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ADAM metallopeptidase with thrombospondin type 1 motif, 1

ADAMTS, ADAMTS-5, ADAMTS-1, C3-C5, aggrecanase-2
This gene encodes a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motif) 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 protein encoded by this gene contains two disintegrin loops and three C-terminal TS motifs and has anti-angiogenic activity. The expression of this gene may be associated with various inflammatory processes as well as development of cancer cachexia. This gene is likely to be necessary for normal growth, fertility, and organ morphology and function. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: thrombospondin-1, aggrecanase, Aggrecan, CAN, HAD
Papers using ADAMTS antibodies
Metalloproteinase expression in PMA-stimulated THP-1 cells. Effects of peroxisome proliferator-activated receptor-gamma (PPARγ) agonists and 9-cis-retinoic acid
Ramji Dipak P. et al., In The International Journal of Biochemistry & Cell Biology, 2002
... Antibodies were from Affinity Bioreagents (ADAMTS-4), Cell Signaling Technology (Smad2/3, p38MAPK, ERK1/2), ...
Papers on ADAMTS
Carboxiterminal pro-endothelin-1 as an endothelial cell biomarker in thrombotic thrombocytopenic purpura.
Prohászka et al., Budapest, Hungary. In Thromb Haemost, Feb 2016
UNASSIGNED: Thrombotic thrombocytopenic purpura (TTP) is characterised by the deficiency of the von Willebrand factor (VWF) cleaving protease (ADAMTS-13).
Expanding the clinical and mutational spectrum of the Ehlers-Danlos syndrome, dermatosparaxis type.
Malfait et al., Gent, Belgium. In Genet Med, Feb 2016
PURPOSE: The Ehlers-Danlos syndrome (EDS), dermatosparaxis type, is a recessively inherited connective tissue disorder caused by deficient activity of ADAMTS-2, an enzyme that cleaves the aminoterminal propeptide domain of types I, II, and III procollagen.
Prospective evaluation of ADAMTS-13 and von Willebrand factor multimers in cardiac surgery.
Miesbach et al., Frankfurt am Main, Germany. In Blood Coagul Fibrinolysis, Feb 2016
UNASSIGNED: Acquired thrombotic-thrombocytopenic purpura, one of the main representatives of thrombotic microangiopathies (TMAs), is caused by the accumulation of antibodies against ADAMTS-13.
Successful treatment of neonatal atypical hemolytic uremic syndrome with C5 monoclonal antibody.
Parvex et al., Genève, Switzerland. In Arch Pediatr, Feb 2016
ADAMTS 13 deficiency, inborn error of the cobalamin pathway, deficiency in the H and I protein, and factor H antibodies were excluded and we concluded in aHUS.
Anti-ADAMTS5 monoclonal antibodies: implications for aggrecanase inhibition in osteoarthritis.
Apte, Cleveland, United States. In Biochem J, Feb 2016
Proteolysis of aggrecan by members of the proteinase family ADAMTS (A disintegrin-like and metalloproteinase domain with thrombospondin type 1 motif), was identified as an early step in the inexorable destruction of cartilage in osteoarthritis (OA).
Plasma ADAMTS-13 protein is not associated with portal hypertension or hemodynamic changes in patients with cirrhosis.
Møller et al., Hvidovre, Denmark. In Dig Liver Dis, Jan 2016
BACKGROUND: Activated hepatic stellate cells synthesize the matrix metalloprotease ADAMTS13, which may be involved in the development of liver cirrhosis and portal hypertension.
Thrombocytopenia-Associated Multiple Organ Failure and Acute Kidney Injury.
Carcillo et al., Houston, United States. In Crit Care Clin, Oct 2015
Von Willebrand factor and ADAMTS-13 play a central role in TTP.
Prophylactic Eculizumab Use in Kidney Transplantation: A Review of the Literature and Report of a Case with Atypical Hemolytic Uremic Syndrome.
Apaydın et al., İstanbul, Turkey. In Ann Transplant, 2014
Our diagnosis was aHUS due to initial results, normal level of ADAMTS activity, and lack of predisposing factors seen in typical HUS.
Advances in understanding cartilage remodeling.
