Genetic analyses of integrin signaling

Wickström, S. A.; Radovanac, K.; Fässler, R.

doi:cshperspect.a005116 [pii] 10.1101/cshperspect.a005116

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Journal Article

Genetic analyses of integrin signaling

MPS-Authors

/persons/resource/persons129350

Wickström, S. A.
Wickström – Skin Homeostasis and Ageing, Max Planck Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society;

External Resource

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21421914
(Any fulltext)

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

Wickström, S. A., Radovanac, K., & Fässler, R. (2011). Genetic analyses of integrin signaling. Cold Spring Harb Perspect Biol, 3(2). doi:cshperspect.a005116 [pii] 10.1101/cshperspect.a005116.

Cite as: https://hdl.handle.net/21.11116/0000-000B-6919-4

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.