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Kruppel-like factor 11
Symbols KLF11; FKLF; FKLF1; MODY7; TIEG2; Tieg3
External IDs OMIM603301 MGI2653368 HomoloGene2668 GeneCards: KLF11 Gene
RNA expression pattern
PBB GE KLF11 218486 at tn.png
More reference expression data
Species Human Mouse
Entrez 8462 194655
Ensembl ENSG00000172059 ENSMUSG00000020653
UniProt O14901 Q8BHJ1
RefSeq (mRNA) XM_001129527 NM_178357
RefSeq (protein) XP_001129527 NP_848134
Location (UCSC) Chr 2:
10.1 - 10.11 Mb
Chr 12:
25.24 - 25.25 Mb
PubMed search [1] [2]

Krueppel-like factor 11 is a protein that in humans is encoded by the KLF11 gene.[1][2][3]



KLF11 has been shown to interact with SIN3A.[4][5]

See also


  1. ^ Cook T, Gebelein B, Mesa K, Mladek A, Urrutia R (Nov 1998). "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". J Biol Chem 273 (40): 25929–36. PMID 9748269.  
  2. ^ Scohy S, Gabant P, Van Reeth T, Hertveldt V, Dreze PL, Van Vooren P, Riviere M, Szpirer J, Szpirer C (Jan 2001). "Identification of KLF13 and KLF14 (SP6), novel members of the SP/XKLF transcription factor family". Genomics 70 (1): 93–101. doi:10.1006/geno.2000.6362. PMID 11087666.  
  3. ^ "Entrez Gene: KLF11 Kruppel-like factor 11".  
  4. ^ Zhang, J S; Moncrieffe M C, Kaczynski J, Ellenrieder V, Prendergast F G, Urrutia R (Aug. 2001). "A conserved alpha-helical motif mediates the interaction of Sp1-like transcriptional repressors with the corepressor mSin3A". Mol. Cell. Biol. (United States) 21 (15): 5041–9. doi:10.1128/MCB.21.15.5041-5049.2001. ISSN 0270-7306. PMID 11438660.  
  5. ^ Ellenrieder, Volker; Zhang Jin-San, Kaczynski Joanna, Urrutia Raul (May. 2002). "Signaling disrupts mSin3A binding to the Mad1-like Sin3-interacting domain of TIEG2, an Sp1-like repressor". EMBO J. (England) 21 (10): 2451–60. doi:10.1093/emboj/21.10.2451. ISSN 0261-4189. PMID 12006497.  

Further reading

  • Asano H, Li XS, Stamatoyannopoulos G (1999). "FKLF, a novel Krüppel-like factor that activates human embryonic and fetal beta-like globin genes.". Mol. Cell. Biol. 19 (5): 3571–9. PMID 10207080.  
  • Zhang JS, Moncrieffe MC, Kaczynski J, et al. (2001). "A conserved alpha-helical motif mediates the interaction of Sp1-like transcriptional repressors with the corepressor mSin3A.". Mol. Cell. Biol. 21 (15): 5041–9. doi:10.1128/MCB.21.15.5041-5049.2001. PMID 11438660.  
  • Jia L, Young MF, Powell J, et al. (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 (2002). "Signaling disrupts mSin3A binding to the Mad1-like Sin3-interacting domain of TIEG2, an Sp1-like repressor.". Embo J. 21 (10): 2451–60. doi:10.1093/emboj/21.10.2451. PMID 12006497.  
  • Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMID 12477932.  
  • Ota T, Suzuki Y, Nishikawa T, et al. (2004). "Complete sequencing and characterization of 21,243 full-length human cDNAs.". Nat. Genet. 36 (1): 40–5. doi:10.1038/ng1285. PMID 14702039.  
  • Ou XM, Chen K, Shih JC (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.". J. Biol. Chem. 279 (20): 21021–8. doi:10.1074/jbc.M312638200. PMID 15024015.  
  • Ellenrieder V, Buck A, Harth A, et al. (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.  
  • Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).". Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMID 15489334.  
  • Cao S, Fernandez-Zapico ME, Jin D, et al. (2005). "KLF11-mediated repression antagonizes Sp1/sterol-responsive element-binding protein-induced transcriptional activation of caveolin-1 in response to cholesterol signaling.". J. Biol. Chem. 280 (3): 1901–10. doi:10.1074/jbc.M407941200. PMID 15531587.  
  • Neve B, Fernandez-Zapico ME, Ashkenazi-Katalan V, et al. (2005). "Role of transcription factor KLF11 and its diabetes-associated gene variants in pancreatic beta cell function.". Proc. Natl. Acad. Sci. U.S.A. 102 (13): 4807–12. doi:10.1073/pnas.0409177102. PMID 15774581.  
  • Lim J, Hao T, Shaw C, et al. (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, et al. (2007). "The tumor suppressor KLF11 mediates a novel mechanism in transforming growth factor beta-induced growth inhibition that is inactivated in pancreatic cancer.". Mol. Cancer Res. 4 (11): 861–72. doi:10.1158/1541-7786.MCR-06-0081. PMID 17114344.  
  • Florez JC, Saxena R, Winckler W, et al. (2007). "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 (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.". J. Cell. Biochem. 101 (3): 712–22. doi:10.1002/jcb.21228. PMID 17252542.  
  • Niu X, Perakakis N, Laubner K, et al. (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

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



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