Activities
Organisms’ development and tissues homeostasis is achieved by a precise control of the fate of differentiating cells. Such regulation is influenced by several cell autonomous and non-autonomous stimuli that are translated into the establishment of specific transcription programs allowing correct fate determination.
Establishment and maintenance of such transcription programs involve several different mechanisms that, by acting at a genetic (i.e., DNA sequence recognition by specific DNA binding transcription factors) and at an epigenetic level (i.e., DNA sequence independent mechanisms of transcriptional regulation), resolve the complex three-dimensional structure of chromatin to set up proper transcriptional information. The latter activity involves different enzymes and adaptor proteins that, by remodeling chromatin structure through nucleosome sliding, eviction, histone post translation modifications and DNA methylation, contribute to establish correct transcription. The bypass of cellular identity is a common feature of all human cancers and several mechanisms involved in determining normal cell identity are also essential for tumors development. This also includes the enzymatic activities that are involved in “placing” and “removing” chromatin modifications which are frequent targets of genomic alterations in a large variety of human tumors (i.e. mutations, deletions, translocations and amplifications) that strongly suggests a selective pressure, during cancer development, for altering the proper epigenetic control of normal cells. Thus, the characterization of the molecular mechanisms underling these activities in normal and pathological contexts as well as studying their role in different neoplastic environments, will help not only to better comprehend the molecular basis of cancer development, maintenance and evolution, but also to highlight novel potential pathways that can be pursued for therapy and prognosis.
EXTERNAL LINKS:
Research Gate: http://www.researchgate.net/profile/Diego_Pasini
OCRID ID: http://orcid.org/0000-0002-9879-6486
ResercherID: http://www.researcherid.com/rid/J-9674-2012