Map3k7, also known as TGF-β -activated kinase 1 (TAK1), is a member of the MAPK kinase kinase (MAPKKK) family. It plays a crucial role in regulating a wide range of physiological and pathological processes, participating in pathways such as NF -κB and MAPKs activation. It functions through assembling with TAK1 -binding proteins (TAB1, TAB2, and TAB3) and can be activated by stimuli like TNFα, IL -1β, and toll -like receptor ligands [3].

In prostate cancer, Map3k7 knockout increased AR protein levels and activity in the mouse prostate, and MAP3K7 and AR protein levels were inversely correlated in patient specimens. This indicates that the inflammation -activated MAP3K7-IKKβ axis has a tumor-suppressive function in degrading AR protein [1].

In hypertensive nephropathy, TRIM31 knockout mice showed aggravated hypertension-induced renal dysfunction, fibrosis, and inflammation, as TRIM31 promotes the proteasomal degradation of MAP3K7, negatively regulating TGF -β1-mediated Smad and MAPK/NF -κB signaling pathways [2].

In mouse embryonic stem cells, inhibiting Map3k7 with a specific inhibitor dramatically decreased endoderm differentiation, suggesting that Map3k7 governs the formation or proliferation of cardiogenic endoderm [4].

In conclusion, Map3k7 is essential in multiple biological processes and disease conditions. Gene knockout models in mice have revealed its significant role in prostate cancer, hypertensive nephropathy, and endoderm differentiation. Understanding Map3k7 functions can provide insights into disease mechanisms and potential therapeutic strategies for related diseases.