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Induced neuronal cells acquire epigenomic signatures specific to matured neurons.

Partial chemical reprogramming is able to reduce the biological age of cells by diverting them to a different metabolic state marked by a strong upregulation of mitochondrial oxidative phosphorylation.

Single cell RNA sequencing reveals that mouse embryonic stem cells can be differentiated into the same terminal motor neuron state via distinct differentiation paths, one of which includes a surprising intermediate state not found in embryos.

Hemodynamic forces regulate endothelial cell metabolism, which in turn regulates endothelial inflammation.

Increased Notch signaling enhances germ cell reprograming in C. elegans by antagonizing PRC2-mediated repression, which results in the activation of UTX-1 and other reprograming-promoting genes.

In patients with coronary artery disease, bone marrow myeloid progenitor cells are reprogrammed towards myeloid skewing and inflammatory activation.

Downregulation of PTBP1 in neurons, but not astrocytes, alleviates motor symptoms in a Parkinson’s disease mouse model by inducing dopaminergic marker expression in striatal neurons and increasing striatal dopamine levels.

Oncoprotein BCL6 confers tumor adaptive resistance to genotoxic stress through the IFN-BCL6-PTEN axis in solid tumors and presents a promising combinational target for chemo-sensitization.

A non-canonical p53 function in adipocyte plays a critical role in energy homeostasis and is involved in obesity-associated metabolic dysfunctions.

Gene knockout in cell lines and mice reveal that store-operated calcium entry is synergistically mediated by Orai1 and Orai3 channel proteins in B cells and is important for signaling to the nucleus and metabolic activity in response to antigenic stimulation.