Editors' ChoiceCellular and Molecular Signaling

Papers of note in Science 355 (6330)

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Sci. Signal.  21 Mar 2017:
Vol. 10, Issue 471, eaan2405
DOI: 10.1126/scisignal.aan2405

This week’s articles include several reviews on targeting signaling pathways to treat cancer, as well as research articles that highlight proteins that drive circadian clocks; how bacteriophages affect the virulence of pathogenic bacteria; a mobile transcription factor in plants; a secreted nucleoside that affects metabolism; and the effects of protein aggregation in aging yeast cells.

CIRCADIAN RHYTHMS

Molecular clockwork from cyanobacteria

Tseng et al. and Snijder et al. performed structural analyses that show how three proteins interact to make the cyanobacterial circadian clock tick.

INFECTION

The parasite of my parasite is my friend?

Diard et al. show that by reducing inflammation, vaccination inhibits transfer of virulence-promoting phages and limits Salmonella spp. evolution during infections in mice.

PLANT BIOLOGY

Making more of your stomata

Raissig et al. demonstrated how a mobile transcription factor builds better stomata in grasses.

PHYSIOLOGY

Uridine’s rise and fall: Food for thought

Deng et al. found that plasma uridine amounts are controlled by feeding behavior, a discovery with possible implications for metabolic disease (see also Jastroch and Tschöp).

AGING

Protein aggregation–mediated aging in yeast

Schlissel et al. report that the sterility of old yeast cells is caused by protein aggregation (see also Gitler and Jarosz).

CANCER THERAPY

PARP inhibitors: Synthetic lethality in the clinic

Lord and Ashworth explain how drugs that amplify the detrimental effects of BRCA mutations on DNA repair cause cell death and have antitumor activity.

Drugging RAS: Know the enemy

Papke and Der review past unsuccessful strategies for targeting mutant RAS in human cancer and illustrate why there are reasons to still be optimistic.

Waste disposal—An attractive strategy for cancer therapy

Salami and Crews highlight an emerging class of cancer drugs that act by targeting specific cancer-causing proteins for selective degradation.

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