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Articles by Signalling Programme
The GPCR adaptor protein Norbin controls the trafficking of C5aR1 and CXCR4 in mouse neutrophils
Keywords agonist-induced internalisation β-arrestin C5aR1 CXCR4 G protein-coupled receptor (GPCR) GPCR trafficking Ncdn Neurochondrin P-Rex1 receptor desensitization receptor endocytosis receptor recycling Abbreviations C5a (complement factor 5a) C5aR1 (complement factor 5a receptor 1, C5a1) DPBS (Dulbecco’s phosphate buffered saline) FVD (fixable viability dye) GPCR (G protein-coupled receptor) GRK (G protein-coupled receptor kinase) GST (glutathione S-transferase) HBSS (Hank’s balanced salt...
Reporter cell lines to screen for inhibitors or regulators of the KRAS-RAF-MEK1/2-ERK1/2 pathway
Keywords: BRAF, ERK1/2, gene reporters, KRAS, MEK1/2, small molecules Subjects: Cancer, Signaling, Therapeutics & Molecular Medicine, Translational Science The RAS-regulated RAF–MEK1/2–ERK1/2 signalling pathway links growth factor-activated receptors to changes in gene expression in the nucleus, thereby controlling whether cells progress through the G1-to-S-phase cell cycle transition or arrest and differentiate [1].
The Rac-GEF Tiam1 controls integrin-dependent neutrophil responses
Introduction Neutrophils are leukocytes of the innate immune system that provide the first line of defence against bacterial and fungal infections, as well as fulfilling important roles in inflammation. They are recruited from the blood stream into infected tissues where they phagocytose, degranulate, and generate reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) to destroy invaded microorganisms (1–3).
Dock2 generates characteristic spatiotemporal patterns of Rac activity to regulate neutrophil polarisation, migration and phagocytosis
Introduction Neutrophils are leukocytes important in host defence against bacterial and fungal infections, as well as a host of other functions.
ERK1/2 inhibitors act as monovalent degraders inducing ubiquitylation and proteasome-dependent turnover of ERK2, but not ERK1
The discovery that intrinsic and acquired resistance to BRAFi and/or allosteric MEKi usually arises through reactivation of ERK1/2 [11,12,15] has fuelled the development of a range of catalytic or dual-mechanism small molecule ERK inhibitors (ERKi), many of which are undergoing clinical evaluation [16,17,23]. We previously noted that ERKi treatment appeared to cause a reduction in ERK1/2 abundance [17].
Non-canonical autophagy drives alternative ATG8 conjugation to phosphatidylserine
Highlights • ATG8 can undergo alternative conjugation to phosphatidylserine in cells • ATG8-PS occurs during non-canonical autophagy via single-membrane ATG8 conjugation • ATG8-PS can be induced by LAP, influenza A, and lysosomal ionic imbalance • ATG8-PS undergoes differential delipidation by ATG4 isoforms Summary Autophagy is a fundamental catabolic process that uses a unique post-translational modification, the conjugation of ATG8 protein to phosphatidylethanolamine (PE).
Programmed axon degeneration: from mouse to mechanism to medicine
Abstract Wallerian degeneration is a widespread mechanism of programmed axon degeneration. In the three decades since the discovery of the Wallerian degeneration slow (WldS) mouse, research has generated extensive knowledge of the molecular mechanisms underlying Wallerian degeneration, demonstrated its involvement in non-injury disorders and found multiple ways to block it.
Selective Autophagy of Mitochondria on a Ubiquitin-Endoplasmic-Reticulum Platform
Highlights • Mitophagy requires coordination of machineries for target recognition and engulfment • IVM-induced mitophagy depends on TRAF2/CIAP1/CIAP2 for ubiquitination of mitochondria • Ubiquitinated mitochondria within ER regions facilitate targeting and autophagy • ULK complex is required, but not for initiation, with FIP200 acting before ATG13 Summary The dynamics and coordination between autophagy machinery and selective receptors during mitophagy are unknown.
PTEN Regulates PI(3,4)P2 Signaling Downstream of Class I PI3K
A Method to Measure PI(3,4)P2 and PI(4,5)P2 by HPLC-MS Identification of the Major Phosphatases Controlling PI(3,4,5)P3 and PI(3,4)P2 Accumulation in EGF-Stimulated Mcf10a Cells PI(3,4,5)P3 and PI(3,4)P2 Accumulate in the Plasma Membrane of EGF-Stimulated Mcf10a Cells The Accumulation of PI(3,4)P2 in EGF-Stimulated Mcf10a Cells Is Class I PI3K Dependent PI(3,4)P2 Accumulation in EGF-Stimulated Mcf10a Cells Correlates with the Activation of AKT and Increased Numbers of Invadopodia How...
cAMP Signaling of Adenylate Cyclase Toxin Blocks the Oxidative Burst of Neutrophils through Epac-Mediated Inhibition of Phospholipase C Activity
cAMP Signaling of Adenylate Cyclase Toxin Blocks the Oxidative Burst of Neutrophils through Epac-Mediated Inhibition of Phospholipase C Activity Ondrej Cerny, Karen E. Anderson, Len R. Stephens, Phillip T. Hawkins, Peter Sebo The Journal of Immunology February 1, 2017, 198 (3) 1285-1296; DOI: 10.4049/jimmunol.1601309
Digesting the Expanding Mechanisms of Autophagy
Autophagy is a catabolic ‘self-eating’ pathway that is emerging as a crucial integration point in cell physiology. With its own set of genes, the autophagy pathway communicates with virtually all signalling networks and organelles. Recent advances have been made in understanding the origin of the autophagosomal membrane, novel regulators, and the mechanisms by which specific intracellular membranes become autophagy substrates.
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