Aging drives chronic disease in part through senescent cells, including macrophages, which fuel inflammation. Senescent macrophages are functionally heterogeneous: canonical p16-high macrophages promote tumorigenesis or, in other contexts, disease tolerance, whereas we previously identified a distinct p21-high, p16-low...
Grasiela Torres, Ivan A. Salladay-Perez, Christina Y. Deng et al.· bioRxiv· 0 citations
Metabolic reprogramming is a hallmark of cancer cells, and stem-like populations often upregulate aldehyde dehydrogenases (ALDHs). Functional studies have established essential roles for individual ALDH isoforms in tumor initiation, progression, and metastasis; however, the mechanisms by which these enzymes promote mal...
Zhi-Ping Feng, Thomas E. Bearrood, Sydney L. Campbell et al.· bioRxiv· 0 citations
A previously unrecognized chromatin-to-metabolism axis connecting gain-of-function ASXL1 truncation to mitochondrial pyruvate transport is defined, identifying MPC as a central mediator of epigenetic-metabolic crosstalk in both a rare developmental syndrome and ASXL1-mutant myeloid malignancy.
Isabella Lin, Michael Sigfrid S. Reyes, A. Krall et al.· bioRxiv· 0 citations
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