High impact information on USF1

• Knockdown of USF1 expression leads to a loss of histone modification recruitment and subsequent encroachment of H3K9 methylation [1].
• Upstream stimulatory factor (USF) is recruited into a steroid hormone-triggered regulatory circuit by the estrogen-inducible transcription factor delta EF1 [2].
• In addition, USF-1 overexpression is able to induce Ov gene promoter activity in transfection experiments [2].
• Moreover, mutating the deltaEF1 binding sites in the 5'-flanking region of the Ov gene abrogates induction of the gene by USF-1 [2].
• The MRE/cMyc complex plays a major role in the basal level expression, and shares some similarities to the upstream stimulatory factor element (USF) identified in the promoter regions of mammalian HO-1 genes and other stress regulated genes [3].

Analytical, diagnostic and therapeutic context of USF1

• Gel mobility shift assays and co-immunoprecipitation experiments identify USF-1 as a component of Chirp-III [2].

References