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Cited by 391

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Role of Rac1 and Oxygen Radicals in Collagenase-1 Expression Induced by Cell Shape Change

Kheradmand, Farrah, Werner, Erica, Tremble, Patrice, Symons, Marc, Werb, Zena·1998·Science

Abstract

Integrin-mediated reorganization of cell shape leads to an altered cellular phenotype. Disruption of the actin cytoskeleton, initiated by binding of soluble antibody to α5β1 integrin, led to increased expression of the collagenase-1 gene in rabbit synovial fibroblasts. Activation of the guanosine triphosphate–binding protein Rac1, which was downstream of the integrin, was necessary for this process, and expression of activated Rac1 was sufficient to increase expression of collagenase-1. Rac1 activation generated reactive oxygen species that were essential for nuclear factor kappa B–dependent transcriptional regulation of interleukin-1α, which, in an autocrine manner, induced collagenase-1 gene expression. Remodeling of the extracellular matrix and consequent alterations of integrin-mediated adhesion and cytoarchitecture are central to development, wound healing, inflammation, and malignant disease. The resulting activation of Rac1 may lead to altered gene regulation and alterations in cellular morphogenesis, migration, and invasion.

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Metadata

Authors
Kheradmand, F., Werner, E., Tremble, P., Symons, M., & Werb, Z.
Venue
Science
Published
1998-05-08
Volume
280
Issue
5365
Pages
898-902
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W1993808418
Cited by
391
References
1
FWCI
12.27
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Role of Rac1 and Oxygen Radicals in Collagenase-1 Expression Induced by Cell Shape Change. https://app.cochat.ai/papers/10.1126/science.280.5365.898
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Kheradmand, F., Werner, E., Tremble, P., Symons, M., & Werb, Z. (1998). Role of Rac1 and Oxygen Radicals in Collagenase-1 Expression Induced by Cell Shape Change. Science. https://doi.org/10.1126/science.280.5365.898

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