-7 cells. In keratinocytes, binds and activates the tyrosine kinase FYN, which in turn blocks epidermal growth factor receptor (EGFR) signaling and leads to keratinocyte growth arrest and differentiation. Associates with the cyclin CCNE1-CDK2-CDKN1B complex and inhibits CDK2 kinase activity, leading to RB1 dephosphorylation and thereby G1 arrest in keratinocytes. In association with RALA activates actin depolymerization, which is necessary for keratinocyte differentiation. In the pre-B cell receptor signaling, functions downstream of BLNK by up-regulating IRF4, which in turn activates L chain gene rearrangement. Regulates epithelial tight junctions (TJs) by phosphorylating occludin (OCLN) on threonine residues, which is necessary for the assembly and maintenance of TJs. In association with PLD2 and via TLR4 signaling, is involved in lipopolysaccharide (LPS)-induced RGS2 down-regulation and foam cell formation. Upon PMA stimulation, mediates glioblastoma cell proliferation by activating the mTOR pathway, the PI3K/AKT pathway and the ERK1-dependent phosphorylation of ELK1. Involved in the protection of glioblastoma cells from irradiation-induced apoptosis by preventing caspase-9 activation. In camptothecin-treated MCF-7 cells, regulates NF-kappa-B upstream signaling by activating IKBKB, and confers protection against DNA damage-induced apoptosis. Promotes oncogenic functions of ATF2 in the nucleus while blocking its apoptotic function at mitochondria. Phosphorylates ATF2 which promotes its nuclear retention and transcriptional activity and negatively regulates its mitochondrial localization.
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Gene ID 5583
Uniprot ID
KPCL_HUMAN
HGNC ID
HGNC:9403
Ensembl Gene ID
ENSG00000027075
KEGG ID
hsa:5583
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
PKC-eta can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
Browse Regulator
Browse Disease
Methyltransferase-like 3 (METTL3) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3
Cell Line Caco-2 cell line Homo sapiens
Treatment: shMETTL3 Caco-2 cells
Control: shNTC Caco-2 cells
GSE167075
Regulation
logFC: 8.88E-01
p-value: 2.37E-29
More Results Click to View More RNA-seq Results
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary Specific depletion of METTL3 in pericytes suppressed diabetes-induced pericyte dysfunction and Microvascular complication in vivo. METTL3 overexpression impaired pericyte function by repressing Protein kinase C eta type (PKC-eta), FAT4, and PDGFRA expression, which was mediated by YTHDF2-dependent mRNA decay.
Target Regulation Down regulation
Responsed Disease Diseases of arteries or arterioles ICD-11: BD5Y
In-vitro Model ACBRI-183 (Human retinal pericytes (ACBRI-183) was obtained from Cell Systems Corp. (CSC, USA))
In-vivo Model Mettl3 floxed mice were purchased from GemPharmatech Co. Ltd (Nanjing, China). Pdgfr-Beta-Cre mice were purchased from Beijing Biocytogen Co. Ltd (Beijing, China) generated on C57BL/6J background. Mettl3 flox/flox mice were crossed with Pdgfr-Beta-Cre mice to generate pericyte-specific Mettl3 knockout mice. All mice were bred under the specific-pathogen free condition with free access to diet and water or their nursing mothers with alternating 12/12 light-dark cycle (lights on at 08:00 and off at 20:00).
Diseases of arteries or arterioles [ICD-11: BD5Y]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Specific depletion of METTL3 in pericytes suppressed diabetes-induced pericyte dysfunction and Microvascular complication in vivo. METTL3 overexpression impaired pericyte function by repressing Protein kinase C eta type (PKC-eta), FAT4, and PDGFRA expression, which was mediated by YTHDF2-dependent mRNA decay.
Responsed Disease Diseases of arteries or arterioles [ICD-11: BD5Y]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
In-vitro Model ACBRI-183 (Human retinal pericytes (ACBRI-183) was obtained from Cell Systems Corp. (CSC, USA))
In-vivo Model Mettl3 floxed mice were purchased from GemPharmatech Co. Ltd (Nanjing, China). Pdgfr-Beta-Cre mice were purchased from Beijing Biocytogen Co. Ltd (Beijing, China) generated on C57BL/6J background. Mettl3 flox/flox mice were crossed with Pdgfr-Beta-Cre mice to generate pericyte-specific Mettl3 knockout mice. All mice were bred under the specific-pathogen free condition with free access to diet and water or their nursing mothers with alternating 12/12 light-dark cycle (lights on at 08:00 and off at 20:00).
References
Ref 1 METTL3-mediated N (6)-methyladenosine modification governs pericyte dysfunction during diabetes-induced retinal vascular complication. Theranostics. 2022 Jan 1;12(1):277-289. doi: 10.7150/thno.63441. eCollection 2022.