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ADAMTS4 encodes a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) protein family. Additionally we are shipping ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 4 Kits (49) and ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 4 Proteins (8) and many more products for this protein.
Showing 10 out of 152 products:
Cow (Bovine) Polyclonal ADAMTS4 Primary Antibody for IHC, WB - ABIN2776877
Lee, Hwang, Park, Lee, Park, Kang, Lee, Kim, Park, Park: Comparison of ADAMTS-1, -4 and -5 expression in culprit plaques between acute myocardial infarction and stable angina. in Journal of clinical pathology 2011
Show all 3 Pubmed References
Human Polyclonal ADAMTS4 Primary Antibody for WB - ABIN391642
Tortorella, Pratta, Liu, Abbaszade, Ross, Burn, Arner: The thrombospondin motif of aggrecanase-1 (ADAMTS-4) is critical for aggrecan substrate recognition and cleavage. in The Journal of biological chemistry 2000
Show all 2 Pubmed References
Human Polyclonal ADAMTS4 Primary Antibody for ELISA, IHC - ABIN6259788
Zhou, Lu, Chen, Ge, Chen, Xu, Shi, Dai, Li, Ju, Cao, Qin, Chen, Teng, Jiang: AMPK deficiency in chondrocytes accelerated the progression of instability-induced and ageing-associated osteoarthritis in adult mice. in Scientific reports 2017
This study demonstrated that ADAMTS-4 is a new marker of mature oligodendrocytes contributing to the myelination processes and thus to the control of motor capacities.
results demonstrate for the first time that ADAMTS4 contributes to diet induced atherosclerosis in ApoE (show APOE Antibodies)(-/-) mice
the reduction of ADAMTS-4 activity during the progression of ALS pathology may be an adaptive change to mitigate its neurodegenerative impact in CNS tissues
Results show that ADAMTS15 (show ADAMTS15 Antibodies) and ADAMTS4 not only exhibit unique cellular expression patterns in the brain but their developmental upregulation by these cell types coincides with critical aspects of neural development
aggrecan (show ACAN Antibodies) and brevican (show BCAN Antibodies) proteolysis is compensated in Adamts4-/- or Adamts5 (show ADAMTS5 Antibodies)-/- mice by ADAMTS (show ADAMTS1 Antibodies) proteoglycanase (show MMP3 Antibodies) family members but a threshold of versican (show Vcan Antibodies) proteolysis is sensitive to the loss of a single ADAMTS (show ADAMTS1 Antibodies) proteoglycanase (show MMP3 Antibodies) during spinal cord injury
ADAMTS4 has roles in melanoma growth and angiogenesis in mice
The serine protease (show F2 Antibodies) tissue plasminogen activator (tPA (show PLAT Antibodies)) and two matrix metalloproteinases, ADAMTS-4 and ADAMTS-5 (show ADAMTS5 Antibodies), were identified as Reelin (show RELN Antibodies) cleaving enzymes.
ADAMTS-4 cleaves Reelin (show RELN Antibodies) in an isoform-specific manner. Among ADAMTS-4 isoforms, p50 (show LSP1 Antibodies) cleaves the N-t site only, while p75 (show NGFR Antibodies) cleaves both sites.
Data demonstrate that Adamts1 (show ADAMTS1 Antibodies) and Adamts4 play redundant and essential roles in perinatal kidney development.
Drastic down-regulation of Adamts4 observed at both E16 (show SLC7A5 Antibodies) and E18; RT-PCR revealed post-natal reduction in expression (Adamts4, 1/3). Results suggest down-regulation of gene is important factor in normal odontogenesis in dental papillae.
ADAMTS 1 (show ADAMTS1 Antibodies), 4, 12, and 13 levels in the maternal and cord blood were lower in the preeclampsia group than in the control group. ADAMTS 1 (show ADAMTS1 Antibodies), 4, and 12 levels in placental tissues were higher in the preeclampsia group.
ADAMTS4 was associated macrophages infiltration and polarization in the tumor microenvironment of CRC (show CALR Antibodies) and ADAMTS4 knockdown had no inhibitory implications on cell proliferation and invasion in vitro, but significantly attenuated tumor growth in vivo.
ADAMTS4 expression was upregulated during carotid atherosclerotic plaque development. Serum levels of ADAMTS4 were associated with increased plaque vulnerability in both symptomatic and asymptomatic patients with carotid artery stenosis.
methylation status of the ADAMTS4 gene is altered in patellar tendinopathy
HipHop-based pharmacophore modeling and virtual screening of the Maybridge database to identify novel ADAMTS-4 inhibitors. These novel lead compounds act as potent and specific inhibitors for the ADAMTS-4 enzyme and could have therapeutic potential in the treatment of OA.
ADAMTS-4 protein expression increased in cartilage tissue from spinal tuberculosis patients.
Using in vitro approaches and cultured breast cancer cell lines authors demonstrate that Fibulin-2 (show FBLN2 Antibodies) is a better substrate for ADAMTS-5 (show ADAMTS5 Antibodies) than it is for ADAMTS-4. Fibulin-2 (show FBLN2 Antibodies) degradation is associated to an enhancement of the invasive potential of T47D, MCF-7 and SK-BR-3 cells.
ADAMTS4 and ADAMTS15 (show ADAMTS15 Antibodies) were upregulated in symptomatic uterine leiomyomas.
The SNP rs4233367 in the exon of ADAMTS-4 gene may be associated with lumbar disc degeneration.
Single Nucleotide Variants of Candidate Genes in Aggrecan (show ACAN Antibodies) Metabolic Pathway Are Associated with Lumbar Disc Degeneration and Modic Changes
ADAMTS4 participates in the regulation of muscle development in cattle.
aggrecanase activity (a) is responsible for early TNFalpha (show TNF Antibodies)-dependent aggrecan (show ACAN Antibodies) cleavage and GAG release in the meniscus and (b) might be involved in meniscal degeneration.
ADAMTS4 and ADAMTS5 (show ADAMTS5 Antibodies) are inhibited by alpha2-macroglobulin (show A2M Antibodies)
identified multiple conserved amino acids within regions N- and C-terminal to the site of scission that may influence enzyme-substrate recognition, and may interact with exosites on ADAMTS-4 and ADAMTS-5 (show ADAMTS5 Antibodies)
This gene encodes a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) protein family. Members of the family share several distinct protein modules, including a propeptide region, a metalloproteinase domain, a disintegrin-like domain, and a thrombospondin type 1 (TS) motif. Individual members of this family differ in the number of C-terminal TS motifs, and some have unique C-terminal domains. The enzyme encoded by this gene lacks a C-terminal TS motif. It is responsible for the degradation of aggrecan, a major proteoglycan of cartilage, and brevican, a brain-specific extracellular matrix protein. The cleavage of aggrecan and brevican suggests key roles of this enzyme in arthritic disease and in the central nervous system, potentially, in the progression of glioma.
A disintegrin and metalloproteinase with thrombospondin motifs 4
, ADAM-TS 4
, a disintegrin-like and metalloprotease (reprolysin type) with thrombospondin type 1 motif, 4
, a disintegrin and metallopeptidase with thrombospondin motifs 4
, a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 4
, ADAM metallopeptidase with thrombospondin type 1 motif, 4
, A disintegrin and metalloproteinase with thrombospondin motifs 4-like
, disintegrin and metalloproteinase with thrombospondin motifs 2
, a disintegrin and metalloproteinase with thrombospondin motifs 4