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Systemic lupus erythematosus

Article Abstract:

Systemic lupus erythematosus (SLE) is an immune system malfunction that causes widespread organ damage. The main cause of SLE is the inability of defective thy-2-type T cells and beta cells to undergo cell death because of a faulty genetic code. The accumulation of these cells in the body triggers abnormal responses that cause the immune system to destroy the various organs of the body. SLE is also characterized by increased levels of antigen-antibody reactions that damage DNA integrity and cellular organelles. Androgens provide SLE resistance due to low SLE manifestations in males.

Author: Kotzin, Brian L.
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1996
Analysis, Physiological aspects, Systemic lupus erythematosus, Antinuclear antibodies, DNA antibodies

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Genetic analysis of autoimmune disease

Article Abstract:

The extensive evaluation of the entire human genetic code will aide in the correction of aberrant genes that causes immunological diseases. The interaction of several faulty genes causes the abnormal metabolic reactions of the immune system. The isolation and eventual correction of these aberrant genes will then result in the formulation of new treatments. The application of the Mendelian laws will aide in the genetic determination of the specific modes of transmission of the disease. Environmental factors have a minor effect on the prevalence of immune system abnormalities.

Author: Todd, John A., Vyse, Timothy J.
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1996
Usage, Genetic screening, Genetic testing, Genetic markers, Chromosome mapping

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Histone deacetylase activity is required for full transcriptional repression by mSin3A

Article Abstract:

Histone deacetylation plays a direct role in mSin3A-mediated transcriptional repression as demonstrated by the use of specific histone deacetylase inhibitor trapoxin in transfected cells. An increase in the transcriptional activity of an mSin3A-silenced reporter gene upon treatment in vivo with trapoxin implies that full transcriptional repressionby mSin3A requires histone deacetylation.

Author: Ayer, Donald E., Schreiber, Stuart L., Hassig, Christian A., Billin, Andrew N., Fleischer, Tracey C.
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1997
Mutation (Biology), Mutation, Leucine, Animal genetics

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Subjects list: Research, Genetic aspects, Immunologic diseases, Immunogenetics
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