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      Transglutaminase 2 in human diseases

      review-article
      1 , * , 2 , 3 , 4 , 4 , 5 , 6
      BioMedicine
      EDP Sciences
      Transglutaminase, Inflammation, Cancer, Fibrosis, Cardiovascular Disease, Neurodegenerative Disease, Celiac Disease

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          Abstract

          Transglutaminase 2 (TG2) is an inducible transamidating acyltransferase that catalyzes Ca(2+)-dependent protein modifications. In addition to being an enzyme, TG2 also serves as a G protein for several seven transmembrane receptors and acts as a co-receptor for integrin β1 and β3 integrins distinguishing it from other members of the transglutaminase family. TG2 is ubiquitously expressed in almost all cell types and all cell compartments, and is also present on the cell surface and gets secreted to the extracellular matrix via non-classical mechanisms. TG2 has been associated with various human diseases including inflammation, cancer, fibrosis, cardiovascular disease, neurodegenerative diseases, celiac disease in which it plays either a protective role, or contributes to the pathogenesis. Thus modulating the biological activities of TG2 in these diseases will have a therapeutic value.

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          Most cited references177

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          Transforming growth factor-beta regulation of immune responses.

          Transforming growth factor-beta (TGF-beta) is a potent regulatory cytokine with diverse effects on hemopoietic cells. The pivotal function of TGF-beta in the immune system is to maintain tolerance via the regulation of lymphocyte proliferation, differentiation, and survival. In addition, TGF-beta controls the initiation and resolution of inflammatory responses through the regulation of chemotaxis, activation, and survival of lymphocytes, natural killer cells, dendritic cells, macrophages, mast cells, and granulocytes. The regulatory activity of TGF-beta is modulated by the cell differentiation state and by the presence of inflammatory cytokines and costimulatory molecules. Collectively, TGF-beta inhibits the development of immunopathology to self or nonharmful antigens without compromising immune responses to pathogens. This review highlights the findings that have advanced our understanding of TGF-beta in the immune system and in disease.
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            Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases.

            Fibroproliferative diseases, including the pulmonary fibroses, systemic sclerosis, liver cirrhosis, cardiovascular disease, progressive kidney disease, and macular degeneration, are a leading cause of morbidity and mortality and can affect all tissues and organ systems. Fibrotic tissue remodeling can also influence cancer metastasis and accelerate chronic graft rejection in transplant recipients. Nevertheless, despite its enormous impact on human health, there are currently no approved treatments that directly target the mechanism(s) of fibrosis. The primary goals of this Review series on fibrotic diseases are to discuss some of the major fibroproliferative diseases and to identify the common and unique mechanisms of fibrogenesis that might be exploited in the development of effective antifibrotic therapies.
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              Transglutaminases: crosslinking enzymes with pleiotropic functions.

              Blood coagulation, skin-barrier formation, hardening of the fertilization envelope, extracellular-matrix assembly and other important biological processes are dependent on the rapid generation of covalent crosslinks between proteins. These reactions--which are catalysed by transglutaminases--endow the resulting supramolecular structure with extra rigidity and resistance against proteolytic degradation. Some transglutaminases function as molecular switches in cytoskeletal scaffolding and modulate protein-protein interactions. Having knowledge of these enzymes is essential for understanding the aetiologies of diverse hereditary diseases of the blood and skin, and various autoimmune, inflammatory and degenerative conditions.
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                Author and article information

                Journal
                Biomedicine (Taipei)
                Biomedicine (Taipei)
                bmdcn
                BioMedicine
                EDP Sciences
                2211-8020
                2211-8039
                25 August 2017
                September 2017
                : 7
                : 3 ( publisher-idID: bmdcn/2017/03 )
                : 15
                Affiliations
                [1 ] Dental Biochemistry, Department of Biochemistry and Molecular Biology, University of Debrecen Debrecen 4010 Hungary
                [2 ] Department of Pediatrics and Biochemistry and Molecular Biology, University of Debrecen Debrecen 4010 Hungary
                [3 ] Celiac Disease Center, Heim Pál Children’s Hospital Budapest 1089 Hungary
                [4 ] Department of Biochemistry and Molecular Biology, University of Debrecen Debrecen 4010 Hungary
                [5 ] Division of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital Taichung 404 Taiwan
                [6 ] School of medicine, College of Medicine, China Medical University Taichung 404 Taiwan
                Author notes
                [* ] Corresponding author. Department of Dental Biochemistry Signaling and Apoptosis Research Group Research Center of Molecular Medicine University of Debrecen H-4012 Debrecen Nagyerdei krt. 98. Hungary. E-mail address: szondy@ 123456med.unideb.hu (Zsuzsa Szondy).
                Article
                bmdcn2017070315 10.1051/bmdcn/2017070315
                10.1051/bmdcn/2017070315
                5571667
                28840829
                407b60d3-ee81-41b2-9e57-e677fde94b38
                © Author(s) 2017. This article is published with open access by China Medical University

                Open Access This article is distributed under terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided original author(s) and source are credited.

                History
                : 23 April 2017
                : 15 May 2017
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 203, Pages: 13
                Categories
                Review Article

                transglutaminase,inflammation,cancer,fibrosis,cardiovascular disease,neurodegenerative disease,celiac disease

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