Human Growth/differentiation factor 5(GDF5) ELISA kit

Growth factor involved in bone and cartilage formation. During cartilage development regulates differentiation of chondrogenic tissue through two pathways. Firstly, positively regulates differentiation of chondrogenic tissue through its binding of high affinity with BMPR1B and of less affinity with BMPR1A, leading to induction of SMAD1-SMAD5-SMAD8 complex phosphorylation and then SMAD protein signaling transduction. Secondly, negatively regulates chondrogenic differentiation through its interaction with NOG. Required to prevent excessive muscle loss upon denervation. This function requires SMAD4 and is mediated by phosphorylated SMAD1/5/8. Binds bacterial lipopolysaccharide (LPS) and mediates LPS-induced inflammatory response, including TNF secretion by monocytes.

1. We found a strong association between the TT genotype and the risk of developing Knee Osteoarthritis (OR = 1.7, 95% CI = 1.12-2.8, p = 0.014), but not in the heterozygous TC state (OR = 1.56, CI 95% = 0.58-4.17, p = 0.367). PMID: 30044130
2. study shows that there exists a relationship between GDF5 (SNP rs143383) and Developmental dysplasia of the hip (DDH) in our population. Second, we found for the first time that the genotype TT and the T allele were overly expressed in the patients and the fathers. More studies on the confirmation of this genetic marker for DDH are called for. PMID: 29797005
3. Two Pakistani families with sequence variants in GDF5 and TRPS1 causing brachydactyly type C and tricho-rhino-phalangeal syndrome type III are described. PMID: 29436063
4. The dysfunctional gene GDF5 was successfully corrected in adipose tissue-derived mesenchymal stem cells using a pair of transcription activatorlike effector nucleases. PMID: 29393424
5. No association has been found between GDF5 +104 T/C promoter polymorphism and osteoarthritis in the Eastern Turkey population. PMID: 28886316
6. The results of the current study revealed that SNP rs143383 of GDF5 is a compelling risk factor for knee OA [Osteoarthritis] and that GDF5 has an etiological effect on the development of OA [Osteoarthritis]. PMID: 29056119
7. A Study of IL-1beta, MMP-3, TGF-beta1, and GDF5 Polymorphisms and Their Association with Primary Frozen Shoulder in a Chinese Han Population PMID: 28676856
8. BMP-14 rs143383 polymorphism reduced the susceptibility to knee osteoarthritis (OA) and hand OA not only in total analysis but also in subgroup analysis; BMP-14 rs143383 polymorphism may be a protective factor against OA occurrence PMID: 29049177
9. The structure of Grem2-GDF5 complex has revealed a number of key findings for DAN-family mediated BMP2 inhibition. PMID: 27524626
10. miR-615-3p negatively regulates the osteogenic differentiation of hLF cells through post-transcriptionally suppressing osteogenic regulators GDF5 and FOXO1. PMID: 28460412
11. p38, c-jun, and NFkappaB pathways activated during intervertebral disc degeneration by IL-1beta but not GDF-5 PMID: 27391542
12. GDF5 elicited significant (p < 0.05) changes in the expression of anabolic, catabolic and hypertrophic genes with several consistent effects in healthy donors and in OA patients PMID: 28481944
13. GDF5 was up regulated in patients after chronic rhinosinusitis developing osteitis. PMID: 27888647
14. Titanium (Ti) surface modification with the combination of hBMP-2 and hGDF-5 for the two growth factor-coated Ti implants can improve the clinical properties of implants for orthopedic and dental applications. PMID: 28124978
15. he large array of modular enhancers for Gdf5 provide a new foundation for studying the spatial specificity of joint patterning in vertebrates, as well as new candidates for regulatory regions that may also influence osteoarthritis risk in human population PMID: 27902701
16. The purpose of this study is to investigate the immunohistochemical expression of cytokeratin 18 (CK18) and the reactivity to GDF5 (CDMP-1), called the morphogenetic protein-1, cartilage-derived, in lingual squamous cell carcinoma. PMID: 27151703
17. homozygous sequence variants in the GDF5 gene underlie acromesomelic dysplasia type-grebe in consanguineous families PMID: 27577507
18. The prevention of IL-1Beta-induced nucleus pulposus extracellular matrix degeneration by miR-7 silencing was attenuated by GDF5 siRNA. PMID: 27583982
19. Mutations in three genes (GDF5, NPR2, BMPR1B) have been reported to cause different forms of acromesomelic dysplasia PMID: 26926249
20. we demonstrate that the transforming growth factor-beta1 and the growth differentiation factor 5 synergistically drive the nucleopulpogenic differentiation process. The commitment of the hASCs was robust and highly specific as attested by the expression of NP-related genes characteristic of young healthy human NP cells PMID: 26661057
