Genetic analyses of integrin signaling
- PMID: 21421914
- PMCID: PMC3039529
- DOI: 10.1101/cshperspect.a005116
Genetic analyses of integrin signaling
Abstract
The development of multicellular organisms, as well as maintenance of organ architecture and function, requires robust regulation of cell fates. This is in part achieved by conserved signaling pathways through which cells process extracellular information and translate this information into changes in proliferation, differentiation, migration, and cell shape. Gene deletion studies in higher eukaryotes have assigned critical roles for components of the extracellular matrix (ECM) and their cellular receptors in a vast number of developmental processes, indicating that a large proportion of this signaling is regulated by cell-ECM interactions. In addition, genetic alterations in components of this signaling axis play causative roles in several human diseases. This review will discuss what genetic analyses in mice and lower organisms have taught us about adhesion signaling in development and disease.
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References
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- Ackerl R, Walko G, Fuchs P, Fischer I, Schmuth M, Wiche G 2007. Conditional targeting of plectin in prenatal and adult mouse stratified epithelia causes keratinocyte fragility and lesional epidermal barrier defects. J Cell Sci 120: 2435–2443 - PubMed
-
- Alon R, Etzioni A 2003. LAD-III, a novel group of leukocyte integrin activation deficiencies. Trends Immunol 24: 561–566 - PubMed
-
- Alt A, Ohba M, Li L, Gartsbein M, Belanger A, Denning MF, Kuroki T, Yuspa SH, Tennenbaum T 2001. Protein kinase Cδ-mediated phosphorylation of α6β4 is associated with reduced integrin localization to the hemidesmosome and decreased keratinocyte attachment. Cancer Res 61: 4591–4598 - PubMed
-
- Araki E, Nakamura K, Nakao K, Kameya S, Kobayashi O, Nonaka I, Kobayashi T, Katsuki M 1997. Targeted disruption of exon 52 in the mouse dystrophin gene induced muscle degeneration similar to that observed in Duchenne muscular dystrophy. Biochem Biophys Res Commun 238: 492–497 - PubMed
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