氨基酸序列
>lcl|BSEQ0008737|Protein kinase C eta type
MSSGTMKFNGYLRVRIGEAVGLQPTRWSLRHSLFKKGHQLLDPYLTVSVDQVRVGQTSTK
QKTNKPTYNEEFCANVTDGGHLELAVFHETPLGYDHFVANCTLQFQELLRTTGASDTFEG
WVDLEPEGKVFVVITLTGSFTEATLQRDRIFKHFTRKRQRAMRRRVHQINGHKFMATYLR
QPTYCSHCREFIWGVFGKQGYQCQVCTCVVHKRCHHLIVTACTCQNNINKVDSKIAEQRF
GINIPHKFSIHNYKVPTFCDHCGSLLWGIMRQGLQCKICKMNVHIRCQANVAPNCGVNAV
ELAKTLAGMGLQPGNISPTSKLVSRSTLRRQGKESSKEGNGIGVNSSNRLGIDNFEFIRV
LGKGSFGKVMLARVKETGDLYAVKVLKKDVILQDDDVECTMTEKRILSLARNHPFLTQLF
CCFQTPDRLFFVMEFVNGGDLMFHIQKSRRFDEARARFYAAEIISALMFLHDKGIIYRDL
KLDNVLLDHEGHCKLADFGMCKEGICNGVTTATFCGTPDYIAPEILQEMLYGPAVDWWAM
GVLLYEMLCGHAPFEAENEDDLFEAILNDEVVYPTWLHEDATGILKSFMTKNPTMRLGSL
TQGGEHAILRHPFFKEIDWAQLNHRQIEPPFRPRIKSREDVSNFDPDFIKEEPVLTPIDE
GHLPMINQDEFRNFSYVSPELQP
具体功能
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.
基因序列
>lcl|BSEQ0013386|Protein kinase C eta type (PRKCH)
ATGTCGTCTGGCACCATGAAGTTCAATGGCTATTTGAGGGTCCGCATCGGTGAGGCAGTG
GGGCTGCAGCCCACCCGCTGGTCCCTGCGCCACTCGCTCTTCAAGAAGGGCCACCAGCTG
CTGGACCCCTATCTGACGGTGAGCGTGGACCAGGTGCGCGTGGGCCAGACCAGCACCAAG
CAGAAGACCAACAAACCCACGTACAACGAGGAGTTTTGCGCTAACGTCACCGACGGCGGC
CACCTCGAGTTGGCCGTCTTCCACGAGACGCCCCTGGGCTACGACCACTTCGTGGCCAAC
TGCACCCTGCAGTTCCAGGAGCTGCTGCGCACGACCGGCGCCTCGGACACCTTCGAGGGT
TGGGTGGATCTCGAGCCAGAGGGGAAAGTATTTGTGGTAATAACCCTTACCGGGAGTTTC
ACTGAAGCTACTCTCCAGAGAGACCGGATCTTCAAACATTTTACCAGGAAGCGCCAAAGG
GCTATGCGAAGGCGAGTCCACCAGATCAATGGACACAAGTTCATGGCCACGTATCTGAGG
CAGCCCACCTACTGCTCTCACTGCAGGGAGTTTATCTGGGGAGTGTTTGGGAAACAGGGT
TATCAGTGCCAAGTGTGCACCTGTGTCGTCCATAAACGCTGCCATCATCTAATTGTTACA
GCCTGTACTTGCCAAAACAATATTAACAAAGTGGATTCAAAGATTGCAGAACAGAGGTTC
GGGATCAACATCCCACACAAGTTCAGCATCCACAACTACAAAGTGCCAACATTCTGCGAT
CACTGTGGCTCACTGCTCTGGGGAATAATGCGACAAGGACTTCAGTGTAAAATATGTAAA
ATGAATGTGCATATTCGATGTCAAGCGAACGTGGCCCCTAACTGTGGGGTAAATGCGGTG
GAACTTGCCAAGACCCTGGCAGGGATGGGTCTCCAACCCGGAAATATTTCTCCAACCTCG
AAACTCGTTTCCAGATCGACCCTAAGACGACAGGGAAAGGAGAGCAGCAAAGAAGGAAAT
GGGATTGGGGTTAATTCTTCCAACCGACTTGGTATCGACAACTTTGAGTTCATCCGAGTG
TTGGGGAAGGGGAGTTTTGGGAAGGTGATGCTTGCAAGAGTAAAAGAAACAGGAGACCTC
TATGCTGTGAAGGTGCTGAAGAAGGACGTGATTCTGCAGGATGATGATGTGGAATGCACC
ATGACCGAGAAAAGGATCCTGTCTCTGGCCCGCAATCACCCCTTCCTCACTCAGTTGTTC
TGCTGCTTTCAGACCCCCGATCGTCTGTTTTTTGTGATGGAGTTTGTGAATGGGGGTGAC
TTGATGTTCCACATTCAGAAGTCTCGTCGTTTTGATGAAGCACGAGCTCGCTTCTATGCT
GCAGAAATCATTTCGGCTCTCATGTTCCTCCATGATAAAGGAATCATCTATAGAGATCTG
AAACTGGACAATGTCCTGTTGGACCACGAGGGTCACTGTAAACTGGCAGACTTCGGAATG
TGCAAGGAGGGGATTTGCAATGGTGTCACCACGGCCACATTCTGTGGCACGCCAGACTAT
ATCGCTCCAGAGATCCTCCAGGAAATGCTGTACGGGCCTGCAGTAGACTGGTGGGCAATG
GGCGTGTTGCTCTATGAGATGCTCTGTGGTCACGCGCCTTTTGAGGCAGAGAACGAAGAT
GACCTCTTTGAGGCCATACTGAATGATGAGGTGGTCTACCCTACCTGGCTCCATGAAGAT
GCCACAGGGATCCTAAAATCTTTCATGACCAAGAACCCCACCATGCGCTTGGGCAGCCTG
ACTCAGGGAGGCGAGCACGCCATCTTGAGACATCCTTTTTTTAAGGAAATCGACTGGGCC
CAGCTGAACCATCGCCAAATAGAACCGCCTTTCAGACCCAGAATCAAATCCCGAGAAGAT
GTCAGTAATTTTGACCCTGACTTCATAAAGGAAGAGCCAGTTTTAACTCCAATTGATGAG
GGACATCTTCCAATGATTAACCAGGATGAGTTTAGAAACTTTTCCTATGTGTCTCCAGAA
TTGCAACCATAG