Department of Neuroscience and Rehabilitation - Clinical Biochemistry Section, University of Ferrara, Ferrara, ItalyInterests: cancer biology; proteomics; transglutaminases; drug discovery; molecular biology; biochemistry; cancer research; oncology; molecular genetics; medicinal chemistry; regulation of gene expression
Dear Colleagues,
The transglutaminase family (TGs-EC 2.3.2.13) is a calcium-dependent, ubiquitously expressed group of enzymes. TGs catalyze post-translational modifications of proteins through a transamidation reaction. TGs are also involved in other metabolic activities, such as guanine nucleotide binding and hydrolysis, protein kinase, and disulfide isomerase activities. Several scientific articles have reported that one of the members of the family, the tissue transglutaminase (TG2), plays a central role in several biological mechanisms and cellular functions, such as cell proliferation, apoptosis, differentiation of various cell types, and tumor response to chemotherapy.
This enzyme has been implicated in a wide variety of altered health states, not only in celiac disease, but also in neurodegenerative diseases, multiple sclerosis, the proliferation and invasion of tumor cells, and lesions of the central nervous system. In this regard, the study of the biological effects of molecules modulating the enzymatic activity of TG2 and/or the effectors that are part of the cascade of triggered events is of enormous interest. The role of TG2 in the pathogenesis of malignancies remains a fascinating area of research, especially considering that this enzyme is involved in the induction of tumor cell differentiation. An important example of modulation of TG2 activity in tumor growth is the polymerization of the cytoskeleton proteins. In this case, TG2 acts on biogenic polyamines as a substrate. The formation of protein-polyamines polymers blocks the growth of tumor cells. Based on these premises, this monograph aims to broaden the knowledge of TG2 in health conditions and pathological states and the cellular functions in which it is involved.
We welcome studies that clarify the molecular mechanisms triggered by TG2 in tumor invasion, but also those aimed at identifying possible natural or synthetic modulators of TG2 activity.
Prof. Simone Beninati and Carlo Mischiati
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