T
Thomas M. Magin
Researcher at Leipzig University
Publications - 132
Citations - 7916
Thomas M. Magin is an academic researcher from Leipzig University. The author has contributed to research in topics: Keratin & Cytoskeleton. The author has an hindex of 43, co-authored 125 publications receiving 7168 citations. Previous affiliations of Thomas M. Magin include Translational Centre for Regenerative Medicine & University of Bonn.
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Journal ArticleDOI
New consensus nomenclature for mammalian keratins
Jürgen Schweizer,Paul Edward Bowden,Pierre A. Coulombe,Lutz Langbein,E. Birgitte Lane,Thomas M. Magin,Lois J. Maltais,M. Bishr Omary,David A.D. Parry,Michael A. Rogers,Mathew W. Wright +10 more
TL;DR: This revised nomenclature accommodates functional genes and pseudogenes, and although designed specifically for the full complement of human keratins, it offers the flexibility needed to incorporate additional keratin proteins from other mammalian species.
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Hormone-sensitive Lipase Deficiency in Mice Causes Diglyceride Accumulation in Adipose Tissue, Muscle, and Testis
Guenter Haemmerle,Robert Zimmermann,Marianne Hayn,Christian Theussl,Georg Waeg,Elke M. Wagner,Wolfgang Sattler,Thomas M. Magin,Erwin F. Wagner,Rudolf Zechner +9 more
TL;DR: In vivo results indicate that HSL is the rate-limiting enzyme for the cellular catabolism of DG in adipose tissue and muscle implying a substrate specificity of the enzyme in vivo.
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Genes for intermediate filament proteins and the draft sequence of the human genome: novel keratin genes and a surprisingly high number of pseudogenes related to keratin genes 8 and 18.
TL;DR: The limits of the analysis are described, the striking unevenness of pseudogene derivation in the IF multigene family is discussed and the nomenclature of Moll and colleagues is proposed to extend to any novel keratin.
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Structural and regulatory functions of keratins
TL;DR: The diversity of epithelial functions is reflected by the expression of distinct keratin pairs that are responsible to protect epithelial cells against mechanical stress and to act as signaling platforms, and experimental evidence accumulating in recent years has led to a much more complex view of the keratin cytoskeleton.
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Keratin-dependent, epithelial resistance to tumor necrosis factor-induced apoptosis.
TL;DR: Moderation of the effects of TNF may be the fundamental function of K8 and K18 common to liver regeneration, inflammatory bowel disease, hepatotoxin sensitivity, and the diagnostic, persistent expression of these keratins in many carcinomas.