دورية أكاديمية
Immune system dysfunction and autoimmune disease in mice lacking Emk (Par-1) protein kinase.
العنوان: | Immune system dysfunction and autoimmune disease in mice lacking Emk (Par-1) protein kinase. |
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المؤلفون: | Hurov JB; Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110-1093, USA., Stappenbeck TS, Zmasek CM, White LS, Ranganath SH, Russell JH, Chan AC, Murphy KM, Piwnica-Worms H |
المصدر: | Molecular and cellular biology [Mol Cell Biol] 2001 May; Vol. 21 (9), pp. 3206-19. |
نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
اللغة: | English |
بيانات الدورية: | Publisher: Taylor & Francis Country of Publication: United States NLM ID: 8109087 Publication Model: Print Cited Medium: Print ISSN: 0270-7306 (Print) Linking ISSN: 02707306 NLM ISO Abbreviation: Mol Cell Biol Subsets: MEDLINE |
أسماء مطبوعة: | Publication: 2023- : [Philadelphia] : Taylor & Francis Original Publication: [Washington, D.C.] : American Society for Microbiology, [c1981- |
مواضيع طبية MeSH: | Caenorhabditis elegans Proteins* , Cell Cycle Proteins*, Autoimmune Diseases/*enzymology , B-Lymphocytes/*immunology , Protein Serine-Threonine Kinases/*immunology , T-Lymphocytes/*immunology, Animals ; Autoimmune Diseases/immunology ; B-Lymphocytes/cytology ; B-Lymphocytes/physiology ; Cell Differentiation ; Colon/abnormalities ; Female ; Gene Expression ; Gene Targeting ; Glomerulonephritis, Membranoproliferative/enzymology ; Hemoglobinuria/enzymology ; Humans ; Immune System/immunology ; Lymphoid Tissue ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Prolapse ; Protein Serine-Threonine Kinases/genetics ; Proteinuria/enzymology ; T-Lymphocytes/cytology ; T-Lymphocytes/physiology |
مستخلص: | Emk is a serine/threonine protein kinase implicated in regulating polarity, cell cycle progression, and microtubule dynamics. To delineate the role of Emk in development and adult tissues, mice lacking Emk were generated by targeted gene disruption. Emk(-/-) mice displayed growth retardation and immune cell dysfunction. Although B- and T-cell development were normal, CD4(+)T cells lacking Emk exhibited a marked upregulation of the memory marker CD44/pgp-1 and produced more gamma interferon and interleukin-4 on stimulation through the T-cell receptor in vitro. In addition, B-cell responses to T-cell-dependent and -independent antigen challenge were altered in vivo. As Emk(-/-) animals aged, they developed splenomegaly, lymphadenopathy, membranoproliferative glomerulonephritis, and lymphocytic infiltrates in the lungs, parotid glands and kidneys. Taken together, these results demonstrate that the Emk protein kinase is essential for maintaining immune system homeostasis and that loss of Emk may contribute to autoimmune disease in mammals. |
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المشرفين على المادة: | 0 (Caenorhabditis elegans Proteins) 0 (Cell Cycle Proteins) EC 2.7.1.- (Mark2 protein, mouse) EC 2.7.11.1 (Protein Serine-Threonine Kinases) |
تواريخ الأحداث: | Date Created: 20010405 Date Completed: 20010517 Latest Revision: 20211203 |
رمز التحديث: | 20221213 |
مُعرف محوري في PubMed: | PMC86958 |
DOI: | 10.1128/MCB.21.9.3206-3219.2001 |
PMID: | 11287624 |
قاعدة البيانات: | MEDLINE |
تدمد: | 0270-7306 |
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DOI: | 10.1128/MCB.21.9.3206-3219.2001 |