Krueppel-like factor 11 is a protein that in humans is encoded by the KLF11 gene.[5][6][7]

KLF11
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesKLF11, FKLF, FKLF1, MODY7, TIEG2, Tieg3, Kruppel-like factor 11, Kruppel like factor 11
External IDsOMIM: 603301; MGI: 2653368; HomoloGene: 2668; GeneCards: KLF11; OMA:KLF11 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001177716
NM_001177718
NM_003597

NM_178357

RefSeq (protein)

NP_001171187
NP_001171189
NP_003588

NP_848134

Location (UCSC)Chr 2: 10.04 – 10.05 MbChr 12: 24.7 – 24.71 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

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.

[8][9][10]

Interactions

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KLF11 has been shown to interact with SIN3A.[11][12]

See also

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References

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  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000172059Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000020653Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Cook T, Gebelein B, Mesa K, Mladek A, Urrutia R (Oct 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". The Journal of Biological Chemistry. 273 (40): 25929–36. doi:10.1074/jbc.273.40.25929. PMID 9748269.
  6. ^ Scohy S, Gabant P, Van Reeth T, Hertveldt V, Drèze PL, Van Vooren P, Rivière M, Szpirer J, Szpirer C (Nov 2000). "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.
  7. ^ "Entrez Gene: KLF11 Kruppel-like factor 11".
  8. ^ Daftary GS, Zheng Y, Tabbaa ZM, Schoolmeester JK, Gada RP, Grzenda AL, Mathison AJ, Keeney GL, Lomberk GA, Urrutia R (2013). "A novel role of the Sp/KLF transcription factor KLF11 in arresting progression of endometriosis". PLOS ONE. 8 (3): e60165. Bibcode:2013PLoSO...860165D. doi:10.1371/journal.pone.0060165. PMC 3610699. PMID 23555910.
  9. ^ Mathison A, Grzenda A, Lomberk G, Velez G, Buttar N, Tietz P, Hendrickson H, Liebl A, Xiong YY, Gores G, Fernandez-Zapico M, Larusso NF, Faubion W, Shah VH, Urrutia R (2013). "Role for Krüppel-like transcription factor 11 in mesenchymal cell function and fibrosis". PLOS ONE. 8 (9): e75311. Bibcode:2013PLoSO...875311M. doi:10.1371/journal.pone.0075311. PMC 3775729. PMID 24069400.
  10. ^ Spittau B, Krieglstein K (2012). "Klf10 and Klf11 as mediators of TGF-beta superfamily signaling". Cell and Tissue Research. 347 (1): 65–72. doi:10.1007/s00441-011-1186-6. PMID 21574058. S2CID 14295737.
  11. ^ 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.
  12. ^ 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.

Further reading

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