Hdac1-flox Mouse

Hdac1, a histone deacetylase, catalyzes lysine deacetylation of histone and non-histone proteins. It is involved in regulating major endothelial functions like angiogenesis, inflammatory signalling, redox homeostasis, and nitric oxide signalling, impacting whole animal physiology [1]. Hdac1 also plays roles in other biological processes such as neuroinflammation, dendritic cell development, and anti-tumor immunity [2,3].

In dendritic cell development, genetic deletion of Hdac1 in hematopoietic progenitors and CD11c-expressing cells impairs pro-pDC and mature pDC generation, and affects ESAM + cDC2 differentiation, while cDC1s are unchanged. Without Hdac1, DCs enhance tumor surveillance through increased cDC1 maturation and interleukin-12 production, driving T helper 1-mediated immunity and CD8+ T cell recruitment [3]. In the Meibomian gland, co-deletion of Hdac1/2 in MG epithelium causes gradual loss of acini and formation of cyst-like structures, indicating their redundant function in adult MG epithelial progenitor cell proliferation and survival [4].

In conclusion, Hdac1 is essential in multiple biological processes. Model-based research, especially KO/CKO mouse models, has revealed its crucial roles in dendritic cell-related anti-tumor immunity and Meibomian gland homeostasis. Understanding Hdac1 function helps in uncovering disease mechanisms and developing potential therapeutic strategies.