Xu et al., Boston, United States. In F1000res, 2014
In this brief review, we focus on the discussion of some current "controversial" observations in articular cartilage degeneration: (1) the biological effect of transforming growth factor-beta 1 on developing and mature articular cartilages, (2) the question of whether aggrecanase 1 (ADAMTS4) and aggrecanase 2 (ADAMTS5) are key enzymes in articular cartilage destruction, and (3) chondrocytes versus chondron in the development of osteoarthritis.
The Function and Roles of ADAMTS-7 in Inflammatory Diseases.
Wei et al., Jinan, China. In Mediators Inflamm, 2014
The ADAMTS proteinases are a group of multidomain and secreted metalloproteinases containing the thrombospondin motifs.
C. elegans Punctin specifies cholinergic versus GABAergic identity of postsynaptic domains.
Bessereau et al., France. In Nature, 2014
These proteins belong to the ADAMTS (a disintegrin and metalloprotease with thrombospondin repeats)-like family, a class of extracellular matrix proteins related to the ADAM proteases but devoid of proteolytic activity.
Regulation of the catabolic cascade in osteoarthritis by the zinc-ZIP8-MTF1 axis.
Chun et al., Kwangju, South Korea. In Cell, 2014
ZIP8-mediated Zn2+ influx upregulated the expression of matrix-degrading enzymes (MMP3, MMP9, MMP12, MMP13, and ADAMTS5) in chondrocytes.
ADAMTS5 functions as an anti-angiogenic and anti-tumorigenic protein independent of its proteoglycanase activity.
Ge et al., Singapore, Singapore. In Am J Pathol, 2012
This is the first report that ADAMTS5 is an anti-angiogenic and anti-tumorigenic protein independent of its proteoglycanase activity.
Rearranging exosites in noncatalytic domains can redirect the substrate specificity of ADAMTS proteases.
Sadler et al., Saint Louis, United States. In J Biol Chem, 2012
chimeric proteases and substrates to examine the role of C-terminal domains of ADAMTS13 and ADAMTS5 in the recognition of their physiological cleavage sites in von Willebrand factor (VWF) and aggrecan, respectively
Novel role of ADAMTS-5 protein in proteoglycan turnover and lipoprotein retention in atherosclerosis.
Mayr et al., London, United Kingdom. In J Biol Chem, 2012
the first evidence implicating ADAMTS-5 in the regulation of proteoglycan turnover and lipoprotein retention in atherosclerosis.
Pericyte TIMP3 and ADAMTS1 modulate vascular stability after kidney injury.
Duffield et al., Boston, United States. In J Am Soc Nephrol, 2012
Pericyte-derived TIMP3 stabilized and ADAMTS1 destabilized the capillary tubular networks
Regulation of aggrecanases from the ADAMTS family and aggrecan neoepitope formation during in vitro chondrogenesis of human mesenchymal stem cells.
Richter et al., Heidelberg, Germany. In Eur Cell Mater, 2011
Data show that the expression of ADAMTS4, 9, 16 and was up-regulated during chondrogenesis, ADAMTS1 and 5 were down-regulated.
Modulating hedgehog signaling can attenuate the severity of osteoarthritis.
Alman et al., Toronto, Canada. In Nat Med, 2009
Furthermore, we show in mice and in human cartilage explants that pharmacological or genetic inhibition of Hh signaling reduces the severity of osteoarthritis and that runt-related transcription factor-2 (RUNX2) potentially mediates this process by regulating a disintegrin and metalloproteinase with thrombospondin type 1 motif-5 (ADAMTS5) expression.
Syndecan-4 regulates ADAMTS-5 activation and cartilage breakdown in osteoarthritis.
Pap et al., Hannover, Germany. In Nat Med, 2009
The occurrence of less severe osteoarthritis-like cartilage destruction in both syndecan-4-deficient mice and syndecan-4-specific antibody-treated wild-type mice results from a marked decrease in ADAMTS-5 activity.
Aberrant ERG expression cooperates with loss of PTEN to promote cancer progression in the prostate.
Pandolfi et al., New York City, United States. In Nat Genet, 2009
ADAMTS1 and CXCR4, two candidate genes strongly associated with cell migration, were upregulated in the presence of ERG overexpression.
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