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ADAMTS9 encodes a member of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) protein family. Additionally we are shipping ADAMTS9 Antibodies (20) and and many more products for this protein.
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Extracellular matrix dynamics is a major influence on umbilical vascular SMC (show DYM ELISA Kits) fate, with ADAMTS9 acting as its principal mediator.
The present study reveals ADAMT-9 expression by mast cells(MCs (show SMCP ELISA Kits)) and that MC activation regulates the expression of the protease, thus implicating the ADAMT-9 of protease in MC function.
Western blot analyses indicated that aggrecanase (show ADAMTS4 ELISA Kits)-generated proteoglycan (show Vcan ELISA Kits) fragments are produced after SCI.
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.
These data identify ADAMTS9 as a novel, constitutive, endogenous angiogenesis inhibitor that operates cell-autonomously in endothelial cells.
ancillary domains of ADAMTS-9 are required both for specific extracellular localization and for its versicanase and aggrecanase (show ADAMTS4 ELISA Kits) activities
Adamts9 is widely expressed during mouse embryo development
show that combinatorial mouse alleles for the secreted metalloproteases Adamts5, Adamts20 (bt), and Adamts9 result in fully penetrant soft-tissue syndactyly.
study identified a suggestive genome-wide significant association of ADAMTS9 with asthma in Spanish subjects
NF-kappaBp65 bound to elements located at -1177 and -1335 in the ADAMTS9 promoter region, in contrast to the untreated samples. The results of the present study suggested that NF-kappaB (show NFKB1 ELISA Kits) may be involved in IL-1beta (show IL1B ELISA Kits)-induced activation of ADAMTS9 in human chondrocytes
A deletion at ADAMTS9-MAGI1 (show MAGI1 ELISA Kits) locus is associated with psoriatic arthritis risk.
LncRNA ADAMTS9-AS2 (show ARSA ELISA Kits) is regulated by DNMT1 (show DNMT1 ELISA Kits) and inhibits migration of glioma cells.
The pathways MAPK (show MAPK1 ELISA Kits) and NF-kappaB (show NFKB1 ELISA Kits) were responsible pathways for the induction of ADAMTS9 gene.
PPARG2 (show PPARG ELISA Kits) and ADAMTS9 variants are both associated with type 2 diabetes mellitus and with insulin (show INS ELISA Kits) resistance, whereas only ADAMTS9 may be related to beta cell function.
ADAMTS9 acts as a functional tumor suppressor in gastric cancer through inhibiting oncogenic AKT (show AKT1 ELISA Kits)/mTOR (show FRAP1 ELISA Kits) signaling pathway
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.
Data show that the expression of ADAMTS4 (show ADAMTS4 ELISA Kits), 9, 16 and was up-regulated during chondrogenesis, ADAMTS1 (show ADAMTS1 ELISA Kits) and 5 were down-regulated.
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.
a disintegrin-like and metalloprotease (reprolysin type) with thrombospondin type 1 motif, 9
, A disintegrin and metalloproteinase with thrombospondin motifs 9
, ADAM-TS 9