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Cell adaptive response to extracellular matrix density is controlled by ICAP-1-dependent beta1-integrin affinity
Angélique Millon-Frémillon1, Daniel Bouvard, Alexei Grichine
1Institut National de la Santé et de la Recherche Médicale U823, France.
The Journal of Cell Biology
|January 30, 2008
Summary
Integrin cytoplasmic domain-associated protein 1 (ICAP-1) regulates focal adhesion assembly by controlling integrin affinity. This finding reveals ICAP-1
Area of Science:
- Cell Biology
- Molecular Biology
- Biophysics
Background:
- Cell migration relies on dynamic assembly and disassembly of adhesion structures.
- The precise mechanisms governing focal adhesion (FA) turnover are not fully understood.
- Integrin cytoplasmic domain-associated protein 1 (ICAP-1) is implicated in cell adhesion.
Purpose of the Study:
- To elucidate the novel mechanistic role of ICAP-1 in focal adhesion dynamics.
- To investigate how ICAP-1 influences integrin affinity and focal adhesion assembly.
- To explore the connection between ICAP-1, integrin conformational changes, and mechanotransduction.
Main Methods:
- Live cell imaging of Icap-1-deficient mouse embryonic fibroblasts.
- Experiments using cells expressing active beta(1) integrin.
- Analysis of focal adhesion assembly, cell spreading, and migration speed.
Main Results:
- ICAP-1 was demonstrated to slow down focal adhesion assembly.
- ICAP-1 antagonistically controls the high-affinity integrin state favored by talin.
- ICAP-1-dependent integrin affinity modulation affects cell spreading and migration.
- ICAP-1 influences cell sensing of matrix surface density via integrin conformational changes.
Conclusions:
- ICAP-1 plays a crucial role in regulating focal adhesion dynamics by modulating integrin affinity.
- Integrin conformational changes, regulated by ICAP-1, are vital for mechanotransduction.
- ICAP-1 is central to the cell's integrated response to its extracellular microenvironment.
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