This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
Information about 22q11 Deletion Syndrome: 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.
Most recent studies have shown that 22q11 Deletion Syndrome shares some biological mechanisms with 22q11-partial-monosomy-syndrome, attention-deficit-hyperactivity-disorder, autistic-disorder, cleft-palate, congenital-abnormality, congenital-heart-defects, congenital-heart-disease, cytogenetic-abnormality, developmental-delay-(disorder), developmental-disabilities, digeorge-syndrome, haploinsufficiency, heart-diseases, hypocalcemia, hypoparathyroidism, mental-disorders, psychotic-disorders, schizophrenia, tetralogy-of-fallot.
Among the many pathways, these few ones have gauged particular interests from scientists studying 22q11 Deletion Syndrome, and have been seen in publications frequently: Artery Development, Brain Development, Cell Cycle, Cell Development, Cell Proliferation, Cognition, Dosage Compensation, Electron Transport, Immune Response, Limb Development, Metaphase, Neural Crest Cell Development, Neurogenesis, Pathogenesis, Prepulse Inhibition, Protein Palmitoylation, Tooth Eruption, Transport, Vasculogenesis, Visual Perception
Quite a number of genes have been found to play important roles in 22q11 Deletion Syndrome, such as CAT, CDC45, COMT, CRAT, CRKL, DHDDS, DHPS, FGF10, FGF8, GNB1L, PRL, PRODH, PRPH2, PTH, SMARCB1, SS18L1, TBX1, ZDHHC8. 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.