Editors' ChoiceCellular and Molecular Signaling

Papers of note in Nature 548 (7666)

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Science Signaling  15 Aug 2017:
Vol. 10, Issue 492, eaao6386
DOI: 10.1126/scisignal.aao6386

This week’s articles describe the consequences of preserving pluripotency in cultured stem cells, how glutamate metabolism in T cells contributes to autoimmune disease, and how inactivating BRAF mutations promote tumor growth.


The costs of preservation

Choi et al. and Yagi et al. report that even short-term preservation of the pluripotency of stem cells in vitro with typical methods using kinase inhibitors alters the expression of genes associated with developmental disorders. In a commentary, Zwaka discusses how these findings raise important and cautionary questions for developmental research and clinical applications.


Harnessing immunometabolism to treat autoimmune disease

Xu et al. showed that metabolism epigenetically controls T cell fate and that targeting a glutamate-dependent metabolic pathway may be therapeutic against TH17 cell–mediated autoimmune disease.


RAS required for BRAF-inactivated tumors

Yao et al. and Nieto et al. found that inactivating mutations in the kinase BRAF drive tumor growth when coexistent with RAS activation.

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