KLF11
KLF11 (KLF transcription factor 11) is a nuclear zinc finger transcription factor of the Sp1 family that binds SP1-like sequences in target promoters. It is also known as Tieg3, TIEG2, FKLF and MODY7, and it inhibits cell growth and induces apoptosis. Browse Assay Genie's current range of KLF11 research reagents below, or read on for the biology behind the target.
KLF11 is a transcription factor that regulates gene expression by binding SP1-like sequences in promoter regions. It activates the epsilon- and gamma-globin gene promoters and, to a much lower degree, the beta-globin gene. It also represses promoters containing SP1-like binding sites, and this repression is associated with inhibition of cell growth. In addition, KLF11 represses transcription of SMAD7, which enhances TGF-beta signalling, and it induces apoptosis.
The KLF11 gene encodes a protein that belongs to the Sp1 C2H2-type zinc-finger family and is classified by HGNC within the zinc fingers C2H2-type group and the KLF transcription factors. The protein is located in the nucleus, consistent with its role in controlling transcription. According to the NCBI Gene summary, three transcript variants encoding two different isoforms have been reported. Researchers working with the KLF11 protein or gene will find a mouse ortholog, Klf11.
The gene was previously named TGFB inducible early growth response 2 and Kruppel like factor 11, and the aliases Tieg3, TIEG2, FKLF and MODY7 are still found in the literature. Defects in the KLF11 gene are a cause of maturity-onset diabetes of the young type 7 (MODY7), which links this transcription factor to disease. Its effects on SMAD7 place it in the regulation of TGF-beta signalling, while its growth-inhibitory and pro-apoptotic activity makes it relevant to studies of cell proliferation and survival.
KLF11 binds SP1-like sequences and both activates and represses promoters, making it a useful model for Sp1-family transcriptional control.
KLF11 activates the epsilon- and gamma-globin promoters and, much less strongly, the beta-globin gene.
KLF11 represses SMAD7 transcription, which enhances TGF-beta signalling, so it is studied as a modulator of this pathway.
Defects in KLF11 cause MODY7, and the protein inhibits cell growth and induces apoptosis, supporting work in disease and cell fate.
KLF11 is a nuclear transcription factor that binds SP1-like sequences. It activates the epsilon- and gamma-globin promoters, represses SP1-like promoters to inhibit cell growth, represses SMAD7 to enhance TGF-beta signalling, and induces apoptosis.
KLF11 is also called Tieg3, TIEG2, FKLF and MODY7. Earlier names include TGFB inducible early growth response 2 and Kruppel like factor 11. The NCBI Gene summary reports three transcript variants encoding two different isoforms.
Defects in the KLF11 gene are a cause of maturity-onset diabetes of the young type 7 (MODY7). A mouse ortholog, Klf11, exists, so rodent models can be used; check the datasheet of any product for its validated reactivity.
Other KLF transcription factors and Sp1-family zinc finger proteins with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt O14901; product specifications from Assay Genie datasheets.