Zobrazeno 1 - 10
of 36
pro vyhledávání: '"Jorunn Stamnaes"'
Publikováno v:
Nature Communications, Vol 14, Iss 1, Pp 1-11 (2023)
Abstract Transglutaminase 3 (TG3), the autoantigen of dermatitis herpetiformis (DH), is a calcium dependent enzyme that targets glutamine residues in polypeptides for either transamidation or deamidation modifications. To become catalytically active
Externí odkaz:
https://doaj.org/article/7086bf68c62a49909723f5d535c05f49
Autor:
Saykat Das, Jorunn Stamnaes, Esko Kemppainen, Kaisa Hervonen, Knut E. A. Lundin, Naveen Parmar, Frode L. Jahnsen, Jørgen Jahnsen, Katri Lindfors, Teea Salmi, Rasmus Iversen, Ludvig M. Sollid
Publikováno v:
Advanced Science, Vol 10, Iss 25, Pp n/a-n/a (2023)
Abstract Dermatitis herpetiformis (DH) is an inflammatory skin disorder often considered as an extra intestinal manifestation of celiac disease (CeD). Hallmarks of CeD and DH are auto‐antibodies to transglutaminase 2 (TG2) and transglutaminase 3 (T
Externí odkaz:
https://doaj.org/article/c03947c46ced4f9ebf35f637435e6e72
Publikováno v:
PLoS ONE, Vol 18, Iss 6, p e0287662 (2023)
BackgroundFormation of complexes between transglutaminase 2 (TG2) and gluten can mechanistically explain why TG2 serves both as B-cell autoantigen and as an enzyme that creates deamidated gluten epitopes in coeliac disease (CeD). A model has been pro
Externí odkaz:
https://doaj.org/article/83d036a54c7942c0b2215694c7cf7cd6
Publikováno v:
PLoS ONE, Vol 17, Iss 4, p e0266543 (2022)
BackgroundCeliac disease is an autoimmune enteropathy driven by dietary intake of gluten proteins. Typical histopathologic features are villous flattening, crypt hyperplasia and infiltration of inflammatory cells in the intestinal epithelium and lami
Externí odkaz:
https://doaj.org/article/d3fca8985a4e418da1abb290ba72482d
Autor:
Jorunn Stamnaes, Daniel Stray, Maria Stensland, Vikas K. Sarna, Tuula A. Nyman, Knut E. A. Lundin, Ludvig M. Sollid
Publikováno v:
Advanced Science, Vol 8, Iss 4, Pp n/a-n/a (2021)
Abstract In celiac disease (CeD), gluten activates adaptive immune cells that cause damage to the small intestinal mucosa. Histological evaluation of intestinal biopsies allows for grading of disease severity. CeD can effectively be treated with a li
Externí odkaz:
https://doaj.org/article/8ddb6a6746be4adabf6f814fe70eda51
Publikováno v:
PLoS ONE, Vol 16, Iss 11 (2021)
A hallmark of celiac disease is the gluten-dependent production of antibodies specific for deamidated gluten peptides (DGP) and the enzyme transglutaminase 2 (TG2). Both types of antibodies are believed to result from B cells receiving help from glut
Externí odkaz:
https://doaj.org/article/fa939a27166143e9a3304aef314a1786
Publikováno v:
PLoS ONE, Vol 10, Iss 8, p e0134922 (2015)
A hallmark of the gluten-driven enteropathy celiac disease is autoantibody production towards the enzyme transglutaminase 2 (TG2) that catalyzes the formation of covalent protein-protein cross-links. Activation of TG2-specific B cells likely involves
Externí odkaz:
https://doaj.org/article/b35cf1b619f24db1a7766060b94a664b
Publikováno v:
PLoS ONE, Vol 7, Iss 2, p e30642 (2012)
Transglutaminase 2 (TG2) is an allosterically regulated enzyme with transamidating, deamidating and cell signaling activities. It is thought to catalyze sequence-specific deamidation of dietary gluten peptides in the small intestines of celiac diseas
Externí odkaz:
https://doaj.org/article/a7329e4082144280994eef493507eef5
Autor:
Jorunn Stamnaes
Publikováno v:
ProteomicsREFERENCES. 21(23-24)
Celiac disease (CeD) is a prevalent intestinal disorder that only develops in genetically susceptible individuals when they mount a harmful CD4+ T-cell response towards gluten peptides. Intake of gluten leads to inflammation and remodeling of the sma
Publikováno v:
PLoS ONE, Vol 16, Iss 11, p e0259082 (2021)
PLoS ONE, Vol 16, Iss 11 (2021)
PLoS ONE
PLoS ONE, Vol 16, Iss 11 (2021)
PLoS ONE
A hallmark of celiac disease is the gluten-dependent production of antibodies specific for deamidated gluten peptides (DGP) and the enzyme transglutaminase 2 (TG2). Both types of antibodies are believed to result from B cells receiving help from glut