Editors' ChoiceCellular and Molecular Signaling

Papers of note in Nature 552 (7683)

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Science Signaling  12 Dec 2017:
Vol. 10, Issue 509, eaar6885
DOI: 10.1126/scisignal.aar6885

This week’s articles highlight a potential therapeutic target for fibrosis; parasite receptors that contribute to malaria; a potential drawback of PD-1 inhibition for cancer immunotherapy; a noncoding RNA that regulates ribosome biogenesis; and a structural analysis of substrate binding by the kinase PINK1.


Reducing fibroblast activation to protect against fibrosis

Schafer et al. found that interleukin-11 (IL-11) produced by activated fibroblasts induced kidney and heart fibrosis and that reducing IL-11 signaling protected mice from fibrosis and organ failure.


Parasite receptors promote malaria

Saito et al. demonstrate that parasite-encoded receptors that are present on the surface of Plasmodium falciparum–infected erythrocytes stimulate receptors that suppress the host immune response.


Unintended consequences of PD-1 inhibition

Wartewig et al. show that although inhibiting the immune receptor PD-1 on T cells can stimulate antitumor immunity, it can also promote T cell non-Hodgkin lymphomas (see commentary by Ludin and Zon).


A tsRNA as a potential target for treating cancer

Kim et al. report that a transfer-RNA–derived small RNA (tsRNA) binds to and promotes translation of a ribosomal protein mRNA and that inhibiting this noncoding RNA reduced liver tumor growth in mice.


How PINK1 targets substrates to promote mitophagy

Schubert et al. present a structural analysis of the kinase PINK1 that shows how this kinase phosphorylates substrates and how mutations associated with autosomal-recessive juvenile Parkinsonism affect substrate binding (see also commentary by Daou and Sicheri).

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