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Disease Info Card
Mandibuloacral Dysostosis
Information about Mandibuloacral Dysostosis: 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 Mandibuloacral Dysostosis
Most recent studies have shown that Mandibuloacral Dysostosis shares some biological mechanisms with acquired-partial-lipodystrophy, acro-osteolysis, atrophy, bone-diseases-developmental, cardiomyopathies, craniofacial-abnormalities, dysplasia, dystrophy, familial-partial-lipodystrophy, hypoplasia, insulin-resistance, lipodystrophy, major-anomalies-of-jaw-size-mandibular-hypoplasia, micrognathism, muscle-contracture, muscular-dystrophy, osteolysis, premature-aging-syndrome, progeria.
Among the many pathways, these few ones have gauged particular interests from scientists studying Mandibuloacral Dysostosis, and have been seen in publications frequently: Aging, Bone Development, Bone Resorption, Cardiac Conduction, Catagen, Cell Adhesion, Cell Cycle, Cell Cycle Arrest, Cell Development, Chromatin Organization, Chromatin Remodeling, Dna Repair, Localization, Mating, Menstruation, Mitosis, Osteoclast Differentiation, Pathogenesis, Pigmentation, Tooth Eruption
Quite a number of genes have been found to play important roles in Mandibuloacral Dysostosis, such as AMPD1, BANF1, EMD, ERMAP, INS, KIF1B, LBR, LMNA, MXD1, PEX7, PHYH, PPARG, ROBO3, ZMPSTE24. 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.