Dnajc10, also known as ERdj5, is a member of the HSP40 family and an ER-resident chaperone protein. It is involved in multiple biological processes, such as regulating the unfolded protein response (UPR) pathway, which is crucial for cells to adapt to endoplasmic reticulum stress. It also seems to be associated with maintaining cell survival, self-renewal, and is potentially involved in cell-cycle and apoptosis-related mechanisms [1,3].

In leukemia, deficiency of Dnajc10 in the MLL-AF9-induced murine leukemia model led to a significant abrogation of AML development and suppression of leukemia stem cell self-renewal. Mechanistically, inhibition of Dnajc10 induced endoplasmic reticulum stress and promoted activation of the PERK-EIF2α-ATF4 branch of the UPR [1]. In mice with alcoholic liver disease, Dnajc10 knockout mice exhibited exacerbated alcohol-induced liver injury, hepatic steatosis, and oxidative stress, indicating its protective role through regulating the Nrf2 pathway and glutathione contents [2].

In conclusion, Dnajc10 is essential for maintaining cell homeostasis, especially in response to endoplasmic reticulum stress. Its deficiency in mouse models has revealed its significance in leukemia development and alcoholic liver disease. These findings suggest that Dnajc10 could potentially be a therapeutic target in these disease areas.