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Disease Info Card
Autoimmune Inflammation Of Skeletal Muscle
Information about Autoimmune Inflammation Of Skeletal Muscle: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Overview of Autoimmune Inflammation Of Skeletal Muscle
Most recent studies have shown that Autoimmune Inflammation Of Skeletal Muscle shares some biological mechanisms with autoimmune-diseases, autoimmune-experimental-myositis, autoimmune-reaction, autoimmunity, connective-tissue-diseases, dermatomyositis, inclusion-body-myositis-(disorder), infective-disorder, inflammation, lupus-erythematosus-systemic, malignant-neoplasms, muscle-weakness, myopathy, myopathy-idiopathic-inflammatory, myositis, neoplasms, polymyositis, primary-sjã¶grens-syndrome, sjogrens-syndrome, weakness.
Among the many pathways, these few ones have gauged particular interests from scientists studying Autoimmune Inflammation Of Skeletal Muscle, and have been seen in publications frequently: B Cell Activation, Cell Activation, Cell Adhesion, Cell Differentiation, Cell Migration, Cell Proliferation, Chemokine Production, Complement Activation, Dna Repair, Er Overload Response, Exocytosis, Glycosylation, Immune Response, Membrane Fusion, Muscle Cell Differentiation, Pathogenesis, Plasma Membrane Repair, Regeneration, T Cell Proliferation, Translation
Quite a number of genes have been found to play important roles in Autoimmune Inflammation Of Skeletal Muscle, such as CD4, CD8A, CHKA, DMPK, HLA-E, IFNG, IL10, IL17A, IL2, IL4, MB, MYH14, PRB1, PSMB10, PSMB8, PSMB9, TLR4, TNF. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.