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Gene Review

KLF11  -  Kruppel-like factor 11

Homo sapiens

Synonyms: FKLF, FKLF1, Krueppel-like factor 11, MODY7, TGFB-inducible early growth response protein 2, ...
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Disease relevance of KLF11

  • The fact that this function of KLF11 is inhibited by oncogenic Erk/mitogen-activated protein kinase in pancreatic cancer cells emphasizes the importance of this mechanism for oncogenesis [1].
  • KLF11-regulated functions require the Mad1-like SID, indicating that these target genes involved in these phenomena are regulated via this corepressor system [2].
  • KLF11 expression renders cells more sensitive to oxidative drugs, an effect that is rescued by infection with recombinant adenoviruses expressing SOD2 and Catalase1 [2].
  • Further characterization of these ABM cultures was determined by following mRNA expression for the transcription factors erythroid Kruppel-like factor (EKLF) and fetal Kruppel-like factor (FKLF) as a function of time in cultures under hypoxia and normoxia [3].

High impact information on KLF11


Biological context of KLF11


Anatomical context of KLF11


Associations of KLF11 with chemical compounds

  • A common glutamine-to-arginine change at codon 62 (Q62R) in its gene KLF11 has been recently associated with type 2 diabetes in two independent samples [8].
  • Neither the Q62R nor any other common variant in KLF11 was associated with T2D in the Pima population [9].

Physical interactions of KLF11


Regulatory relationships of KLF11

  • In luciferase assays FKLF activated the gamma- and epsilon-globin gene promoters, and, to a much lower degree, the beta-globin promoter [7].
  • KLF11 is a biochemical paradigm for a subset of proteins that repress transcription via a Mad1-like mSin3A interacting domain (SID) [2].

Other interactions of KLF11


Analytical, diagnostic and therapeutic context of KLF11

  • A combination of random oligonucleotide binding, EMSA, luciferase reporter, and chromatin immunoprecipitation assays shows that KLF11 binds to the insulin promoter and regulates its activity in beta cells [4].
  • Molecular cloning and characterization of TIEG2 reveals a new subfamily of transforming growth factor-beta-inducible Sp1-like zinc finger-encoding genes involved in the regulation of cell growth [6].


  1. KLF11 mediates a critical mechanism in TGF-beta signaling that is inactivated by Erk-MAPK in pancreatic cancer cells. Ellenrieder, V., Buck, A., Harth, A., Jungert, K., Buchholz, M., Adler, G., Urrutia, R., Gress, T.M. Gastroenterology (2004) [Pubmed]
  2. An mSin3A interaction domain links the transcriptional activity of KLF11 with its role in growth regulation. Fernandez-Zapico, M.E., Mladek, A., Ellenrieder, V., Folch-Puy, E., Miller, L., Urrutia, R. EMBO J. (2003) [Pubmed]
  3. The effect of hypoxia and stem cell source on haemoglobin switching. Narayan, A.D., Ersek, A., Campbell, T.A., Colón, D.M., Pixley, J.S., Zanjani, E.D. Br. J. Haematol. (2005) [Pubmed]
  4. Role of transcription factor KLF11 and its diabetes-associated gene variants in pancreatic beta cell function. Neve, B., Fernandez-Zapico, M.E., Ashkenazi-Katalan, V., Dina, C., Hamid, Y.H., Joly, E., Vaillant, E., Benmezroua, Y., Durand, E., Bakaher, N., Delannoy, V., Vaxillaire, M., Cook, T., Dallinga-Thie, G.M., Jansen, H., Charles, M.A., Clément, K., Galan, P., Hercberg, S., Helbecque, N., Charpentier, G., Prentki, M., Hansen, T., Pedersen, O., Urrutia, R., Melloul, D., Froguel, P. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  5. KLF11-mediated repression antagonizes Sp1/sterol-responsive element-binding protein-induced transcriptional activation of caveolin-1 in response to cholesterol signaling. Cao, S., Fernandez-Zapico, M.E., Jin, D., Puri, V., Cook, T.A., Lerman, L.O., Zhu, X.Y., Urrutia, R., Shah, V. J. Biol. Chem. (2005) [Pubmed]
  6. Molecular cloning and characterization of TIEG2 reveals a new subfamily of transforming growth factor-beta-inducible Sp1-like zinc finger-encoding genes involved in the regulation of cell growth. Cook, T., Gebelein, B., Mesa, K., Mladek, A., Urrutia, R. J. Biol. Chem. (1998) [Pubmed]
  7. FKLF, a novel Krüppel-like factor that activates human embryonic and fetal beta-like globin genes. Asano, H., Li, X.S., Stamatoyannopoulos, G. Mol. Cell. Biol. (1999) [Pubmed]
  8. The Kruppel-Like Factor 11 (KLF11) Q62R Polymorphism Is Not Associated With Type 2 Diabetes in 8,676 People. Florez, J.C., Saxena, R., Winckler, W., Burtt, N.P., Almgren, P., Bengtsson Bostr??m, K., Tuomi, T., Gaudet, D., Ardlie, K.G., Daly, M.J., Altshuler, D., Hirschhorn, J.N., Groop, L. Diabetes (2006) [Pubmed]
  9. Association analysis of Krüppel-like factor 11 variants with type 2 diabetes in Pima Indians. Ma, L., Hanson, R.L., Que, L.N., Mack, J.L., Franks, P.W., Infante, A.M., Kobes, S., Bogardus, C., Baier, L.J. J. Clin. Endocrinol. Metab. (2008) [Pubmed]
  10. Dual functions of transcription factors, transforming growth factor-beta-inducible early gene (TIEG)2 and Sp3, are mediated by CACCC element and Sp1 sites of human monoamine oxidase (MAO) B gene. Ou, X.M., Chen, K., Shih, J.C. J. Biol. Chem. (2004) [Pubmed]
  11. Modulation of transforming growth factor beta (TGFbeta)/Smad transcriptional responses through targeted degradation of TGFbeta-inducible early gene-1 by human seven in absentia homologue. Johnsen, S.A., Subramaniam, M., Monroe, D.G., Janknecht, R., Spelsberg, T.C. J. Biol. Chem. (2002) [Pubmed]
  12. A conserved alpha-helical motif mediates the interaction of Sp1-like transcriptional repressors with the corepressor mSin3A. Zhang, J.S., Moncrieffe, M.C., Kaczynski, J., Ellenrieder, V., Prendergast, F.G., Urrutia, R. Mol. Cell. Biol. (2001) [Pubmed]
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