Disease relevance of Klf4

• Furthermore, a GKLF overexpressing adenovirus inhibited whereas GKLF morpholino antisense oligos increased expression of endogenous SMC marker genes [1].

High impact information on Klf4

• Krüppel-like factor 4 (KLF4/GKLF) is a target of bone morphogenetic proteins and transforming growth factor beta 1 in the regulation of vascular smooth muscle cell phenotype [2].
• Results of transient transfection studies showed that GKLF-induced repression of a SM alpha-actin promoter/luciferase reporter gene partially depended on the TCE [1].
• GKLF is thought to participate in the switch from cell proliferation to differentiation [3].

Biological context of Klf4

• The aims of the present studies were to: 1) determine the role of the SM alpha-actin TCE in vivo through mutagenesis studies in transgenic mice and 2) further characterize the possible role and mechanisms by which the TCE-binding factor GKLF/KLF4 induces repression of SMC marker genes in various SMC model systems in vitro [1].

Other interactions of Klf4

• A transforming growth factor-beta control element required for SM alpha-actin expression in vivo also partially mediates GKLF-dependent transcriptional repression [1].

Analytical, diagnostic and therapeutic context of Klf4

• Results of chromatin immunoprecipitation assays showed GKLF binding to TCE containing regions of various SMC marker gene promoters within intact chromatin [1].

References