Sensing the environment: a historical perspective on integrin signal transduction

By C. Miranti, J. Brugge. Nature Cell Biology, 2002

886 citations recorded by the source corpus.

Subfields: Immunology, Immunology and Allergy, Oncology

View Paper: https://www.semanticscholar.org/paper/50783d5106b646e07c70be577560054644bb7614

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Citations in the corpus

Foreign body reaction to biomaterials. (2008, background): “[38,39] FAK becomes activated following integrin binding and is responsible for regulating cytoskeletal dynamics and in turn the assembly and disassembly of focal adhesions[40] FAK is recruited to the focal adhesion complex and is tyrosine phosphorylated.”
A mechanical checkpoint controls multicellular growth through YAP/TAZ regulation by actin-processing factors. (2013, positive): “…are cell shape, cell geometry, deformation generated by the pulling forces of the extracellular matrix (ECM) and of neighboring cells, and the associated changes in cytoskeletal organization and tension (Berrier and Yamada, 2007; Miranti and Brugge, 2002; Schwartz, 2010; Vogel and Sheetz, 2006).”
Integrins and extracellular matrix in mechanotransduction. (2010, background): “Integrins can also associate laterally in the plasma membrane with other cell surface proteins, including tetraspanins, growth factor receptors, matricellular proteins, and matrix protease receptors.(8) The ECM is a complex mixture of matrix molecules, including glycoproteins, collagens, laminins, g”
Focal adhesion kinase: the first ten years (2003, background): “In the interim, much progress has been made regarding integrin signaling and the role of protein tyrosine kinases, and FAK in particular, in this pathway (Miranti and Brugge, 2002; Schwartz and Ginsberg, 2002).”
Integrin signalling at a glance (2009, background): “…the affinity of integrins for their extracellular ligands (integrin activation and inactivation) was first appreciated in blood cells, whose aggregation within the circulation or integrin-dependent adhesion to vessel walls must be strictly localised to appropriate sites (Miranti and Brugge, 2002).”
Matrix Crosslinking Forces Tumor Progression by Enhancing Integrin signaling (2009, background): “The findings suggest that ECM stiffness, as induced byelevatedcollagencrosslinking could promote breast malignancy by enhancing integrinGFR crosstalk (Figure 7I) (Miranti and Brugge, 2002).”
The epigenetic progenitor origin of human cancer (2006, background): “Explanted haematopoietic and solid tumour cells not only acquire other phenotypes in vitro or in vivo , but these phenotypes can be modified depending on the cellular and tissue matrix milieu into which they are introduce”
Integrin signalling during tumour progression (2004, background): “Both integrins bind to the latent complex that holds TGF-β inactive, but each uses a distinct mechanism to induce the release of active TGF-&beta”
Functional structure and composition of the extracellular matrix (2003, background): “This involves separation of the cytoplasmic tails of the α and β chains and probably leads to conformational changes in the extracellular domain of the heterodimer, allowing it to effectively interact with its ligand [16,19].”