This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
, No Gclids
Disease Info Card
Pseudo-hurler Polydystrophy
Information about Pseudo-hurler Polydystrophy: 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 Pseudo-hurler Polydystrophy
Most recent studies have shown that Pseudo-hurler Polydystrophy shares some biological mechanisms with bone-diseases-developmental, carpal-tunnel-syndrome, congenital-abnormality, dwarfism, dysplasia, joint-stiffness, lysosomal-storage-diseases, mucolipidoses, mucopolysaccharidoses, mucopolysaccharidosis-i, mucopolysaccharidosis-ii, mucopolysaccharidosis-iii, muscle-contracture, pain, pfaundler-hurler-syndrome, storage-disease, type-i-mucolipidosis, type-ii-mucolipidosis.
Among the many pathways, these few ones have gauged particular interests from scientists studying Pseudo-hurler Polydystrophy, and have been seen in publications frequently: Autophagy, Bone Resorption, Cell Growth, Cell Proliferation, Cholesterol Esterification, Excretion, Fibroblast Proliferation, Glycosylation, Hormone Secretion, Intracellular Transport, Localization, Pathogenesis, Regulation Of Cell Growth, Regulation Of Cell Proliferation, Secretion, Translational Termination, Transport
Quite a number of genes have been found to play important roles in Pseudo-hurler Polydystrophy, such as ARSA, ASAH1, CTSB, CTSD, CTSH, GLB1, GNPTAB, GNPTG, GUSB, INS, NAGPA, RFC1, RFC2, SOX3, SQSTM1. 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.