21. The data suggest that Ad-GDF-5 gene therapy is a potential treatment for IDD, which restores the functions of degenerative intervertebral disc through enhancing the ECM production of human NP cells. PMID: 26739524
22. An association of SNP in GDF5 with temporomandibular joint osteoarthritis in female Han Chinese. PMID: 25757091
23. 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] PMID: 25894512
24. Two novel homozygous missense mutations in the GDF5 gene cause brachydactyly type C. PMID: 25820810
25. our results showed that GDF-5 and BMPRII expressed both in normal and degenerated intervertebral disc tissues, and GDF-5 might have an inhibition effect on degenerated lumbar intervertebral discs PMID: 25755766
26. This meta-analysis finds that the C allele and CC genotype of the GDF5 gene are protective for knee osteoarthritis susceptibility. PMID: 25467786
27. Our results revealed that the GDF5 SNP was associated with susceptibility to the meniscus injury and postoperative function recovery in Chinese male soldiers. PMID: 24227118
28. 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. PMID: 25092592
29. The proregion is stabilized by an intramolecular disulfide bond. The isolated proregion folds independently of the mature domain. PMID: 25174448
30. Growth differentiation factor 5 and canonical Wnt signaling may contribute to molecular mechanisms of osteoarthritis. PMID: 24561281
31. 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 pathway. PMID: 25223801
32. results suggested that GDF5 polymorphism is associated with susceptibility to symptomatic lumbar disc herniation in Chinese Han population and type II collagen in the nucleus pulposus may be a factor in susceptibility to symptomatic lumbar disc herniation PMID: 24105021
33. Osteoarthritis chondrocytes do not respond in a predictable manner to culture with exogenous GDF5. PMID: 24466161
34. High GDF5 expression is associated with osteoarthritis. PMID: 24861163
35. The expression of growth differentiation factor 5 (GDF5) and aggrecan in 15 cases of salivary gland pleomorphic adenomas, was investigated. PMID: 24398992
36. established an association between two SNPs (rs224332 and rs224333) of GDF5 and DDH development in a female Chinese population. PMID: 24114442
37. In vitro findings suggest that the degenerating disc milieu, with high proinflammatory cytokine levels, may limit expression of GDF-5, resulting in limited regenerative capacity of the intact disc. PMID: 24582800
38. These novel insights into the biology of GDF5 might also provide further clues on the pathophysiology of OA. PMID: 24098149
39. The novel missense mutation p.Leu176Pro causes impaired secretion of GDF5 in Brachydactyly type C and mild Grebe type chondrodyslplasia. PMID: 23812741
40. GDF5 is the only osteoarthritis susceptibility gene so far identified with definite evidence.[Review] PMID: 24003854
41. Overall, a statistically significant association was found between the +104T/C polymorphism of GDF5 and risk of knee osteoarthritis PMID: 23151597
42. GDF5 harbors a C/A transversion located -41 bp relative to the transcription start site that leads to increased gene expression. PMID: 22929025
43. GDF5 polymorphisms are associated with susceptibility to low back pain during military training in Chinese soldiers. PMID: 23725396
44. In conclusion, the rs143383 variant was not found to associate with the risk of ACL rupture. PMID: 23090674
45. we have identified four trans-acting factors that are binding to GDF5, three of which are modulating GDF5 expression via the OA susceptibility locus rs143383. PMID: 23825960
46. Although the effect size of the association between OA and GDF5 is small, there is suggestive evidence for an association. PMID: 23423687
47. GDF5 regulates TGF-beta-dependent angiogenesis in breast carcinoma cells. PMID: 23226264
48. Growth differentiation factor 5 modulation of chondrogenesis of self-assembled constructs involves gap junction-mediated intercellular communication. PMID: 23121099
49. analysis of positive selection on the osteoarthritis-risk and decreased-height associated variants at the GDF5 gene in East Asians PMID: 22905146
50. Our findings in 5 population cohorts from Northern Europe indicate that a variant in the GDF5 gene is a risk factor for lumbar disc degeneration in women. PMID: 21360499

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Acromesomelic chondrodysplasia, Grebe type (AMDG); Acromesomelic chondrodysplasia, Hunter-Thompson type (AMDH); Brachydactyly C (BDC); Du Pan syndrome (DPS); Symphalangism, proximal 1B (SYM1B); Multiple synostoses syndrome 2 (SYNS2); Brachydactyly A2 (BDA2); Osteoarthritis 5 (OS5); Brachydactyly A1, C (BDA1C)

Secreted. Cell membrane.

TGF-beta family

Predominantly expressed in long bones during embryonic development. Expressed in monocytes (at protein level).

HGNC: 4220

OMIM: 112600

KEGG: hsa:8200

STRING: 9606.ENSP00000363489

UniGene: Hs.1573