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Disease Info Card
Congenital Anomaly Of Skeletal Bone
Information about Congenital Anomaly Of Skeletal Bone: 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 Congenital Anomaly Of Skeletal Bone
Most recent studies have shown that Congenital Anomaly Of Skeletal Bone shares some biological mechanisms with antley-bixler-syndrome-autosomal-dominant, bone-diseases-developmental, campomelic-dysplasia, chromosomal-translocation, cleft-palate, congenital-abnormality, cytogenetic-abnormality, disorders-of-sex-development, dysostoses, dysplasia, fetal-death, fetal-growth-retardation, growth-retardation, haploinsufficiency, hereditary-diseases, hypoplasia, mutation-out-of-frame, neoplasms, osteochondrodysplasias, teratogenic-effect.
Among the many pathways, these few ones have gauged particular interests from scientists studying Congenital Anomaly Of Skeletal Bone, and have been seen in publications frequently: Cell Differentiation, Cell Fate Determination, Chondrocyte Differentiation, Copulation, Endochondral Ossification, Gene Conversion, Interphase, Limb Development, Lung Development, Mating, Mesoderm Formation, Ossification, Osteoblast Differentiation, Pathogenesis, Regulation Of Gene Expression, Sex Determination, System Development, Translation, Tube Morphogenesis, Vasculogenesis
Quite a number of genes have been found to play important roles in Congenital Anomaly Of Skeletal Bone, such as BMP4, COL2A1, CYCS, CYP17A1, DLK1, FBN1, GDF5, HNRNPC, MTSS1, NOG, POR, PORCN, SHH, SHOX, SOX5, SOX6, SOX9, SRY, VDAC2. 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.