The RASputin effect

Genes and Development

Volumn 16, Issue 16, 2002, Pages 2033-2038

  Boettner, Benjamin ^a   Van Aelst, Linda ^a  

^a Howard Hughes Medical Institute Cold Spring Harbor Laboratory Cold Spring Harbor   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

RAS PROTEIN;

ANGIOGENESIS; APOPTOSIS; CARCINOGENICITY; CELL CYCLE; DISEASE ASSOCIATION; DYSPLASIA; GENE MUTATION; METASTASIS; PRIORITY JOURNAL; PROTEIN EXPRESSION; REVIEW; VASCULARIZATION;

ANIMALS; CELL TRANSFORMATION, NEOPLASTIC; MAP KINASE SIGNALING SYSTEM; MICE; MODELS, BIOLOGICAL; MUTATION; NEOPLASMS; RAS PROTEINS;

EID: 0037102450     PISSN: 08909369     EISSN: None     Source Type: Journal    
DOI: 10.1101/gad.1020602     Document Type: Review

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5. New insights into tumor suppression: PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase/AKT pathway
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13. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
14. Mechanisms and consequences of activation of protein kinase B/Akt
15. Integrin αvβ3 requirement for sustained mitogen-activated protein kinase activity during angiogenesis
16. The importance of being K-Ras
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34. Lessons from hereditary colorectal cancer
35. PIK3CA as an oncogene in cervical cancer
36. Mice deficient in the Rac activator Tiam1 are resistant to Ras-induced skin tumours
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38. The exocyst is a Ra1 effector complex
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51. Ras partners
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53. 1 progression through the independent regulation of cyclin D1 and p27
54. Multiple Ras functions can contribute to mammalian cell transformation
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56. EGF receptor signaling stimulates SRC kinase phosphorylation of clathrin, influencing clathrin redistribution and EGF uptake
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