http://www.cnr.it/ontology/cnr/individuo/prodotto/ID5073
Emery-dreifuss muscular dystrophy, nuclear cell signaling and chromatin remodeling (Articolo in rivista)
- Type
- Label
- Emery-dreifuss muscular dystrophy, nuclear cell signaling and chromatin remodeling (Articolo in rivista) (literal)
- Anno
- 2002-01-01T00:00:00+01:00 (literal)
- Alternative label
Maraldi N.M., Squarzoni S., Sabatelli P., Lattanzi G., Ognibene A., Manzoli F.A. (2002)
Emery-dreifuss muscular dystrophy, nuclear cell signaling and chromatin remodeling
in Advances in enzyme regulation
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Maraldi N.M., Squarzoni S., Sabatelli P., Lattanzi G., Ognibene A., Manzoli F.A. (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
- Note
- ISI Web of Science (WOS) (literal)
- Titolo
- Emery-dreifuss muscular dystrophy, nuclear cell signaling and chromatin remodeling (literal)
- Abstract
- The physiological control of transcription is mediated by protein–DNA and
protein–protein interactions at promoter elements, through the nuclear
commitment of a wide spectrum of transcription factors (TFs) generated in
response to signaling pathways. However, the regulatory elements are
necessary but not sufficient to support expression in the biological
context. The extent to which genes are activated and/or suppressed, in
fact, depends on the chromatin structure that provides the linkage between
gene organization and components of transcriptional control (Stein et al.,
1999). The conceptual and experimental basis for involvement of multiple
parameters of nuclear organization in transcriptional control has been
greatly improved in recent years. In this paper, we will address some key
findings that account for the molecular mechanisms that mediate chromatin
remodeling as a prerequisite of gene transcription. We will also consider
the possibility that modifications in these mechanisms could be causally
related to compromised gene expression under pathological conditions,
namely in a group of human muscular dystrophies. (literal)
Incoming links:
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi