Abstract:
:The E2F transcription factors (TFs), which control the progression of the cell cycle in response to DNA-damage and various stresses, are known to interact with a tumor suppressor, Retinoblastoma 1 (RB1). We previously showed that the response of the human RB1 promoter to a 12-O-tetradecanoylphorbol-13-acetate (TPA) in HL-60 cells is mediated by a duplicated GGAA-motif, which is also present in the 5'-upstream of the E2F family genes. The motifs are especially rich in the 5'-upstream of the E2F4 gene. In the present study, we constructed Luciferase (Luc) expression vectors containing a 466-bp of the 5'-upstream of the human E2F4 gene. The transfection of this plasmid and deletion/mutation-introduced derivatives into HL-60 cells and a Luc reporter assay showed that duplicated and triplicated GGAA (TTCC) motifs in the E2F4 promoter respond to TPA. As expected, electrophoretic mobility shift assay (EMSA) indicated that SPI1 (PU.1) binds to the GGAA-motif containing element. A quantitative RT-PCR and Western blotting showed that the E2F4 transcripts and its encoding proteins accumulate during the differentiation of HL-60 into macrophage-like cells. In contrast, the expression of the E2F1 gene and the protein, which possibly acts as a cell cycle accelerator, was greatly diminished.
journal_name
J Biochemjournal_title
Journal of biochemistryauthors
Hamada H,Goto Y,Arakawa J,Murayama E,Ogawa Y,Konno M,Oyama T,Asai M,Sato A,Tanuma SI,Uchiumi Fdoi
10.1093/jb/mvz047subject
Has Abstractpub_date
2019-06-14 00:00:00eissn
0021-924Xissn
1756-2651pii
5519121pub_type
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pub_type: 杂志文章
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journal_title:Journal of biochemistry
pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Journal of biochemistry
pub_type: 杂志文章
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abstract::Heat-stable malate dehydrogenase isolated from Thermus flavus AT62 was completely inactivated by treatment with diethylpyrocarbonate. The inactivation was accompanied by the loss of 1.2 histidine residues per subunit of the enzyme. The enzyme was protected from inactivation by NADH. The enzyme was also inactivated by ...
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pub_type: 杂志文章
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更新日期:1986-06-01 00:00:00
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