Foto del docente

Irene Faenza

Full Professor

Department of Biomedical and Neuromotor Sciences

Academic discipline: BIO/16 Human Anatomy

Research

Keywords: phospholipase C beta nuclear signalling myogenic differentiation Ostosarcomas, Rabdomyosarcomas

 

The research of Dr. Irene Faenza is directed mainly to the study of the mechanisms underlying the growth and differentiation in relation to signals generated by the nuclear cycle polyphosphoinositide (PI) and the morphological and functional significance of the topography of this system signal transduction. Her studies focus on nuclear enzymes that metabolize PI and in particular is interested in the study of Phospholipase C inositide dependent. The studies conducted so far by Dr. Irene Faenza are geared to deepen the role in the nucleus polyphosphoinositide and identify specific targets of PLCb1. All these studies have contributed greatly to the identification and determination of the functional role of the nuclear cycle polyphosphoinositide in both differentiation and proliferation processes. Especially it was highlighted the importance of topographical subcellular localization and determination of specific functions of signaling inositide-dependent. For this reason these works have been cited in the most important articles and reviews by the leading experts in the field. Her work covers the following fields: Autonomous nuclear signalling via inositol lipid cycle, is aimed to the identification at nuclear level of the key steps leading to cell growth and differentiation. In particular the main interest is the study in normal and cancer cells of the nuclear localisation and signalling activity of polyphosphoinositides. She has contributed to the discovery of the localisation at the nucleus of this signalling pathway, as internationally recognised, and currently she is furthering the pathophysiological significance of this peculiar location. Through morpho functional studies both in the differentiation and proliferation processes it was identified cyclin D3 as a final target of this nuclear lipid signaling. In recent years Dr Irene Faenza is dedicated to investigations in the field of functional proteomics for the identification of proteins that interact at the nuclear level with PLCβ1 and for the determination of its molecular targets. Recently Dr. Faenza is dedicated to the study and analysis of miRNAs. In mammals, miRNAs are involved in embryonic development, neural and muscle but also in the regulation of hematopoiesis, of 'organogenesis and apoptosis. Dr. Faenza is dedicated to the development of a project which envisaged to identify miRNAs involved in erythroid differentiation following the differentiation of K562 which had been modulated the expression of PLCβ1. In particular since the last years her main interest is the study of the nuclear localisation and signalling activity and the identification of novel downstream effectors of nuclear polyphosphoinositides also through the high-resolution 2-DE-based proteomic analysis. Namely she has furtherd the role of this signalling pathway in the nucleus during myogenic differentiation, giving new insight to its role in myotonic dystrophies. Moreover she has contributed to the study of haemopoietic differentiation, envisaging the pathophysiological significance of nuclear phosphoinositide signalling in MDS. Very recently she has investigated the mechanism of osteogenic differentiation to clarify the molecular events which control this process. AKT regulates many cellular functions, such as growth and proliferation and differentiation. Dr Faenza has contributed to identify the nuclear substrates of AKT that were phosphorylated after ATRA treatment through a proteomics-based analysis by using 2D-electrophoresis/mass spectrometry (MS) in combination with an anti-AKT phospho-substrate antibody. Furthermore research has been conducted to elucidate the nuclear role of the double-strand RNA-dependent protein kinase, PKR, which plays a central role in inflammatory/chronic stress-mediated pathologies such as cancer, diabetes, and neuro/muscular degenerative diseases.

Metrix: From Google Scholar 

Documents:87 ; total citations: 2880 ; h-index: 33