The Krüppel‐like transcriptional factors Zf9 and GKLF coactivate the human keratin 4 promoter and physically interact

Okano, Jun-ichi; Opitz, Oliver G.; Nakagawa, Hiroshi; Jenkins, Timothy D.; Friedman, Scott L.; Rustgi, Anil K.

doi:10.1016/s0014-5793(00)01468-x

Cited by 62 publications

(42 citation statements)

References 15 publications

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“…A potential explanation for the apparent discrepancies stated above is that certain tumors may contain mutated forms of KLF4, which may exert a dominant negative effect on cell function. Previous studies indicating that KLF4 interacts with multiple regulatory proteins including Sp1 (40), p53 (19), Zf9 (41), and p300/ CBP (34) distinctly suggest that this latter hypothesis may be a possibility.…”

Section: Discussionmentioning

confidence: 94%

Krüppel-like Factor 4 (Gut-enriched Krüppel-like Factor) Inhibits Cell Proliferation by Blocking G1/S Progression of the Cell Cycle

Chen¹,

Johns²,

Geiman³

et al. 2001

Journal of Biological Chemistry

231

219

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Krü ppel-like factor 4 (KLF4) is an epithelial cell-enriched, zinc finger-containing transcription factor, the expression of which is associated with growth arrest. Previous studies show that constitutive expression of KLF4 inhibits DNA synthesis but the manner by which KLF4 exerts this effect is unclear. In the present study, we developed a system in which expression of KLF4 is controlled by a promoter that is induced upon treatment of cells containing the receptors for the insect hormone, ecdysone, with ponasterone A, an ecdysone analogue. The rate of proliferation of a stably transfected colon cancer cell line, RKO, was significantly decreased following addition of ponasterone A when compared with untreated cells. Flow cytometric analyses indicated that the inducible expression of KLF4 caused a block in the G 1 /S phase of the cell cycle. A similar block was observed when ecdysone receptor-containing RKO cells were infected with a replication-defective recombinant adenovirus containing an inducible KLF4 and treated with ponasterone A. Results of these studies provide evidence that the inhibitory effect of KLF4 on cell proliferation is mainly exerted at the G 1 /S boundary of the cell cycle.

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Section: Discussionmentioning

confidence: 94%

Krüppel-like Factor 4 (Gut-enriched Krüppel-like Factor) Inhibits Cell Proliferation by Blocking G1/S Progression of the Cell Cycle

Chen¹,

Johns²,

Geiman³

et al. 2001

Journal of Biological Chemistry

231

219

View full text Add to dashboard Cite

show abstract

“…The second set of data demonstrates that the minimal cyclin D1 promoter also contains multiple CACCC elements that bind KLF4 in vitro and that KLF4 binding results in in vivo repression of the promoter, an effect not seen after transfection of Sp1 (21). Finally, KLF4 activates late differentiation genes such as keratin 4 (22). Together these data argue that KLF4 levels play a critical role in the decision between proliferation and cell cycle arrest/differentiation.…”

Section: Proliferation or Differentiationmentioning

confidence: 90%

Krüppel-like Factors: Three Fingers in Many Pies

Bieker

2001

Journal of Biological Chemistry

559

496

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“…The molecular requirements for p21 WAF1/cip1 up-regulation by KLF6 have not been defined, and information about transcriptional coactivators within KLF6 transcriptional complexes is limited. Heterologous interaction of KLF6 with KLF4 or Sp1 is required for keratin (19) or endoglin gene expression (20), respectively, but potential interacting proteins in that context have not be explored.…”

Section: Introductionmentioning

confidence: 99%

Regulation of Krüppel-like Factor 6 Tumor Suppressor Activity by Acetylation

Li¹,

Yea²,

Dolios³

et al. 2005

Cancer Research

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Krüppel-like factor 6 (KLF6) is a zinc finger transcription factor and tumor suppressor that is inactivated in a number of human cancers by mutation, allelic loss, and/or promoter methylation. A key mechanism of growth inhibition by wildtype KLF6 is through p53-independent up-regulation of p21 WAF1/cip1 (CDKN1A), which is abrogated in several tumor-derived mutants. Here we show by chromatin immunoprecipitation that transactivation of p21 WAF1/cip1 by KLF6 occurs through its direct recruitment to the p21 WAF1/cip1 promoter and requires acetylation by histone acetyltransferase activity of either cyclic AMP-responsive element binding protein-binding protein or p300/CBP-associated factor. Direct lysine acetylation of KLF6 peptides can be shown by mass spectrometry. A single lysine-to-arginine point mutation (K209R) derived from prostate cancer reduces acetylation of KLF6 and abrogates its capacity to up-regulate endogenous p21WAF1/cip1 and reduce cell proliferation. These data indicate that acetylation may regulate KLF6 function, and its loss in some tumor-derived mutants could contribute to its failure to suppress growth in prostate cancer. (Cancer Res 2005; 65(20): 9216-25)

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The Krüppel‐like transcriptional factors Zf9 and GKLF coactivate the human keratin 4 promoter and physically interact

Cited by 62 publications

References 15 publications

Krüppel-like Factor 4 (Gut-enriched Krüppel-like Factor) Inhibits Cell Proliferation by Blocking G1/S Progression of the Cell Cycle

Krüppel-like Factor 4 (Gut-enriched Krüppel-like Factor) Inhibits Cell Proliferation by Blocking G1/S Progression of the Cell Cycle

Krüppel-like Factors: Three Fingers in Many Pies

Regulation of Krüppel-like Factor 6 Tumor Suppressor Activity by Acetylation

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