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- Table of Contents
, No Gclids
pathway Info Card
At Binding
Information about At Binding: 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 At Binding
Most recent studies have shown that At Binding shares some biological mechanisms with cell-adhesion, cell-growth, cell-proliferation, chemotaxis, coagulation, complement-activation, dna-methylation, dna-repair, dna-replication, excretion, localization, methylation, pathogenesis, platelet-activation, proteolysis, secretion, sulfation, transport, tropism, tumor-necrosis-factor-production.
Among the many pathways, these few ones have gauged particular interests from scientists studying At Binding, and have been seen in publications frequently: cell-adhesion, cell-growth, cell-proliferation, chemotaxis, coagulation, complement-activation, dna-methylation, dna-repair, dna-replication, excretion, localization, methylation, pathogenesis, platelet-activation, proteolysis, secretion, sulfation, transport, tropism, tumor-necrosis-factor-production
Quite a number of genes have been found to play important roles in At Binding, such as AGT, ARHGAP4, CD14, CDKN1A, F10, FGF2, HNRNPC, LDLR, MAP3K14, PF4, PFDN4, POMC, PRL, PRLR, PRNP, SERPINC1, TNF, VEGFA. 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 pathway. Plesae stay updated.