Title : Periodic mechanical stress stimulates the FAK mitogenic signal in rat chondrocytes through ERK1/2 activity.

Pub. Date : 2013

PMID : 24217647






4 Functional Relationships(s)
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1 Reduction of FAK with targeted shRNA via transfection of NH2-terminal tyrosine phosphorylation-deficient FAK mutant Y397F or Y576F-Y577F abolished periodic mechanical stress-induced chondrocyte proliferation and matrix synthesis, accompanied by attenuated ERK1/2 phosphorylation. Tyrosine mitogen activated protein kinase 3 Rattus norvegicus
2 CONCLUSION: Our findings collectively suggest that periodic mechanical stress promotes chondrocyte proliferation and matrix synthesis through at least two pathways, integrin beta1-Src-Rac1-FAK(Tyr(576/577))-ERK1/2 and integrin beta1-FAK (Tyr(397))-ERK1/2. Tyrosine mitogen activated protein kinase 3 Rattus norvegicus
3 CONCLUSION: Our findings collectively suggest that periodic mechanical stress promotes chondrocyte proliferation and matrix synthesis through at least two pathways, integrin beta1-Src-Rac1-FAK(Tyr(576/577))-ERK1/2 and integrin beta1-FAK (Tyr(397))-ERK1/2. Tyrosine mitogen activated protein kinase 3 Rattus norvegicus
4 CONCLUSION: Our findings collectively suggest that periodic mechanical stress promotes chondrocyte proliferation and matrix synthesis through at least two pathways, integrin beta1-Src-Rac1-FAK(Tyr(576/577))-ERK1/2 and integrin beta1-FAK (Tyr(397))-ERK1/2. Tyrosine mitogen activated protein kinase 3 Rattus norvegicus