Abstract
Overexpression of Lck was shown, by our previous study, to suppress gene transcription from various viral and cellular promoters. The suppression of transcription from human T-cell leukemia virus promoter by Lck was independent of the presence of the enhancer core sequences within the long terminal repeat. The suppression of transcription was observed with Lck mutants that had either diminished or enhanced tyrosine-kinase activity. A mutant lacking the myristylation site also suppressed transcription. From the analysis with various deletion mutants of Lck, it was suggested that Src-homology domain 2 (SH2) is both necessary and sufficient for the suppression of transcription. A similar effect was also observed with the SH2 domain of the v-src gene. Thus, overexpression of Lck could suppress gene expression through a unique function of the SH2 domain.
| Original language | English |
|---|---|
| Pages (from-to) | 989-997 |
| Number of pages | 9 |
| Journal | Oncogene |
| Volume | 12 |
| Issue number | 5 |
| Publication status | Published - 1996 |
| Externally published | Yes |
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Keywords
- Lck
- SH2
- Src
- Transcriptional suppression
- Tyrosine kinase
ASJC Scopus subject areas
- Molecular Biology
- Genetics
- Cancer Research
Cite this
Src-homology domain 2 is responsible for transcriptional suppression induced by expression of Lck. / Ohta, M.; Nagai, H.; Nyunoya, Hiroshi; Shimotohno, K.
In: Oncogene, Vol. 12, No. 5, 1996, p. 989-997.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Src-homology domain 2 is responsible for transcriptional suppression induced by expression of Lck
AU - Ohta, M.
AU - Nagai, H.
AU - Nyunoya, Hiroshi
AU - Shimotohno, K.
PY - 1996
Y1 - 1996
N2 - Overexpression of Lck was shown, by our previous study, to suppress gene transcription from various viral and cellular promoters. The suppression of transcription from human T-cell leukemia virus promoter by Lck was independent of the presence of the enhancer core sequences within the long terminal repeat. The suppression of transcription was observed with Lck mutants that had either diminished or enhanced tyrosine-kinase activity. A mutant lacking the myristylation site also suppressed transcription. From the analysis with various deletion mutants of Lck, it was suggested that Src-homology domain 2 (SH2) is both necessary and sufficient for the suppression of transcription. A similar effect was also observed with the SH2 domain of the v-src gene. Thus, overexpression of Lck could suppress gene expression through a unique function of the SH2 domain.
AB - Overexpression of Lck was shown, by our previous study, to suppress gene transcription from various viral and cellular promoters. The suppression of transcription from human T-cell leukemia virus promoter by Lck was independent of the presence of the enhancer core sequences within the long terminal repeat. The suppression of transcription was observed with Lck mutants that had either diminished or enhanced tyrosine-kinase activity. A mutant lacking the myristylation site also suppressed transcription. From the analysis with various deletion mutants of Lck, it was suggested that Src-homology domain 2 (SH2) is both necessary and sufficient for the suppression of transcription. A similar effect was also observed with the SH2 domain of the v-src gene. Thus, overexpression of Lck could suppress gene expression through a unique function of the SH2 domain.
KW - Lck
KW - SH2
KW - Src
KW - Transcriptional suppression
KW - Tyrosine kinase
UR - http://www.scopus.com/inward/record.url?scp=0029939317&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029939317&partnerID=8YFLogxK
M3 - Article
C2 - 8649816
AN - SCOPUS:0029939317
VL - 12
SP - 989
EP - 997
JO - Oncogene
JF - Oncogene
SN - 0950-9232
IS - 5
ER -