KLF11 Antibody – Mouse Monoclonal

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]

TIEG2: Transcription factor. Activates the epsilon- and gamma- globin gene promoters and, to a much lower degree, the beta-globin gene and represses promoters containing SP1-like binding inhibiting cell growth. Represses transcription of SMAD7 which enhances TGF-beta signaling. Induces apoptosis. Defects in KLF11 are the cause of maturity-onset diabetes of the young type 7 (MODY7). MODY is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease. Belongs to the Sp1 C2H2-type zinc-finger protein family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: DNA-binding; C2H2-type zinc finger protein; Transcription factor

Chromosomal Location of Human Ortholog: 2p25

Cellular Component: nucleus

Molecular Function: metal ion binding; transcription factor activity

Biological Process: transcription from RNA polymerase II promoter; G1/S-specific transcription in mitotic cell cycle; negative regulation of cell proliferation; positive regulation of apoptosis; apoptosis; negative regulation of transcription from RNA polymerase II promoter

Disease: Maturity-onset Diabetes Of The Young, Type 7