Gtf2h4-flox Mouse

Gtf2h4, or general transcription factor IIH subunit 4, is involved in transcription-dependent DNA repair mechanisms [2]. It is part of the major histocompatibility complex (MHC) class II region and may play a role in the immune system [3].

In ischemic diseases, Gtf2h4 promotes partial endothelial-to-mesenchymal transition (EndMT) and angiogenesis after ischemic injury. It activates NF-κB through NCOA3 phosphorylation at serine 1330, which enhances the interaction between NCOA3 and p65, thus activating the NF-κB/Snail signaling axis during partial EndMT [1]. Genetic variant rs114596632 in Gtf2h4 is associated with lung cancer risk, as the T allele is related to decreased DNA repair capacity phenotype and decreased mRNA expression levels [4]. In prostate cancer, Gtf2h4 is highly expressed, and high expression is associated with a higher biochemical recurrence rate, indicating a poor prognosis [5].

In summary, Gtf2h4 has significant functions in processes like EndMT and angiogenesis in ischemic diseases, and is associated with the risk and prognosis of diseases such as lung cancer and prostate cancer. Studies on Gtf2h4 contribute to understanding disease mechanisms and may offer potential therapeutic targets for hypoxic/ischemic diseases, lung cancer, and prostate cancer.