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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Growth differentiation factor 5

GDF5, CDMP-1, growth differentiation factor-5, cartilage-derived morphogenetic protein-1
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: glycodelin, CAN, HAD, TGF-beta, BMP-7
Papers using GDF5 antibodies
Papers on GDF5
Adenovirus-mediated GDF-5 promotes the extracellular matrix expression in degenerative nucleus pulposus cells.
Feng et al., Nanchong, China. In J Zhejiang Univ Sci B, Jan 2016
OBJECTIVE: To construct a recombinant adenovirus vector-carrying human growth and differentiation factor-5 (GDF-5) gene, investigate the biological effects of adenovirus-mediated GDF-5 (Ad-GDF-5) on extracellular matrix (ECM) expression in human degenerative disc nucleus pulposus (NP) cells, and explore a candidate gene therapy method for intervertebral disc degeneration (IDD).
Identification of plasma microRNA expression profile in radiographic axial spondyloarthritis-a pilot study.
Haseeb et al., Cleveland, United States. In Clin Rheumatol, Jan 2016
The most repressed miRNA was miR-16 and is predicted to regulate the expression of activin A receptor (ACVR2B), a receptor for growth, and differentiation factor-5 (GDF-5).
TGF-β1 and GDF5 act synergistically to drive the differentiation of human adipose stromal cells towards Nucleus pulposus -like cells.
Guicheux et al., Nantes, France. In Stem Cells, Jan 2016
Here, we demonstrate that the TGF-β1 and the GDF5 factors synergistically drive the nucleopulpogenic differentiation process.
Long-Range Communication Network in the Type 1B Bone Morphogenetic Protein Receptor.
Lee et al., Galveston, United States. In Biochemistry, Jan 2016
In preparation for testing the long-range effects of mutations of distal residues for future studies, we examined the extent of measurable perturbation of the four conserved residues by determination of the conformation and relative affinities of these BMPR-1B mutants for ligands BMP-2, -6, and -7 and GDF-5.
The function and interrelationship between GDF5 and ERG-010 during chondrogenesis in vitro.
Wallis et al., Pittsburgh, United States. In In Vitro Cell Dev Biol Anim, Dec 2015
Both GDF5 and ERG are proposed as regulators of chondrocyte differentiation during and post interzone formation.
Generation and periodontal differentiation of human gingival fibroblasts-derived integration-free induced pluripotent stem cells.
Luan et al., Beijing, China. In Biochem Biophys Res Commun, Nov 2015
Furthermore, treatment of the iPSCs in vitro with enamel matrix derivative (EMD) or growth/differentiation factor-5 (GDF-5) significantly up-regulated the expression of periodontal tissue markers associated with bone, periodontal ligament and cementum respectively.
Lessons from rare diseases of cartilage and bone.
Boyde et al., Liverpool, United Kingdom. In Curr Opin Pharmacol, Jun 2015
Investigation of rare cartilage syndromes is identifying new potential targets in OA including GDF5 and lubricin.
A comprehensive meta-analysis of association between genetic variants of GDF5 and osteoarthritis of the knee, hip and hand.
Ma et al., Xi'an, China. In Inflamm Res, Jun 2015
OBJECTIVE: A number of studies have reported an association of GDF5 with osteoarthritis (OA) but have produced some divergent findings and their interpretation may not be straightforward.
Growth and differentiation factor-5 contributes to the structural and functional maintenance of the intervertebral disc.
Zhou et al., Chongqing, China. In Cell Physiol Biochem, 2014
Growth factors including transforming growth factor-β (TGF-β), fibroblast growth factor (FGF), insulin-like growth factor-1 (IGF-1) and growth and differentiation factor-5 (GDF-5), among others, have been demonstrated to enhance anabolism in IVD cells and to induce NP-like differentiation of MSCs.
Biologic Agents for Periodontal Regeneration and Implant Site Development.
