Mouse embryonic fibroblasts null for the Krüppel-like factor 4 gene are genetically unstable

Krüppel-like factor 4 is a radioprotective factor for the intestine following γ-radiation-induced gut injury in mice

“…Furthermore, results of DNA-damage repair (Fig. 10) strongly support a role for Klf4 in DNA-damage repair response in vivo, consistent with its role in this response that was previously shown in vitro (12,24). Our data suggest a plausible model where, in the absence of Klf4 and following DNA damage, p21 could be driving the cell toward apoptosis and senescence, probably attributable to a defect in the DNA repair mechanism in Klf4 ⌬IS mice, as evident by the ␥H2AX staining.…”

A Small Ubiquitin-related Modifier-interacting Motif Functions as the Transcriptional Activation Domain of Krüppel-like Factor 4

“…Known to play a critical role in development, differentiation, metabolism, and physiology, KLF4 has been extensively investigated in recent years, especially after it was reported to be one of the four transcription factors that induce pluripotent stem cells (14,23,26,39). Thus, unveiling a general mechanism that regulates KLF4 transcriptional activity will greatly help understand the many basic events orchestrated by this multifunctional transcription factor and design better therapeutic strategies.…”

“…Co-immunoprecipitation-To independently detect binding of SUMO-1 to KLF4, Klf4-null (Klf4 Ϫ/Ϫ ), mouse embryonic fibroblasts (39) were co-transfected with the indicated KLF4 construct and Myc-tagged SUMO-1 lacking two carboxyl-terminal glycine residues that support SUMOylation (Myc-SUMO-1⌬GG). Three days later, cells were lysed in lysis buffer containing phosphatase inhibitors (Active Motif, catalog #54001).…”

Krüppel-like factor 4 (KLF4): What we currently know

“…Also, KLF4 has been shown to suppress transcription of CCNE to prevent centrosome amplification following DNA damage by γ-irradiation (33). Not only does KLF4 play a role in regulating centrosome duplication following DNA damage, but it regulates both centrosome duplication and chromosome number (genetic stability) both in vitro and in vivo (34,35). …”

“…Here following radiation-induced DNA damage, p53 induces KLF4 expression which in turn suppresses the expression of estrogen receptor-alpha, and thus abrogating estrogen-dependent breast cancer cell growth (161). In MEFs it was shown that KLF4 plays an essential role in modulating the DNA damage response and repair mechanisms (34,35). In vivo , KLF4 plays a role as a radio-protective factor against gastrointestinal syndrome in mice following total body γ-irradiation, does so both by inhibiting apoptosis in the acute response to irradiation and by contributing to crypt regeneration (39,41).…”