This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
, No Gclids
Disease Info Card
Common Ventricle Disorder
Information about Common Ventricle Disorder: 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 Common Ventricle Disorder
Most recent studies have shown that Common Ventricle Disorder shares some biological mechanisms with atresia, cardiac-arrhythmia, congenital-atresia-of-pulmonary-valve, congenital-heart-defects, congenital-heart-disease, cyanosis, double-outlet-right-ventricle, heart-diseases, heart-failure, heart-septal-defects, hypoplastic-left-heart-syndrome, pulmonary-stenosis, regurgitation, stenosis, tetralogy-of-fallot, transposition-of-great-vessels, tricuspid-atresia, ventricular-septal-defects.
Among the many pathways, these few ones have gauged particular interests from scientists studying Common Ventricle Disorder, and have been seen in publications frequently: Cardiac Conduction, Catecholamine Secretion, Cell Migration, Coagulation, Complement Activation, Cytokine Production, Developmental Process, Glomerular Filtration, Heart Development, Inflammatory Response, Neural Crest Cell Migration, Neuroprotection, Pathogenesis, Regulation Of Biological Process, Secretion, Transport, Transposition, Vasoconstriction, Vasodilation, Wound Healing
Quite a number of genes have been found to play important roles in Common Ventricle Disorder, such as ACE, AMY2A, BCHE, BLOC1S6, CELA3B, CPB1, ENOPH1, EPB42, GDF1, GNL3, KRAS, NDUFB6, NPPB, PRH1, PVR, SLC17A5, TBX1. 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.