Contents
Vol 10, Issue 482
Research Articles
- IRE1α promotes viral infection by conferring resistance to apoptosis
A prosurvival signaling pathway in cells infected with hepatitis C virus overrides interferon responses to impair antiviral resistance.
- Intercellular transmission of the unfolded protein response promotes survival and drug resistance in cancer cells
Prostate cancer cells release an ER stress response signal that enhances tumor growth and drug resistance.
- Radiation inhibits salivary gland function by promoting STIM1 cleavage by caspase-3 and loss of SOCE through a TRPM2-dependent pathway
Radiation for head and neck cancers causes dry mouth by suppressing store-operated Ca2+ entry in salivary glands.
Podcast
- Science Signaling Podcast for 6 June 2017: Calcium signaling and dry mouth
Radiation therapy for head and neck cancers causes dry mouth by interfering with Ca2+ signaling in salivary gland cells (Liu et al. in 6 June 2017 issue).
Editors' Choice
- Highlight: Understanding radiation sialadenitis
A nonapoptotic function of caspase-3 underlies the salivary gland complications of radiation therapy of head and neck cancers.
- An adenosine receptor for olfaction
Extracellular processing of ATP in the fish olfactory epithelium produces adenosine that is perceived by olfactory neurons.
- Paper of note in Science 356 (6341)
This week’s article is about a lipid that stimulates or inhibits mTORC1 signaling depending on where in the cell the lipid is made.
- Papers of note in Science Translational Medicine 9 (392)
This week’s articles describe a new drug conjugate to treat pain, a target for preventing cognitive decline in Alzheimer’s disease, and a strategy for sensitizing RAS-mutant cancers to PARP inhibitors.
- Papers of note in Nature 546 (7656)
This week’s articles highlight the role of follicle-stimulating hormone in postmenopausal adipose tissue accumulation, the importance of a sphingolipid for T cell survival, and the cryo-EM structure of a G protein–coupled receptor complex.
About The Cover

Online Cover This week features a Research Article that shows that cells lacking the transcription factor XBP1, which stimulates type I interferon (IFN) production as part of the unfolded protein response, are defective in controlling infection by the hepatitis C virus (HCV). Instead of being defective in IFN production, however, the XBP1-deficient infected cells failed to undergo apoptosis, thus facilitating increased viral replication. The image is an illustration of HCV. [Image: Dr_Microbe/istockphoto]