KLF11

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External IDs	GeneCards: [1]
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Species	Human	Mouse
Entrez	n/a	n/a
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RefSeq (mRNA)	n/a	n/a
RefSeq (protein)	n/a	n/a
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Wikidata
View/Edit Human

Krueppel-like factor 11 is a protein that in humans is encoded by the KLF11 gene.

KLF11 is a mesoderm derived, zinc finger transcription factor in the Krüppel-like factor (KLF) family. It binds to SP1- like GC- rich sequences in epsilon and gamma globin gene promoters inhibiting cellular growth and causing apoptosis. In the regulation of genes, it is involved in cellular inflammation and differentiation, making it an essential factor in early embryonic development. This transcription factor binds to promoters of genes involved in cholesterol, prostaglandin, neurotransmitter, fat, and sugar metabolism, specifically pancreatic beta cell function. Defects in KLF11 affect glucose metabolism, insulin transcription, insulin processing, and insulin secretion which cause type 2 diabetes in adults and maturity-onset diabetes of the young type 7. These types of diabetes are caused by KLF11 interacting with co-repressors in the pancreatic islet beta cells. KLF11 has recently been shown to be involved in endometriosis since it regulated the expression of extracellular matrix genes. Its absence in extracellular matrix genes created a more fibrogenic response by the tissue. This was proved by creating a “knockout” model. The experiment showed that the absence of KLF11 showed higher amounts of fibrosis indicating that it prevents the growth of endometriotic lesions and inhibits pathological scarring.

Interactions

KLF11 has been shown to interact with SIN3A.

See also

• Krüppel-like factors
• Maturity onset diabetes of the young

Further reading

• Asano H, Li XS, Stamatoyannopoulos G (May 1999). "FKLF, a novel Krüppel-like factor that activates human embryonic and fetal beta-like globin genes". Molecular and Cellular Biology. 19 (5): 3571–9. PMC 84149. PMID 10207080.
• Zhang JS, Moncrieffe MC, Kaczynski J, Ellenrieder V, Prendergast FG, Urrutia R (Aug 2001). "A conserved alpha-helical motif mediates the interaction of Sp1-like transcriptional repressors with the corepressor mSin3A". Molecular and Cellular Biology. 21 (15): 5041–9. doi:10.1128/MCB.21.15.5041-5049.2001. PMC 87230. PMID 11438660.
• Jia L, Young MF, Powell J, Yang L, Ho NC, Hotchkiss R, Robey PG, Francomano CA (Jan 2002). "Gene expression profile of human bone marrow stromal cells: high-throughput expressed sequence tag sequencing analysis". Genomics. 79 (1): 7–17. doi:10.1006/geno.2001.6683. PMID 11827452.
• Ellenrieder V, Zhang JS, Kaczynski J, Urrutia R (May 2002). "Signaling disrupts mSin3A binding to the Mad1-like Sin3-interacting domain of TIEG2, an Sp1-like repressor". The EMBO Journal. 21 (10): 2451–60. doi:10.1093/emboj/21.10.2451. PMC 126002. PMID 12006497.
• Ou XM, Chen K, Shih JC (May 2004). "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". The Journal of Biological Chemistry. 279 (20): 21021–8. doi:10.1074/jbc.M312638200. PMID 15024015.
• Ellenrieder V, Buck A, Harth A, Jungert K, Buchholz M, Adler G, Urrutia R, Gress TM (Aug 2004). "KLF11 mediates a critical mechanism in TGF-beta signaling that is inactivated by Erk-MAPK in pancreatic cancer cells". Gastroenterology. 127 (2): 607–20. doi:10.1053/j.gastro.2004.05.018. PMID 15300592.
• Cao S, Fernandez-Zapico ME, Jin D, Puri V, Cook TA, Lerman LO, Zhu XY, Urrutia R, Shah V (Jan 2005). "KLF11-mediated repression antagonizes Sp1/sterol-responsive element-binding protein-induced transcriptional activation of caveolin-1 in response to cholesterol signaling". The Journal of Biological Chemistry. 280 (3): 1901–10. doi:10.1074/jbc.M407941200. PMID 15531587.
• Neve B, Fernandez-Zapico ME, Ashkenazi-Katalan V, Dina C, Hamid YH, Joly E, Vaillant E, Benmezroua Y, Durand E, Bakaher N, Delannoy V, Vaxillaire M, Cook T, Dallinga-Thie GM, Jansen H, Charles MA, Clément K, Galan P, Hercberg S, Helbecque N, Charpentier G, Prentki M, Hansen T, Pedersen O, Urrutia R, Melloul D, Froguel P (Mar 2005). "Role of transcription factor KLF11 and its diabetes-associated gene variants in pancreatic beta cell function". Proceedings of the National Academy of Sciences of the United States of America. 102 (13): 4807–12. doi:10.1073/pnas.0409177102. PMC 554843. PMID 15774581.
• Lim J, Hao T, Shaw C, Patel AJ, Szabó G, Rual JF, Fisk CJ, Li N, Smolyar A, Hill DE, Barabási AL, Vidal M, Zoghbi HY (May 2006). "A protein-protein interaction network for human inherited ataxias and disorders of Purkinje cell degeneration". Cell. 125 (4): 801–14. doi:10.1016/j.cell.2006.03.032. PMID 16713569.
• Buck A, Buchholz M, Wagner M, Adler G, Gress T, Ellenrieder V (Nov 2006). "The tumor suppressor KLF11 mediates a novel mechanism in transforming growth factor beta-induced growth inhibition that is inactivated in pancreatic cancer". Molecular Cancer Research. 4 (11): 861–72. doi:10.1158/1541-7786.MCR-06-0081. PMID 17114344.
• Florez JC, Saxena R, Winckler W, Burtt NP, Almgren P, Bengtsson Boström K, Tuomi T, Gaudet D, Ardlie KG, Daly MJ, Altshuler D, Hirschhorn JN, Groop L (Dec 2006). "The Krüppel-like factor 11 (KLF11) Q62R polymorphism is not associated with type 2 diabetes in 8,676 people". Diabetes. 55 (12): 3620–4. doi:10.2337/db06-0867. PMID 17130512.
• Spittau B, Wang Z, Boinska D, Krieglstein K (Jun 2007). "Functional domains of the TGF-beta-inducible transcription factor Tieg3 and detection of two putative nuclear localization signals within the zinc finger DNA-binding domain". Journal of Cellular Biochemistry. 101 (3): 712–22. doi:10.1002/jcb.21228. PMID 17252542.
• Niu X, Perakakis N, Laubner K, Limbert C, Stahl T, Brendel MD, Bretzel RG, Seufert J, Päth G (Jul 2007). "Human Krüppel-like factor 11 inhibits human proinsulin promoter activity in pancreatic beta cells". Diabetologia. 50 (7): 1433–41. doi:10.1007/s00125-007-0667-3. PMID 17479246.

External links

• KLF11+protein,+human at the US National Library of Medicine Medical Subject Headings (MeSH)

This article incorporates text from the United States National Library of Medicine, which is in the public domain.