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Disease Info Card
Pure Red-cell Aplasia
Information about Pure Red-cell Aplasia: 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 Pure Red-cell Aplasia
Most recent studies have shown that Pure Red-cell Aplasia shares some biological mechanisms with anemia, anemia-hemolytic, aplasia-nos, aplastic-anemia, autoimmune-diseases, autoimmune-hemolytic-anemia, autoimmune-reaction, chronic-lymphocytic-leukemia, disease-due-to-parvoviridae, erythema-infectiosum, hypoplasia, kidney-diseases, kidney-failure-chronic, leukemia, lymphoid-leukemia, neoplasms, parvovirus-b19-(disease), thymoma, thymus-neoplasms.
Among the many pathways, these few ones have gauged particular interests from scientists studying Pure Red-cell Aplasia, and have been seen in publications frequently: Antibody-dependent Cellular Cytotoxicity, Cell Activation, Cell Cycle, Cell Death, Cell Differentiation, Cell Growth, Cell Maturation, Cell Proliferation, Coagulation, Glycosylation, Hemopoiesis, Hypersensitivity, Immune Response, Pathogenesis, Regeneration, Response To Erythropoietin, Ribosome Biogenesis, Secretion, Translation, Tropism
Quite a number of genes have been found to play important roles in Pure Red-cell Aplasia, such as ABO, ALB, CD4, CD8A, CTLA4, EPCAM, EPO, EPX, FLOT2, HLA-DQA1, IL2, NOD2, PON1, RPS19, TCN2, TIMP1. 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.