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ADAM metallopeptidase with thrombospondin type 1 motif, 9

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. Members of the ADAMTS family have been implicated in the cleavage of proteoglycans, the control of organ shape during development, and the inhibition of angiogenesis. This gene is localized to chromosome 3p14.3-p14.2, an area known to be lost in hereditary renal tumors. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ADAMTS, thrombospondin-1, JAZF1, metalloprotease, CO-029
Papers on ADAMTS9
A deletion at ADAMTS9-MAGI1 locus is associated with psoriatic arthritis risk.
Marsal et al., Barcelona, Spain. In Ann Rheum Dis, Oct 2015
We found a highly significant association of an intergenic deletion between ADAMTS9 and MAGI1 genes on chromosome 3p14.1 (p=0.00014).
Interleukin-1β induced nuclear factor-κB binds to a disintegrin-like and metalloproteinase with thrombospondin type 1 motif 9 promoter in human chondrosarcoma cells.
Demircan et al., Ankara, Turkey. In Mol Med Report, Jul 2015
A disintegrin-like and metalloproteinase with thrombospondin type 1 motif 9 (ADAMTS9) is a type of proteoglycanase, which proteolytically cleaves versican and aggrecan.
ADAMTS9-Mediated Extracellular Matrix Dynamics Regulates Umbilical Cord Vascular Smooth Muscle Differentiation and Rotation.
Apte et al., Cleveland, United States. In Cell Rep, Jul 2015
Here, the secreted metalloprotease ADAMTS9 is shown to be necessary for murine umbilical cord vascular development.
Altered gene expression profile in ovarian follicle in rats treated with indomethacin and RU486.
Nakayama et al., In J Toxicol Sci, Jun 2015
In RU486-treated rats, Adamts1, Adamts9, Edn2, Ednra, Lyve1, Plat, and Pparg were down-regulated.
Vascular signal transducer and activator of transcription-3 promotes angiogenesis and neuroplasticity long-term after stroke.
Harms et al., Berlin, Germany. In Circulation, Jun 2015
Gene array analysis of a CD31-enriched cell population of the neurovascular niche showed that endothelial Stat3 ablation led to a shift toward an antiangiogenic and axon growth-inhibiting micromilieu after stroke, with an increased expression of Adamts9.
Insights on ADAMTS proteases and ADAMTS-like proteins from mammalian genetics.
Apte et al., Cleveland, United States. In Matrix Biol, May 2015
Genome-wide analyses have determined an association of some ADAMTS loci such as ADAMTS9 and ADAMTS7, with specific traits and acquired disorders.
Comparative transcriptome profiling in human bicuspid aortic valve disease using RNA sequencing.
Semsarian et al., Sydney, Australia. In Physiol Genomics, Mar 2015
Downregulation of matrix protease ADAMTS9 and protein aggrecan were observed in BAVr compared with TAV.
Relationship between gene expression and lung function in Idiopathic Interstitial Pneumonias.
Yang et al., Nashville, United States. In Bmc Genomics, 2014
This analysis identified 58 transcripts that are associated with mild vs severe disease (categorical analysis), including those with established role in fibrosis (ADAMTS4, ADAMTS9, AGER, HIF-1α, SERPINA3, SERPINE2, and SELE) as well as novel IIP candidate genes such as rhotekin 2 (RTKN2) and peptidase inhibitor 15 (PI15).
Loss of C. elegans GON-1, an ADAMTS9 Homolog, Decreases Secretion Resulting in Altered Lifespan and Dauer Formation.
Mitani et al., Tokyo, Japan. In Plos One, 2014
ADAMTS9 is a metalloprotease that cleaves components of the extracellular matrix and is also implicated in transport from the endoplasmic reticulum (ER) to the Golgi.
Interplay between promoter methylation and chromosomal loss in gene silencing at 3p11-p14 in cervical cancer.
Lyng et al., Oslo, Norway. In Epigenetics, 2014
Integrated analysis of methylation, gene dosage, and expression of the 26 hypermethylated genes identified 3 regulation patterns encompassing 8 hypermethylated genes; a methylation driven pattern (C3orf14, GPR27, ZNF717), a gene dosage driven pattern (THOC7, PSMD6), and a combined methylation and gene dosage driven pattern (FHIT, ADAMTS9, LRIG1).
