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The protein encoded by GDF5 is a member of the bone morphogenetic protein (BMP) family and the TGF-beta superfamily. Additionally we are shipping GDF5 Kits (51) and GDF5 Proteins (42) and many more products for this protein.
Showing 10 out of 114 products:
Human Polyclonal GDF5 Primary Antibody for EIA, WB - ABIN357461
Kusafuka, Luyten, De Bondt, Hiraki, Shukunami, Kayano, Takemura: Immunohistochemical evaluation of cartilage-derived morphogenic protein-1 and -2 in normal human salivary glands and pleomorphic adenomas. in Virchows Archiv : an international journal of pathology 2003
Show all 5 references for ABIN357461
Human Polyclonal GDF5 Primary Antibody for IHC (p), WB - ABIN388820
Liu, Lin, Sytwu, Chang: GDF-5 is suppressed by IL-1beta and enhances TGF-beta3-mediated chondrogenic differentiation in human rheumatoid fibroblast-like synoviocytes. in Experimental and molecular pathology 2010
Show all 4 references for ABIN388820
Human Polyclonal GDF5 Primary Antibody for EIA, IHC (p) - ABIN950667
Posthumus, Collins, Cook, Handley, Ribbans, Smith, Schwellnus, Raleigh: Components of the transforming growth factor-beta family and the pathogenesis of human Achilles tendon pathology--a genetic association study. in Rheumatology (Oxford, England) 2010
Show all 2 references for ABIN950667
Changes in the expression of downstream regulators of skeletal differentiation, like barx1 (show BARX1 Antibodies) and gdf5, is one mechanism by which head skeletal element number and articulation are altered during evolution.
Results suggest that CDMP1/GDF5 requires cleavage by two distinct proteolytic enzymes.
An association of SNP in GDF5 with temporomandibular joint osteoarthritis in female Han Chinese.
results demonstrate that SNP rs143383 of GDF5 is a compelling risk factor for both knee and hand osteoarthritis (OA) and provide further support for GDF5 in the etiology of OA [meta-analysis]
Two novel homozygous missense mutations in the GDF5 gene cause brachydactyly type C.
our results showed that GDF-5 and BMPRII (show BMPR2 Antibodies) expressed both in normal and degenerated intervertebral disc tissues, and GDF-5 might have an inhibition effect on degenerated lumbar intervertebral discs
This meta-analysis finds that the C allele and CC genotype of the GDF5 gene are protective for knee osteoarthritis susceptibility.
Our results revealed that the GDF5 SNP was associated with susceptibility to the meniscus injury and postoperative function recovery in Chinese male soldiers.
missense mutations p.T201P and p.L263P interfere with the protein structure and thereby reduce the amount of fully processed, biologically active GDF5, finally causing the clinical loss of function phenotype.
Growth differentiation factor 5 and canonical Wnt (show WNT2 Antibodies) signaling may contribute to molecular mechanisms of osteoarthritis.
These results suggest that obesity leads to upregulation of GDF5 expression responsible for the promotion of brown adipogenesis through a mechanism relevant to activation of the NF-kappaB (show NFKB1 Antibodies) pathway.
results suggested that GDF5 polymorphism is associated with susceptibility to symptomatic lumbar disc herniation in Chinese Han population and type II collagen (show COL2A1 Antibodies) in the nucleus pulposus may be a factor in susceptibility to symptomatic lumbar disc herniation
Dach2 (show DACH2 Antibodies) and Hdac9 (show HDAC9 Antibodies) mediate the effects of muscle activity on muscle reinnervation; Myog (show MYOG Antibodies) and Gdf5 appear to stimulate muscle reinnervation through parallel pathways
Gdf-5 induced the expression of the alpha5 sub-unit, while Bmp-7 (show BMP7 Antibodies) induced the expression of the alphaV sub-unit.
Clonal expansion of Gdf5 progenitors contributes to linear growth of the enthesis.
GDF5 might play a critical role in 3T3-L1 preadipocyte differentiation
These results suggest that PI3K/Akt (show AKT1 Antibodies) signals play a role in the GDF5-mediated brown adipogenesis through a mechanism related to activation of the Smad (show SMAD1 Antibodies) pathway.
These results suggest that brown adipogenesis and energy homeostasis are both positively regulated by the GDF5/BMPR (show BMPR1A Antibodies)/Smad (show SMAD1 Antibodies)/PGC-1alpha (show PPARGC1A Antibodies) signaling pathway in adipose tissues.
apical and basal dendritic arbours of pyramidal cells throughout the hippocampus were stunted in both homozygous and heterozygous Gdf5 null mutants, indicating that dendrite size and complexity are sensitive to the level of endogenous GDF5 synthesis.
This work implicates SOX11 (show SOX11 Antibodies) as a potential regulator of GDF5 expression in joint maintenance and suggests a possible role in the pathogenesis of osteoarthritis
A novel molecular mechanism of a GDF5 mutation affecting chondrogenesis and osteogenesis, is reported.
Data show that revealed notochord cells in Gdf-5-null mice correctly form nuclei pulposi.
These results suggest that the SNP of the GDF5 gene could be a very useful genetic marker for body measurement traits in the bovine reproduction and breeding.
The protein encoded by this gene is a member of the bone morphogenetic protein (BMP) family and the TGF-beta superfamily. This group of proteins is characterized by a polybasic proteolytic processing site which is cleaved to produce a mature protein containing seven conserved cysteine residues. The members of this family are regulators of cell growth and differentiation in both embryonic and adult tissues. Mutations in this gene are associated with acromesomelic dysplasia, Hunter-Thompson type\; brachydactyly, type C\; and chondrodysplasia, Grebe type. These associations confirm that the gene product plays a role in skeletal development.
growth factor GDF5
, growth differentiation factor 5
, growth/differentiation factor 5-like
, cartilage-derived morphogenetic protein-1
, growth/differentiation factor 5
, cartilage-derived morphogenetic protein 1
, growth differentiation factor 5 preproprotein
, growth differentiation factor 5 (cartilage-derived morphogenetic protein-1)