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Metabolism

The mitochondrial unfolded protein response inhibits pluripotency acquisition and mesenchymal-to-epithelial transition in somatic cell reprogramming

mitochondrial function

TMEM65 regulates and is required for NCLX-dependent mitochondrial calcium efflux

TMEM65

Hyperglycemia-triggered lipid peroxidation destabilizes STAT4 and impairs anti-viral Th1 responses in type 2 diabetes

type 2 diabetes
hyperglycemia
T helper 1 responses
lipid peroxidation

Misregulation of mitochondrial 6mA promotes the propagation of mutant mtDNA and causes aging in C. Elegans

6mA
mtDNA
mitochondrial genome
mitochondria

Spatial single-cell isotope tracing reveals heterogeneity of de novo fatty acid synthesis in cancer

heterogeneity
fatty acid

Organization of a functional glycolytic metabolon on mitochondria for metabolic efficiency

mitochondria
glucose
glucose metabolism

Futile lipid cycling: from biochemistry to physiology

Metabolism
glyceride

PNPO–PLP axis senses prolonged hypoxia in macrophages by regulating lysosomal activity

PNPO

Lysine acetyltransferase 6A maintains CD4+ T cell response via epigenetic reprogramming of glucose metabolism in autoimmunity

glucose metabolism
histone acetylation
autoimmune
KAT6A

Mitochondrial fatty acid synthesis is an emergent central regulator of mammalian oxidative metabolism

mitochondria
mitochondrial fatty acid synthesis
mtFAS
fatty acids

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Autophagy, Inflammation, & Metabolism Center of Biomedical Research Excellence

The AIM Center is funded by NIH grant P20GM121176, and it endows the state of New Mexico and the surrounding region with a state-of-the-art biomedical center and an intellectual and technological hub for cutting-edge research. On a larger scale, the AIM Center promises to be a nationally important center for the advancement of research on autophagy.

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