http://www.cnr.it/ontology/cnr/individuo/prodotto/ID11245
Selective repression of myod transcription by v-Myc prevents terminal differentiation of quail embryo myoblasts transformed by the MC29 strain of avian myelocytomatosis virus (Articolo in rivista)
- Type
- Label
- Selective repression of myod transcription by v-Myc prevents terminal differentiation of quail embryo myoblasts transformed by the MC29 strain of avian myelocytomatosis virus (Articolo in rivista) (literal)
- Anno
- 2002-01-01T00:00:00+01:00 (literal)
- Alternative label
La Rocca S.A., Vannucchi S., Pompili M., Pinney D.F., Emerson C.P. Jr., Grossi M., Tato F. (2002)
Selective repression of myod transcription by v-Myc prevents terminal differentiation of quail embryo myoblasts transformed by the MC29 strain of avian myelocytomatosis virus
in Oncogene (Basingstoke)
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- La Rocca S.A., Vannucchi S., Pompili M., Pinney D.F., Emerson C.P. Jr., Grossi M., Tato F. (literal)
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- Rivista
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- progetto di ricerca n.65 (literal)
- Note
- ISI Web of Science (WOS) (literal)
- Titolo
- Selective repression of myod transcription by v-Myc prevents terminal differentiation of quail embryo myoblasts transformed by the MC29 strain of avian myelocytomatosis virus (literal)
- Abstract
- We have investigated the mechanism by which expression of the v-myc
oncogene interferes with the competence of primary quail myoblasts to
undergo terminal differentiation. Previous studies have established that
quail myoblasts transformed by myc oncogenes are severely impaired in the
accumulation of mRNAs encoding the myogenic transcription factors Myf-5,
MyoD and Myogenin. However, the mechanism responsible for such a
repression remains largely unknown. Here we present evidence that v-Myc
selectively interferes with quail myoD expression at the transcriptional
level. Cis-regulatory elements involved in the auto-activation of qmyoD
are specifically targeted in this unique example of transrepression by v-
Myc, without the apparent participation of Myc-specific E-boxes or InR
sequences. Transiently expressed v-Myc efficiently interfered with MyoD-
dependent transactivation of the qmyoD regulatory elements, while the
myogenin promoter was unaffected. Finally, we show that forced expression
of MyoD in v-myc-transformed quail myoblasts restored myogenin expression
and promoted extensive terminal differentiation. These data suggest that
transcriptional repression of qmyoD is a major and rate-limiting step in
the molecular pathway by which v-Myc severely inhibits terminal
differentiation in myogenic cells.
(literal)
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