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Walerych et al. show that p53 missense mutants upregulate the proteasome and increase breast cancer cell resistance to proteasome inhibitors. Combined inhibition of p53 mutants and the proteasome leads to increased therapeutic efficacy.
Luschnig and colleagues present a model in which Staccato, in combination with Rab39, mediates the control of apical membrane fusion by interacting with components of the SNARE machinery in the formation of anastomoses in the tracheal tube.
Banh et al. show that PTP1B decreases non-mitochondrial oxygen consumption by regulating the RNF213/α-KGDD pathway, thus promoting hypoxic survival of cancer cells.
Galanos and colleagues observe p21 accumulation in proliferating cancer cells, and show that in cultured p53-null cells, p21 can cause genomic instability by perturbing replication licensing through inhibition of the CRL4-CDT ubiquitin ligase.
Baer et al. report that macrophage-specific DICER deletion abolishes TAM immunosuppressive activity and promotes anti-tumour immunity by recruitment and activation of cytotoxic T cells and increased IFN-γ production.
Kopito and Schrul show that the peroxisome proteins PEX19 and PEX3 mediate the correct insertion of the lipid droplet protein UBXD8 into ER subdomains.
Lee et al. report that aberrantly folded cytosolic proteins are recruited to the ER by the USP19 deubiquitylase, and are then encapsulated in late endosomes that fuse with the plasma membrane, leading to their secretion.
Torrano et al. use bioinformatics analyses to identify PGC1α as a transcriptional regulator of a metabolic program downstream of ERRα that opposes metastatic dissemination in prostate cancer.
Seokho et al. report that Wnt ligands bind the extracellular domain of polycystin 1 (PKD1) and induce Ca2+ influx through the Ca2+-permeable ion channel TRPP2. This activity is abrogated by PKD1 mutations linked to polycystic kidney disease.
Orhon et al. report that primary-cilium-mediated fluid flow sensing triggers autophagy through LKB1–AMPK–mTOR signalling, and thereby controls the volume of kidney epithelial cells.
Using long-term lineage tracing and mathematical modelling, Tumbar and colleagues define two separate stem cell populations in the epidermis that are regionally clustered, molecularly distinct and show different proliferation dynamics.
Mikkola and colleagues show that medial HOXA gene expression, induced by retinoic acid signalling, marks the establishment of the definitive HSC fate and controls HSC identity and function.
Welte et al. report that mTOR signalling regulates G-CSF production and accumulation of myeloid-derived suppressor cells (MDSCs) to the tumour site, which promotes the tumour-initiating capacity of cancer cells by activating Notch signalling.
Mendoza and colleagues provide insights into the specificity of the NoCut checkpoint, showing that although different types of chromosomal defects delay cytokinetic abscission, only after replication stress does this prevent DNA damage.
Nielsen et al. show that granulin is secreted by metastasis-associated macrophages to promote pancreatic cancer metastasis. Granulin activates hepatic stellate cells, which secrete periostin, thereby resulting in a fibrotic, pro-metastatic liver milieu.
Li et al. show that the c-Myc-dependent splicing switch from ketohexokinase-C (KHK-C) to KHK-A activates phosphoribosyl pyrophosphate synthetase 1 (PRPS1), resulting in enhanced de novo nucleic acid synthesis and hepatocellular carcinoma formation.
Rudolph and colleagues identify Per2 as a negative regulator of lymphoid-biased haematopoietic stem cells, and show that it reduces cell maintenance and function in response to DNA damage and ageing.
Tchorz and colleagues identify a role for the RSPO–LGR4/5–ZNRF3/RNF43 module as master regulator of Wnt/β-catenin-mediated metabolic liver zonation and hepatic growth/size control during development, homeostasis and regeneration.
Integrins and talin are parts of a ‘molecular clutch’ that mechanically links the actin cytoskeleton to the extracellular matrix. Elosegui-Artola et al. now reveal a tunable rigidity threshold, above which talin unfolds to mediate force transduction.