In humans, the protein is 513 amino acids, with a predicted molecular weight of approximately 55kDa, and is encoded by the KLF4 gene.

[10] The KLF4 gene is conserved in chimpanzee, rhesus monkey, dog, cow, mouse, rat, chicken, zebrafish, and frog.

[43] KLF4 is expressed in a variety of tissues and organs such as: the cornea where it is required for epithelial barrier function[44][45] and is a regulator of genes required for corneal homeostasis;[46] the skin where it is required for the development of skin permeability barrier function;[47][48][49] the bone and teeth tissues where it regulates normal skeletal development;[50][51][52][53] epithelial cell of the mouse male and female reproductive tract[54] where in the males it is important for proper spermatogenesis;[55][56][57] vascular endothelial cells[58] where it is critical in preventing vascular leakage in response to inflammatory stimuli;[59] white blood cells where it mediates inflammatory responses cellular differentiation[60][61][62][63] and proliferation;[63][64] the kidneys where it is involved in the differentiation of embryonic stem cells and induced pluripotent stem (iPS) cells to renal lineage in vitro[65] and its dysregulation has been linked to some renal pathologies.

[76] Also, overexpression of KLF4 in skin resulted in hyperplasia and dysplasia,[77] which lead to the development of squamous cell carcinoma.

It may suppress angiogenesis by regulating NOTCH1 activity,[97] while in the central nervous system its overexpression leads to vascular dysplasia.

[98] KLF4 may promote inflammation by mediating NF-κB-dependent inflammatory pathway such as in macrophages,[18] esophageal epithelium[79] and in chemically-induced acute colitis in mice.

[99] Additionally, KLF-4 downregulates TNF-α-induced VCAM1 expression by targeting and blocking the binding site of NF-κB to the VCAM1 promoter.

[34] Takahashi and Yamanaka were the first to identify KLF4 as one of four factors ( oct-3/4 + sox2 + Klf4 + c-Myc ) that are required to induce mouse embryonic and adult fibroblasts into pluripotent stem cells (iPS).

This article incorporates text from the United States National Library of Medicine, which is in the public domain.