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Showing 1-6 of 6 results for "MAK156" within Papers
Mona S Nilsen et al.
Diabetes, 69(9), 1903-1916 (2020-06-27)
Circulating branched-chain amino acids (BCAAs) associate with insulin resistance and type 2 diabetes. 3-Hydroxyisobutyrate (3-HIB) is a catabolic intermediate of the BCAA valine. In this study, we show that in a cohort of 4,942 men and women, circulating 3-HIB is
Rong Huang et al.
JCI insight, 4(18) (2019-09-20)
Age is a well-established risk factor for impaired bone fracture healing. Here, we identify a role for apolipoprotein E (ApoE) in age-associated impairment of bone fracture healing and osteoblast differentiation, and we investigate the mechanism by which ApoE alters these
Nikos Koundouros et al.
Cell, 181(7), 1596-1611 (2020-06-20)
Oncogenic transformation is associated with profound changes in cellular metabolism, but whether tracking these can improve disease stratification or influence therapy decision-making is largely unknown. Using the iKnife to sample the aerosol of cauterized specimens, we demonstrate a new mode
Stephanie Kim et al.
Environmental health perspectives, 129(7), 77006-77006 (2021-07-30)
Chemicals in disparate structural classes activate specific subsets of the transcriptional programs of peroxisome proliferator-activated receptor-γ (PPARγ) to generate adipocytes with distinct phenotypes. Our objectives were to a) establish a novel classification method to predict PPARγ ligands and modifying chemicals;
Stephanie Kim et al.
Archives of toxicology, 94(9), 3087-3103 (2020-07-20)
Triphenyl phosphate (TPhP) is an environmental PPARγ ligand, and growing evidence suggests that it is a metabolic disruptor. We have shown previously that the structurally similar ligand, tributyltin, does not induce brite adipocyte gene expression. Here, using in vivo and
Xingzhe Ma et al.
Cell metabolism, 33(5), 1001-1012 (2021-03-11)
Understanding the mechanisms underlying how T cells become dysfunctional in a tumor microenvironment (TME) will greatly benefit cancer immunotherapy. We found that increased CD36 expression in tumor-infiltrating CD8+ T cells, which was induced by TME cholesterol, was associated with tumor progression and
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