Guangjin Zhou

TL;DR: KLF4 was found to cooperate with Stat6 to induce an M2 genetic program and inhibit M1 targets via sequestration of coactivators required for NF-κB activation and mice bearing myeloid-specific deletion of KLF4 exhibited delayed wound healing and were predisposed to developing diet-induced obesity, glucose intolerance, and insulin resistance.

TL;DR: It is shown that endothelial KLF4 is an essential determinant of atherogenesis and thrombosis andMechanistically, it is demonstrated that KLF 4 differentially regulated pertinent endothelial targets via competition for the coactivator p300, and cogent evidence is provided implicated as essential in vivo regulators of vascular function in the adult animal.

TL;DR: It is shown that KLF4 is necessary for maintenance of the epithelial phenotype in non-transformed MCF-10A mammary epithelial cells, and E-cadherin is identified as a novel transcriptional target of KLf4.

TL;DR: It is shown that endothelial KLF2 and KLF4 control a large segment of the endothelial transcriptome, thereby affecting virtually all key endothelial functions, and establishing an absolute requirement for KLF 2/4 for maintenance of endothelial and vascular integrity in the adult animal.

TL;DR: In this paper, the authors identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo, and demonstrate that exposure to either hypoxia and/or bacterial products reduced KLF2 expression while inducing hypoxyia inducible factor 1α (HIF-1α), findings that were recapitulated in human septic patients.