ArticleBiochemistry and biophysics reports2021
KLF4 transactivates TRIM29 expression and modulates keratin network.
Article in Biochemistry and biophysics reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- ALK5 inhibition reduces HDM-induced inflammation and oxidative injury by regulating KLF4-mediated glycolysis in BEAS-2B cells.Journal of bioenergetics and biomembranes · 2026Article
- The role of KLF4 in phagocyte activation during infectious diseases.Frontiers in immunology · 2025Review
- O-GlcNAcylation of TRIM29 and OGT translation forms a feedback loop to promote adaptive response of PDAC cells to glucose deficiency.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- The Kruppel-like factor 4-signal transducer and activator of transcription 5A axis promotes pancreatic fibrosis in mice with caerulein-induced chronic pancreatitis.Experimental animals · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Krüppel-like factor 4 (KLF4) is well known to be a conserved zinc-containing transcription factor that participates in diverse biological processes such as cell proliferation and differentiation. In this study, we found KLF4 can bind specific site in the promoter of TRIM29 to transactivate its transcription, and sumoylation modification on 278 lysine site was not essential for KLF4 to transactivate TRIM29 transcription. It also was showed that KLF4 promoted cell migration when overexpressed, and knockdown of TRIM29 abrogated the migration triggered by KLF4. In addition, overexpression of KLF4 reduced the phosphorylation level of keratin 8 at 432 amino acid site. Our study demonstrated that KLF4 is an important transcription factor on regulating TRIM29 expression and modulates the keratin network.
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Registered trials
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