[Misregulation of P-TEFb activity: pathological consequences]. / Perturbations de la transcription liées à une dérégulation de P-TEFb : cancer, Sida et hypertrophie cardiaque.
Med Sci (Paris)
; 28(2): 200-5, 2012 Feb.
Article
em Fr
| MEDLINE
| ID: mdl-22377309
ABSTRACT
P-TEFb stimulates transcription elongation by phosphorylating the carboxy-terminal domain of RNA pol II and antagonizing the effects of negative elongation factors. Its cellular availability is controlled by an abundant non coding RNA, conserved through evolution, the 7SK RNA. Together with the HEXIM proteins, 7SK RNA associates with and sequesters a fraction of cellular P-TEFb into a catalytically inactive complex. Active and inactive forms of P-TEFb are kept in a functional and dynamic equilibrium tightly linked to the transcriptional requirement of the cell. Importantly, cardiac hypertrophy and development of various types of human malignancies have been associated with increased P-TEFb activity, consequence of a disruption of this regulatory equilibrium. In addition, the HIV-1 Tat protein also releases P-TEFb from the 7SK/HEXIM complex during viral infection to promote viral transcription and replication. Here, we review the roles played by the 7SK RNP in cancer development, cardiac hypertrophy and AIDS.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Regulação da Expressão Gênica
/
Doença
/
Fator B de Elongação Transcricional Positiva
Tipo de estudo:
Etiology_studies
/
Prognostic_studies
Limite:
Humans
Idioma:
Fr
Revista:
Med Sci (Paris)
Assunto da revista:
MEDICINA
Ano de publicação:
2012
Tipo de documento:
Article
País de afiliação:
França
País de publicação:
FR
/
FRANCE
/
FRANCIA
/
FRANÇA