Wang et al., Ann Arbor, United States. In Biomed Res Int, 2014
It was the purpose of this comprehensive review to describe the origin and rationale, evidence, and the most current understanding of the following biologic agents: Recombinant Human Platelet-Derived Growth Factor-BB (rhPDGF-BB), Enamel Matrix Derivate (EMD), Platelet-Rich Plasma (PRP) and Platelet-Rich Fibrin (PRF), Recombinant Human Fibroblast Growth Factor-2 (rhFGF-2), Bone Morphogenic Proteins (BMPs, BMP-2 and BMP-7), Teriparatide PTH, and Growth Differential Factor-5 (GDF-5).
Genetic contribution to radiographic severity in osteoarthritis of the knee.
Doherty et al., London, United Kingdom. In Ann Rheum Dis, 2012
In conclusion, we find that GDF5, but not COG5 or MCF2L, influence the extent of radiographic damage in knee osteoarthritis
New insights into the molecular mechanism of multiple synostoses syndrome (SYNS): mutation within the GDF5 knuckle epitope causes noggin-resistance.
Knaus et al., Berlin, Germany. In J Bone Miner Res, 2012
A novel molecular mechanism of a GDF5 mutation affecting chondrogenesis and osteogenesis, is reported.
Delayed fracture healing in growth differentiation factor 5-deficient mice: a pilot study.
Tuan et al., Bethesda, United States. In Clin Orthop Relat Res, 2011
Although GDF-5 deficiency did not compromise long-term fracture healing, a delay in cartilage formation and remodeling supports roles for GDF-5 in the early phase of bone repair.
Expression of the osteoarthritis-associated gene GDF5 is modulated epigenetically by DNA methylation.
Loughlin et al., Newcastle upon Tyne, United Kingdom. In Hum Mol Genet, 2011
Data demonstrates that the genetic effect of the rs143383 SNP on GDF5 expression is modulated epigenetically by DNA methylation.
A genetic association study between growth differentiation factor 5 (GDF 5) polymorphism and knee osteoarthritis in Thai population.
Wajanavisit et al., Bangkok, Thailand. In J Orthop Surg Res, 2010
GDF5 polymorphism has an association with knee osteoarthritis in Thai ethnic.
Common variants in the GDF5-UQCC region are associated with variation in human height.
Mohlke et al., Ann Arbor, United States. In Nat Genet, 2008
Common variants in the GDF5-UQCC region are associated with variation in human height.
A functional polymorphism in the 5' UTR of GDF5 is associated with susceptibility to osteoarthritis.
Ikegawa et al., Tokyo, Japan. In Nat Genet, 2007
GDF5 is a susceptibility gene for osteoarthritis and decreased GDF5 expression is involved in the pathogenesis of osteoarthritis.
Disruption of human limb morphogenesis by a dominant negative mutation in CDMP1.
Luyten et al., Bethesda, United States. In Nat Genet, 1997
We have identified a causative point mutation in the gene encoding the bone morphogenetic protein (BMP)-like molecule, cartilage-derived morphogenetic protein-1 (CDMP-1).
A human chondrodysplasia due to a mutation in a TGF-beta superfamily member.
Luyten et al., Bethesda, United States. In Nat Genet, 1996
The disorder, characterized by skeletal abnormalities restricted to the limbs andlimb joints, is phenotypically similar to murine brachypodism (bp) which is due to mutations in growth/differentiation factor-5 (Gdf-5) (6), the mouse homologue of hCDMP-1.
Limb alterations in brachypodism mice due to mutations in a new member of the TGF beta-superfamily.
Lee et al., Stanford, United States. In Nature, 1994
We now report the isolation of three new members of the transforming growth factor-beta (TGF-beta) superfamily (growth/differentiation factors (GDF) 5,6 and 7) and show by mapping, expression patterns and sequencing that mutations in Gdf5 are responsible for skeletal alterations in bp mice.
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