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ADAM metallopeptidase with thrombospondin type 1 motif, 18

ADAMTS18, ADAM metallopeptidase with thrombospondin type 1 motif, 18
This gene encodes a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) protein family. ADAMTS family members 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 has a high sequence similarity to the protein encoded by gene ADAMTS16, another family member. It is thought to function as a tumor suppressor. Alternatively spliced transcript variants have been identified, but their biological validity has not been determined. [provided by RefSeq, Jul 2008] (from NCBI)
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Top mentioned proteins: ADAMTS, thrombospondin-1, AGE, HAD, POLYMERASE
Papers on ADAMTS18
Evaluation of ADAMTS12, ADAMTS16, ADAMTS18 and IL-33 serum levels in pre-eclampsia.
New
Demircan et al., Ankara, Turkey. In J Matern Fetal Neonatal Med, Oct 2015
The aim of this study was to compare serum molecules including IL-33, ADAMTS12, ADAMTS16 and ADAMTS18 levels between pre-eclampsia and control groups and to investigate the role of these molecules in pre-eclampsia.
Hypermethylation of the 16q23.1 tumor suppressor gene ADAMTS18 in clear cell renal cell carcinoma.
Jin et al., Beijing, China. In Int J Mol Sci, 2014
ADAMTS18, located at 16q23.1, has been reported to be a critical TSG in multiple primary tumors; however, this has not yet been verified in clear cell renal cell carcinoma (ccRCC).
Expansion of ocular phenotypic features associated with mutations in ADAMTS18.
Moore et al., London, United Kingdom. In Jama Ophthalmol, 2014
IMPORTANCE: We describe novel ocular phenotypic features caused by mutations in ADAMTS18.
A meta-analysis of somatic mutations from next generation sequencing of 241 melanomas: a road map for the study of genes with potential clinical relevance.
Zhao et al., Nashville, United States. In Mol Cancer Ther, 2014
Third, we identified 12 significantly mutated genes in "pan-negative" samples (ALK, STK31, DGKI, RAC1, EPHA4, ADAMTS18, EPHA7, ERBB4, TAF1L, NF1, SYK, and KDR), including five genes (RAC1, ADAMTS18, EPHA7, TAF1L, and NF1) with a recurrent mutation in at least two "pan-negative" tumor samples.
ADAMTS-18: a metalloproteinase with multiple functions.
Review
Li et al., In Front Biosci, 2013
ADAMTS-18 is a member of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family of proteases, which are known to play important roles in development, angiogenesis and coagulation; dysregulation and mutation of these enzymes have been implicated in many disease processes, such as inflammation, cancer, arthritis and atherosclerosis.
The syndrome of microcornea, myopic chorioretinal atrophy, and telecanthus (MMCAT) is caused by mutations in ADAMTS18.
Alkuraya et al., Riyadh, Saudi Arabia. In Hum Mutat, 2013
Consistent with the presumed pseudodominant inheritance in one of the original families, we show that MMCAT maps to a single autozygous locus on chr16q23.1 in which exome sequencing revealed a homozygous missense change in ADAMTS18.
Comparative gene expression analysis of the human periodontal ligament in deciduous and permanent teeth.
Choi et al., Seoul, South Korea. In Plos One, 2012
The up-regulated genes in permanent PDL tissues were related to tissue degradation (IL6 and ADAMTS18), myocontraction (PDE3B, CASQ2, and MYH10), and neurological responses (FOS, NCAM2, SYT1, SLC22A3, DOCK3, LRRTM1, LRRTM3, PRSS12, and ARPP21).
The ADAMTS18 gene is responsible for autosomal recessive early onset severe retinal dystrophy.
Banfi et al., Napoli, Italy. In Orphanet J Rare Dis, 2012
Functional tests were performed in the medaka fish (Oryzias latipes) model organism to gain further insight into the pathogenic role of the ADAMTS18 gene in eye and central nervous system (CNS) dysfunction.
Atrial fibrillation in pigs induces left atrial endocardial transcriptional remodelling.
Hermida et al., Pamplona, Spain. In Thromb Haemost, 2012
p=0.005) and ADAMTS-18 (FC=-0.69;
A genome-wide search for genetic influences and biological pathways related to the brain's white matter integrity.
Deary et al., Edinburgh, United Kingdom. In Neurobiol Aging, 2012
There was genome-wide suggestive evidence for two SNPs, one in ADAMTS18 (p = 1.65 × 10(-6)), which is related to tumor suppression and hemostasis, and another in LOC388630 (p = 5.08 × 10(-6)), which is of unknown function.
The distinct ophthalmic phenotype of Knobloch syndrome in children.
Alkuraya et al., Riyadh, Saudi Arabia. In Br J Ophthalmol, 2012
METHODS: Case series of Saudi children with previously documented homozygous mutations in COL18A1 or ADAMTS18.
Identification of a thrombin cleavage site and a short form of ADAMTS-18.
Li et al., New York City, United States. In Biochem Biophys Res Commun, 2012
We previously reported that C-terminal fragment of ADAMTS-18 induces platelet fragmentation through ROS release.
Optimized refolding and characterization of active C-terminal ADAMTS-18 fragment from inclusion bodies of Escherichia coli.
Zhang et al., Shanghai, China. In Protein Expr Purif, 2012
The human ADAMTS-18 (a disintegrin and metalloproteinase with thrombospondin type-1 modules 18) is a new member of the ADAMTS family.
Endothelium--role in regulation of coagulation and inflammation.
Review
van Hinsbergh, Amsterdam, Netherlands. In Semin Immunopathol, 2012
Thrombin-cleaved ADAMTS18 induces disintegration of platelet aggregates while tissue-type plasminogen activator initiates fibrinolysis.
A polyclonal antibody against active C-terminal ADAMTS-18 fragment.
Zhang et al., Shanghai, China. In Hybridoma (larchmt), 2011
The human ADAMTS-18, a disintegrin and metalloproteinase with thrombospondin type-1 modules 18, is a secreted Zn-metalloproteinase.
Identification of ADAMTS18 as a gene mutated in Knobloch syndrome.
GeneRIF
Alkuraya et al., Riyadh, Saudi Arabia. In J Med Genet, 2011
the study identified ADAMTS18 as the only gene carrying a homozygous protein altering mutation.
Mutational and functional analysis reveals ADAMTS18 metalloproteinase as a novel driver in melanoma.
GeneRIF
Samuels et al., Bethesda, United States. In Mol Cancer Res, 2010
ADAMTS18 mutations promote growth, migration, and metastasis in melanoma
High-resolution melting analysis of ADAMTS18 methylation levels in gastric, colorectal and pancreatic cancers.
GeneRIF
Yu et al., Zhengzhou, China. In Med Oncol, 2010
ADAMTS18 gene methylation in 3 types of cancers was significantly higher than normal tissues. No significant association was found between methylation status & TNM staging. Epigenetic regulation of ADAMTS18 was associated with carcinogenesis.
Genome-wide association and follow-up replication studies identified ADAMTS18 and TGFBR3 as bone mass candidate genes in different ethnic groups.
GeneRIF
Deng et al., Kansas City, United States. In Am J Hum Genet, 2009
ADAMTS18 and TGFBR3 might underlie BMD determination in the major human ethnic groups.
Epigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas.
GeneRIF
Tao et al., Hong Kong, Hong Kong. In Oncogene, 2007
Functional epigenetics show ADAMTS18 to be a novel functional tumor suppressor, being frequently inactivated epigenetically in multiple carcinomas.
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