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Disease Info Card
Familial Periodic Paralysis
Information about Familial Periodic Paralysis: 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 Periodic Paralysis
Most recent studies have shown that Familial Periodic Paralysis shares some biological mechanisms with acidosis, cardiac-arrhythmia, channelopathies, hyperkalemic-periodic-paralysis, hyperthyroidism, hypokalemic-periodic-paralysis, muscle-weakness, muscular-atrophy, muscular-dystrophy, myasthenia-gravis, myopathy, myotonia-congenita, myotonic-dystrophy, neuromuscular-diseases, paramyotonia-congenita-(disorder), periodic-paralysis-(finding), thyrotoxic-periodic-paralysis, thyrotoxicosis, weakness.
Among the many pathways, these few ones have gauged particular interests from scientists studying Familial Periodic Paralysis, and have been seen in publications frequently: Aldosterone Secretion, Cation Transport, Excretion, Glomerular Filtration, Insulin Secretion, Ion Transport, Mating, Membrane Depolarization, Muscle Atrophy, Parturition, Pathogenesis, Pinocytosis, Relaxation Of Muscle, Reverse Transcription, Secretion, Transport
Quite a number of genes have been found to play important roles in Familial Periodic Paralysis, such as CACNA1S, CST7, DBNL, DPYD, DPYS, INS, KCNC4, KCNE3, KCNJ2, MB, MSX2, PSMC1, REST, RPS4X, RPS4Y1, SCN4A, SPTA1. 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.