重组人 KLF5 蛋白 (GST tag N-Terminus)

补充信息

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KLF5 (Kruppel-like factor 5) also referred to as BTEB2 is a transcription factor with a molecular mass of approximately 54 kDa. It belongs to the KLF family characterized by its three C2H2-type zinc finger domains which bind to specific DNA sequences regulating gene expression. KLF5 displays ubiquitous expression but is highly concentrated in epithelial tissues specifically in the gastrointestinal tract and skin. This factor plays an essential role in the regulation of cell proliferation and differentiation.

Biological function summary

Kruppel-like factor 5 modulates gene transcription by binding to GC-rich elements in promoter regions influencing various cellular processes. KLF5 can interact with other transcription factors and co-regulators forming complexes important for its function. It significantly impacts epithelial cell dynamics affecting cell transformation differentiation and migration. In particular it plays a pivotal role in maintaining the proliferative capacity of epithelial cells and supporting wound healing processes.

Pathways

Kruppel-like factor 5 holds a notable position in the TGF-beta and Wnt signaling pathways which govern cellular growth control and development. In the TGF-beta pathway KLF5 can antagonize SMAD-mediated transcription suppression promoting cell proliferation particularly in epithelial stem cells. In the Wnt pathway it influences beta-catenin activity essential for epithelial cell renewal and maintenance. Through these pathways KLF5 interacts with proteins such as SMAD3 and beta-catenin coordinating cell turnover and tissue homeostasis.

KLF5 impacts cancer and cardiovascular diseases. It plays a complex role in oncogenesis where its overexpression is associated with colorectal breast and prostate cancers due to its ability to enhance proliferation. KLF5's interaction with proteins like p53 influences tumorigenic potentials. In cardiovascular disorders KLF5 contributes to vascular pathology affecting smooth muscle cell proliferation and atherosclerosis. Through its regulation of cyclin D1 it integrates into pathways leading to abnormal vascular smooth muscle growth linking it further to cardiovascular complications.