Disrupting the scaffold to improve focal adhesion kinase-targeted cancer therapeutics.

Disrupting the scaffold to improve focal adhesion kinase-targeted cancer therapeutics.
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DOI:
10.1126/scisignal.2004021
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发表时间:
2013-03-26
期刊:
影响因子:
7.3
通讯作者:
Golubovskaya V
Golubovskaya V
中科院分区:
生物学1区
文献类型:
--
作者:
Cance WG;Kurenova E;Marlowe T;Golubovskaya V

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Focal adhesion kinase (FAK) is emerging as a promising cancer target because it is highly expressed at both the transcriptional and translational level in cancer and is involved in many aspects of tumor growth, invasion, and metastasis. Existing FAK-based therapeutics focus on inhibiting the kinase's catalytic function and not the large scaffold it creates that includes many oncogenic receptor tyrosine kinases and tumor suppressor proteins. Targeting the FAK scaffold is a feasible and promising approach for developing highly specific therapeutics that disrupt FAK signaling pathways in cancer.
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