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Anti-KLF4 serum, from rabbit

ITEM#: 3042-ABE2860100UL

MFR#: ABE2860-100UL

Krueppel-like factor 4 (UniProt: Q60793; also known as Epithelial zinc finger protein EZF, Gut-enriched krueppel-like factor, KLF4) is encoded by the Klf4 (also known as Ezf, Gklf, Zie) gene (Gene ID: 16600) in murine species. Klf4 is a member of the

Krueppel-like factor 4 (UniProt: Q60793; also known as Epithelial zinc finger protein EZF, Gut-enriched krueppel-like factor, KLF4) is encoded by the Klf4 (also known as Ezf, Gklf, Zie) gene (Gene ID: 16600) in murine species. Klf4 is a member of the krueppel C2H2-type zinc-finger protein family that regulates multiple biological processes, including proliferation, differentiation, development, and apoptosis. KLF4 is a developmentally regulated transcription factor that plays an important role in maintaining the pluripotent state in embryonic stem cells (ESCs) and can be used as a marker of the pluripotent state for cells in culture. It can serve both as activator and as repressor depending upon its environment, but its most prominent function is growth suppression. Interestingly, increased expression of Klf4 leads to an increase in expression of P21WAF1/CIP1, which is an important checkpoint protein that inhibits cell cycle progression and is essential in mediating the cell cycle arrest at both the G1/S and G2/M boundaries. Klf4 also mediates the normal functions of the tumor suppressor p53 and contributes to the down-regulation of p53/TP53 transcription. Mutations in Klf4 gene can lead to unchecked growth and tumor formation. KLF4 is shown to be often mutated in many colon cancer cell lines and the lack of Klf4 expression is correlated with colorectal cancer pathogenesis. Elevated expression of Klf4 gene has been linked to gastric cancer, breast cancer, and squamous cell carcinomas. KLF4 is reported to target the primary miR1-2 loop promoter and stimulates miR-1 expression. Loss of KLF4 expression is considered as a mechanistic link between aggressive prostate cancer progression and low canonical AR output through miR-1 inactivation. (Ref.: Jiang, J., et al. (2008). Nat. Cell Biol. 10(3); 353-360; Siu, MK et al. (2016). Oncogenesis 5: e282).