It has long been recognized that adhesion receptors cooperate with the cytoskeleton during morphogenesis, tissue remodeling and homeostasis. But how this occurs is less well-understood. A host of cytoskeletal regulators have been reported to have functional and biochemical linkage with adhesion receptors. The challenge remains to find functionally-coherent patterns within this increasingly large corpus of molecular information. In this review we discuss one approach, to identify distinctive functional modules that contribute to different adhesive processes. We illustrate this by considering Arp2/3-driven surface protrusion, which is utilized at both integrin-based cell-matrix adhesions and cadherin-based cell-cell adhesions. We further argue that regulatory proteins, such as cortactin, serve to coordinate the molecular components of this protrusive apparatus into a cohesive module.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1002/cm.20380 | DOI Listing |
J Biol Chem
January 2025
Department of Psychiatry, Columbia University Vagelos College of Physicians and Surgeons, New York, NY, USA; Department of Molecular Pharmacology and Therapeutics, Columbia University Vagelos College of Physicians and Surgeons, New York, NY, USA; Division of Molecular Therapeutics, New York State Psychiatric Institute, New York, NY, USA. Electronic address:
Most adhesion GPCRs undergo autoproteolytic cleavage during receptor biosynthesis, resulting in non-covalently bound N- and C-terminal fragments (NTF and CTF) that remain associated during receptor trafficking to the plasma membrane. While substantial evidence supports increased G protein signaling when just the CTF is expressed, there is an ongoing debate about whether NTF removal is required to initiate signaling in the context of the wild-type receptor. Here, we use adhesion GPCR latrophilin-3 (ADGRL3) as a model receptor to investigate tethered agonist-mediated activation.
View Article and Find Full Text PDFViruses
November 2024
Department of Microbiology, University of Washington School of Medicine, Seattle, WA 98109, USA.
Certain species D human adenoviruses (HAdV-D19, -D37, and -D64) are causative agents of epidemic keratoconjunctivitis. HAdV-D37 has previously been shown to bind CD46 (membrane cofactor protein) and sialic acid as adhesion receptors. HAdV-D64 is genetically highly similar to HAdV-D37, with an identical fiber protein sequence, but differs substantially in its penton base and hexon proteins, two other major capsid components, due to genetic recombination.
View Article and Find Full Text PDFInt J Biol Macromol
December 2024
Research Institute for Prevention of Non-Communicable Diseases, Cellular and Molecular Research Center, Qazvin University of Medical Sciences, Qazvin, Iran. Electronic address:
Integrin αvβ3, a primary cell-adhesion receptor, plays a crucial role in various biological processes, including angiogenesis, pathological neovascularization, and tumor metastasis. Its expression increases during tumor angiogenesis. The insulin-like growth factor 1 receptor (IGF1R) is a transmembrane protein that stimulates vital signaling pathways, promoting cancer cell growth, survival, and metabolism.
View Article and Find Full Text PDFDev Cell
December 2024
Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany; Technische Universität Dresden, Biotechnologisches Zentrum, Center for Molecular and Cellular Bioengineering (CMCB), Dresden, Germany; Cluster of Excellence Physics of Life, TU Dresden, Dresden, Germany. Electronic address:
Tight junctions play an essential role in sealing tissues, by forming belts of adhesion strands around cellular perimeters. Recent work has shown that the condensation of ZO1 scaffold proteins is required for tight junction assembly. However, the mechanisms by which junctional condensates initiate at cell-cell contacts and elongate around cell perimeters remain unknown.
View Article and Find Full Text PDFJ Pediatr Hematol Oncol
January 2025
Department of Pediatrics, The University of North Carolina at Chapel Hill, Chapel Hill, NC.
Constitutional platelet disorders have become better understood since Bernard and Soulier first described a case in 1948. Their diagnosis can also be challenging due to overlap in clinical presentation and lab findings with platelet type von Willebrand. Bernard-Soulier syndrome is a disorder caused by GPIb receptor mutations that decrease its affinity for von Willebrand factor resulting in reduced platelet function and macrothrombocytopenia.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!