The Association of Type 2 Diabetes Loci Identified in Genome-Wide Association Studies with Metabolic Syndrome and Its Components in a Chinese Population with Type 2 Diabetes.
Yang et al., Beijing, China. In Plos One, 2014
In addition, genetic variants of BCL11A, GCKR, ADAMTS9, CDKAL1, KLF14, CDKN2BAS, TCF7L2, CDC123/CAMK1D, HHEX, MTNR1B, and KCNQ1 contributed to the risk for T2D without MetS (P < 0.05).
Transcriptome analysis of hen preadipocytes treated with an adipogenic cocktail (DMIOA) with or without 20(S)-hydroxylcholesterol.
Kim et al., Winnipeg, Canada. In Bmc Genomics, 2014
Genes over-expressed in DMIOA compared to control cells include those involved in cellular development (ADAM22, ADAMTS9, FIGF), lipid metabolism (FABP3, 4 and 5), and molecular transport (MAP3K8, PDK4, AGTR1).
Seven new loci associated with age-related macular degeneration.
AMD Gene Consortium et al., Regensburg, Germany. In Nat Genet, 2013
Our results include seven loci with associations reaching P < 5 × 10(-8) for the first time, near the genes COL8A1-FILIP1L, IER3-DDR1, SLC16A8, TGFBR1, RAD51B, ADAMTS9 and B3GALTL.
Identification of a novel ADAMTS9/GON-1 function for protein transport from the ER to the Golgi.
Mitani et al., Tokyo, Japan. In Mol Biol Cell, 2012
ADAMTS9 and GON-1 in the ER that promotes protein transport from the ER to the Golgi. This function is GON-domain dependent but protease activity independent.
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.
Lentiviral shRNA knock-down of ADAMTS-5 and -9 restores matrix deposition in 3D chondrocyte culture.
Barker et al., Sheffield, United Kingdom. In J Tissue Eng Regen Med, 2010
four of the six aggrecanases are expressed in immortalized chondrocyte cell-lines and can be upregulated in response to inflammatory cytokines
Cooperation of two ADAMTS metalloproteases in closure of the mouse palate identifies a requirement for versican proteolysis in regulating palatal mesenchyme proliferation.
Apte et al., Cleveland, United States. In Development, 2010
These findings support a model in which cooperative versican proteolysis by ADAMTS9 in vascular endothelium and by ADAMTS20 in palate mesenchyme drives palatal shelf sculpting and extension.
Meta-analysis identifies 13 new loci associated with waist-hip ratio and reveals sexual dimorphism in the genetic basis of fat distribution.
Lindgren et al., Regensburg, Germany. In Nat Genet, 2010
We identified 13 new loci in or near RSPO3, VEGFA, TBX15-WARS2, NFE2L3, GRB14, DNM3-PIGC, ITPR2-SSPN, LY86, HOXC13, ADAMTS9, ZNRF3-KREMEN1, NISCH-STAB1 and CPEB4 (P = 1.9 × 10⁻⁹ to P = 1.8 × 10⁻⁴⁰) and the known signal at LYPLAL1.
Extracellular protease ADAMTS9 suppresses esophageal and nasopharyngeal carcinoma tumor formation by inhibiting angiogenesis.
Lung et al., Hong Kong, Hong Kong. In Cancer Res, 2010
Results indicate that ADAMTS9 contributes an important function in the tumor microenvironment that acts to inhibit angiogenesis and tumor growth in both esophageal cancer and nasophageal cancer.
Meta-analysis of genome-wide association data and large-scale replication identifies additional susceptibility loci for type 2 diabetes.
Altshuler et al., Oxford, United Kingdom. In Nat Genet, 2008
We detected at least six previously unknown loci with robust evidence for association, including the JAZF1 (P = 5.0 x 10(-14)), CDC123-CAMK1D (P = 1.2 x 10(-10)), TSPAN8-LGR5 (P = 1.1 x 10(-9)), THADA (P = 1.1 x 10(-9)), ADAMTS9 (P = 1.2 x 10(-8)) and NOTCH2 (P = 4.1 x 10(-8)) gene regions.
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