Jmjd1c-flox Mouse

Jmjd1c, a member of JmjC domain histone demethylase, is involved in multiple biological processes. It participates in pathways related to cell differentiation, metabolism, and immune regulation, which are crucial for maintaining normal physiological functions and are associated with various diseases [1,2,3,4,5,6]. Genetic models, especially gene knockout (KO) and conditional knockout (CKO) mouse models, have been instrumental in studying its functions.

In B cells, Jmjd1c deficiency promotes plasma cell differentiation, leading to enhanced disease severity in rheumatoid arthritis (RA) as it causes STAT3 Lys140 hypermethylation, disrupting its interaction with Ptpn6 and sustaining abnormal phosphorylation and activity [1]. In tumor Treg cells, JMJD1C deletion enhances AKT and STAT3 signals, leading to interferon-γ production and Treg cell fragility, suggesting its role in tumor immune evasion [2]. In pulmonary arterial hypertension, JMJD1C knockdown suppresses hypoxia-induced pulmonary arterial smooth muscle cell (PASMC) hyperproliferation and glycolysis by inhibiting STAT3 activation [3].

In conclusion, Jmjd1c is a key regulator in multiple biological processes. Its KO/CKO mouse models have revealed its significance in diseases such as RA, cancer, and pulmonary arterial hypertension, contributing to our understanding of disease mechanisms and potential therapeutic targets.