C. Chi

Mitochondrial Fatty Acid Synthesis and Mecr Regulate CD4+ T Cell Function and Oxidative Metabolism

This study shows that Mecr, a mitochondrial fatty acid synthesis gene, is critical for CD4+ T cell metabolism, function, and survival, with implications for inflammatory diseases and mitochondrial disorders.

Tissue-Specific Dependence of Th1 Cells on the Amino Acid Transporter SLC38A1 in Inflammation

This study identifies tissue- and subset-specific roles of SLC38A1 in Th1 cell function during inflammation, showing its importance in EAE and IBD but not lung inflammation.

Androgen Signaling Restricts Glutaminolysis to Drive Sex-Specific Th17 Metabolism

The paper shows that androgen signaling reduces glutaminolysis in male Th17 cells, leading to sex-specific metabolic differences that affect Th17-mediated inflammation.

Functional Overlap of Inborn Errors of Immunity and Metabolism Genes Define T Cell Immunometabolic Vulnerabilities

The paper identifies functional overlap between inborn errors of immunity and metabolism genes, revealing immunometabolic vulnerabilities in T cells.

Subset-specific mitochondrial and DNA damage shapes T cell responses to fever and inflammation

The paper shows that fever increases inflammatory activity in CD4+ T cells but causes mitochondrial dysfunction and DNA damage specifically in Th1 cells, leading to p53-dependent apoptosis to prevent mutations.

The dynamic properties of a nuclear coactivator binding domain are evolutionarily conserved

The paper compares the dynamic properties of an ancient NCBD from a bilaterian ancestor to human NCBD, finding conserved dynamics despite increased thermodynamic stability.

Suppression of canonical TGF-β signaling enables GATA4 to interact with H3K27me3 demethylase JMJD3 to promote cardiomyogenesis

The paper identifies how TGF-β signaling inhibition allows GATA4 to interact with JMJD3, promoting cardiomyogenesis by demethylating H3K27me3 at cardiac gene promoters.

Maturation of human induced pluripotent stem cell-derived cardiomyocytes for modeling hypertrophic cardiomyopathy

This study develops a method to mature hiPSC-CMs, enabling them to model adult-onset cardiovascular disease like hypertrophic cardiomyopathy.