This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
, No Gclids
Disease Info Card
Familial Hemiplegic Migraine
Information about Familial Hemiplegic Migraine: 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 Familial Hemiplegic Migraine
Most recent studies have shown that Familial Hemiplegic Migraine shares some biological mechanisms with ataxia, ataxia-spinocerebellar, atrophy, cerebellar-ataxia, channelopathies, comatose, common-migraine, depressive-disorder, epilepsy, episodic-ataxia-type-2-(disorder), headache, hemiparesis, hemiplegia, migraine-disorders, migraine-with-aura, nervous-system-disorder, spinocerebellar-ataxia-type-6-(disorder).
Among the many pathways, these few ones have gauged particular interests from scientists studying Familial Hemiplegic Migraine, and have been seen in publications frequently: Cell Adhesion, Cell Death, Cell Growth, Exocytosis, Habituation, Hypersensitivity, Immune Response, Ion Homeostasis, Ion Transport, Localization, Menopause, Menstruation, Muscle Contraction, Pathogenesis, Reflex, Secretion, Sensitization, Synaptic Transmission, Transport, Vasodilation
Quite a number of genes have been found to play important roles in Familial Hemiplegic Migraine, such as ATP1A2, ATP1A4, AURKA, CACNA1A, CALCA, CSAD, DRD2, GDI1, INSR, MTHFR, NOTCH3, PSMC1, RPS4Y1, S100A12, SCN1A, SCN2A, TG, TGFBI. 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.