Loss of focal adhesion kinase (FAK) inhibits epidermal growth factor receptor-dependent migration and induces aggregation of NH2-terminal FAK in the nuclei of apoptotic glioblastoma cells

Cancer Research

Volumn 61, Issue 13, 2001, Pages 4978-4981

  Jones, Graham ^a   Machado, Joel ^a   Merlo, Adrian ^a  

^a UNIVERSITY OF BASEL   (Switzerland)

Author keywords

[No Author keywords available]

Indexed keywords

4 (3 BROMOANILINO) 6,7 DIMETHOXYQUINAZOLINE; CASPASE 3; EPIDERMAL GROWTH FACTOR RECEPTOR; FOCAL ADHESION KINASE;

APOPTOSIS; ARTICLE; CELL MEMBRANE; CELL MIGRATION; CELL NUCLEUS; ENZYME ACTIVITY; ENZYME INHIBITION; GLIOBLASTOMA; HUMAN; HUMAN CELL; PRIORITY JOURNAL; SIGNAL TRANSDUCTION;

APOPTOSIS; CELL MOVEMENT; CELL NUCLEUS; FOCAL ADHESION KINASE 1; FOCAL ADHESION PROTEIN-TYROSINE KINASES; GLIOBLASTOMA; HUMANS; PHOSPHORYLATION; PROTEIN-TYROSINE KINASES; RECEPTOR, EPIDERMAL GROWTH FACTOR; SIGNAL TRANSDUCTION; TUMOR CELLS, CULTURED;

EID: 0035392952     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (22)

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2. Focal adhesion targeting: The critical determinant of FAK regulation and substrate phosphorylation
3. The N-termini of FAK and JAKs contain divergent band 4.1 domains
4. Focal adhesion kinase and paxillin bind to peptides mimicking β integrin cytoplasmic domains
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6. 2-terminal kinase
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