Estrogen receptor beta signaling in CD8⁺ T cells boosts T cell receptor activation and antitumor immunity through a phosphotyrosine switch.

ABSTRACT: BackgroundThe non-overlapping functions of the two estrogen receptor subtypes, ERα (Estrogen Receptor α)and ERβ (Estrogen Receptor β), in tumor cells have been studied extensively. However, their counterparts in host cells is vastly underinterrogated. Even less is known about how ERα and ERβ activities are regulated in a subtype-specific manner. We previously identified a phosphotyrosine residue (pY36) of human ERβ that is important for tumor ERβ to inhibit growth of breast cancer cells in vitro and in vivo. A role of this ERβ phosphotyrosine switch in regulating host ERβ remains unclear.Conventional gene editing was used to mutate the corresponding tyrosine residue of endogenous mouse ERβ (Y55F) in mouse embryonic stem cells. The derived homozygous mutant Esr2^Y55F/Y55F m

SUBMITTER: Yuan B 

PROVIDER: S-EPMC7816924 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature