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GeneQ18032954· pop 5· linked from 814 articles

Also known as FKLF, FKLF1, MODY7, TIEG2, Tieg3, Kruppel-like factor 11, Kruppel like factor 11

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

Gene data

KLF11
Name
KLF transcription factor 11
Type
protein-coding
Aliases
FKLF, FKLF1, MODY7, TIEG2, Tieg3

The protein encoded by this gene is a zinc finger transcription factor that binds to SP1-like sequences in epsilon- and gamma-globin gene promoters. This binding inhibits cell growth and causes apoptosis. Defects in this gene are a cause of maturity-onset diabetes of the young type 7 (MODY7). Three transcript variants encoding two different isoforms have been found for this gene. [provided by RefSeq, Apr 2010].

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Gene · Ensembl

KLF transcription factor 11

Symbol
KLF11
Biotype
Protein coding
Organism
Homo sapiens
Location
2:10,042,849-10,054,958
Strand
Forward (+)
Assembly
GRCh38
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via Ensembl · EMBL-EBI

Wikidata facts

Show 5 more facts
HomoloGene ID
2668
genomic end
10194963
genomic start
10182976
cytogenetic location
2p25.1
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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.

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