Abstract
The past decade has seen the definition of key signalling pathways downstream of receptor tyrosine kinases (RTKs) in terms of their components and the protein-protein interactions that facilitate signal transduction. Given the strong evidence that links signalling by certain families of RTKs to the progression of breast cancer, it is not surprising that the expression profile of key downstream signalling intermediates in this disease has also come under scrutiny, particularly because some exhibit transforming potential or amplify mitogenic signalling pathways when they are overexpressed. Reflecting the diverse cellular processes regulated by RTKs, it is now clear that altered expression of such signalling proteins in breast cancer may influence not only cellular proliferation (eg Grb2) but also the invasive properties of the cancer cells (eg EMS1/cortactin).
MeSH terms
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Adaptor Proteins, Signal Transducing*
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Breast / metabolism
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Breast Neoplasms / genetics
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Breast Neoplasms / metabolism*
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Cortactin
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Drosophila Proteins*
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Female
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GRB2 Adaptor Protein
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GRB7 Adaptor Protein
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Gene Expression Regulation, Neoplastic
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Genes, src / physiology
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Homeodomain Proteins / metabolism
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Humans
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Isoenzymes / metabolism
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Microfilament Proteins / physiology
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Phospholipase C gamma
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Protein-Tyrosine Kinases / genetics
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Protein-Tyrosine Kinases / metabolism*
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Proteins / genetics
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Proteins / metabolism
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Signal Transduction*
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Type C Phospholipases / metabolism
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src Homology Domains / genetics
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src Homology Domains / physiology
Substances
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Adaptor Proteins, Signal Transducing
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CTTN protein, human
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Cortactin
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Drosophila Proteins
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GRB2 Adaptor Protein
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GRB2 protein, human
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GRB7 protein, human
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Homeodomain Proteins
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Isoenzymes
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Microfilament Proteins
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Proteins
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ems protein, Drosophila
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GRB7 Adaptor Protein
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Protein-Tyrosine Kinases
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Type C Phospholipases
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Phospholipase C gamma