Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Molecular and Cellular Biology |
| Vol/bind | 6 |
| Udgave nummer | 5 |
| Sider (fra-til) | 1843-6 |
| Antal sider | 3 |
| ISSN | 0270-7306 |
| Status | Udgivet - 1986 |
Bibliografisk note
Keywords: Animals; Antibodies, Monoclonal; Cell Transformation, Neoplastic; Cells, Cultured; Chromosome Deletion; Epitopes; Mice; Mutation; Oncogene Proteins, Viral; OncogenesAdgang til dokumentet
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I: Molecular and Cellular Biology, Bind 6, Nr. 5, 1986, s. 1843-6.
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - A transforming ras gene can provide an essential function ordinarily supplied by an endogenous ras gene.
AU - Papageorge, A G
AU - Willumsen, B M
AU - Johnsen, M
AU - Kung, H F
AU - Stacey, D W
AU - Vass, W C
AU - Lowy, D R
N1 - Keywords: Animals; Antibodies, Monoclonal; Cell Transformation, Neoplastic; Cells, Cultured; Chromosome Deletion; Epitopes; Mice; Mutation; Oncogene Proteins, Viral; Oncogenes
PY - 1986
Y1 - 1986
N2 - Microinjection of monoclonal antibody Y13-259, which reacts with all known mammalian and yeast ras-encoded proteins, has previously been shown to prevent NIH 3T3 cells from entering the S phase (L. S. Mulcahy, M. R. Smith, and D. W. Stacey, Nature [London] 313:241-243, 1985). We have now found several transformation-competent mutant v-rasH genes whose protein products in transformed NIH 3T3 cells are not immunoprecipitated by this monoclonal antibody. These mutant proteins are, however, precipitated by a different anti-ras antibody. Each of these mutants lacks Met-72 of v-rasH. In contrast to the result for cells transformed by wild-type v-rasH, Y13-259 microinjection of NIH 3T3 cells transformed by these mutant ras genes did not prevent the cells from entering the S phase. These results imply that a transformation-competent ras gene can supply a normal essential function for NIH 3T3 cells. When the proteins encoded by the mutant ras genes were overproduced in Escherichia coli, several mutant proteins that lacked Met-72 failed to bind Y13-259 in a Western blot. However, a ras protein from a mutant lacking amino antibody, but a ras protein from a mutant lacking amino acids 72 to 84 did not. These results suggest that Y13-259 may bind to a higher ordered structure that has been restored in the mutant lacking amino acids 72 to 82.
AB - Microinjection of monoclonal antibody Y13-259, which reacts with all known mammalian and yeast ras-encoded proteins, has previously been shown to prevent NIH 3T3 cells from entering the S phase (L. S. Mulcahy, M. R. Smith, and D. W. Stacey, Nature [London] 313:241-243, 1985). We have now found several transformation-competent mutant v-rasH genes whose protein products in transformed NIH 3T3 cells are not immunoprecipitated by this monoclonal antibody. These mutant proteins are, however, precipitated by a different anti-ras antibody. Each of these mutants lacks Met-72 of v-rasH. In contrast to the result for cells transformed by wild-type v-rasH, Y13-259 microinjection of NIH 3T3 cells transformed by these mutant ras genes did not prevent the cells from entering the S phase. These results imply that a transformation-competent ras gene can supply a normal essential function for NIH 3T3 cells. When the proteins encoded by the mutant ras genes were overproduced in Escherichia coli, several mutant proteins that lacked Met-72 failed to bind Y13-259 in a Western blot. However, a ras protein from a mutant lacking amino antibody, but a ras protein from a mutant lacking amino acids 72 to 84 did not. These results suggest that Y13-259 may bind to a higher ordered structure that has been restored in the mutant lacking amino acids 72 to 82.
M3 - Journal article
C2 - 2431287
SN - 0270-7306
VL - 6
SP - 1843
EP - 1846
JO - Molecular and Cellular Biology
JF - Molecular and Cellular Biology
IS - 5
ER -