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ADAMTS10 belongs to the ADAMTS (a disintegrin and metalloproteinase domain with thrombospondin type-1 motifs) family of zinc-dependent proteases. Additionally we are shipping ADAMTS10 Kits (22) and and many more products for this protein.
Showing 10 out of 41 products:
Human Polyclonal ADAMTS10 Primary Antibody for EIA, WB - ABIN950271
Morales, Al-Sharif, Khalil, Shinwari, Bavi, Al-Mahrouqi, Al-Rajhi, Alkuraya, Meyer, Al Tassan: Homozygous mutations in ADAMTS10 and ADAMTS17 cause lenticular myopia, ectopia lentis, glaucoma, spherophakia, and short stature. in American journal of human genetics 2009
Show all 5 references for ABIN950271
Human Polyclonal ADAMTS10 Primary Antibody for WB - ABIN654061
Ben Yahia, Ouechtati, Jelliti, Nouira, Chakroun, Abdelhak, Khairallah: Clinical and genetic investigation of isolated microspherophakia in a consanguineous Tunisian family. in Journal of human genetics 2009
Show all 3 references for ABIN654061
these studies support the notion that sperm-oocyte interactions involve considerable functional redundancy and identify ADAMTS10 as a novel candidate in the mediation of these fundamentally important events.
TGF-beta (show TGFB1 Antibodies) stimulation of renal cells results in a significant up-regulation of Adams 10, 17, 12, and 19
ADAMTS10 is a functional metalloprotease (show ADAMTS7 Antibodies) as demonstrated by cleavage of alpha2-macroglobulin (show A2M Antibodies)
These findings support the Gly661Arg mutation of ADAMTS10 as the likely cause of POAG in beagles.
ADAMTS10 participates in microfibril biogenesis rather than in fibrillin-1 (show FBN1 Antibodies) turnover
ADAMTS10 is a functional metalloprotease (show ADAM8 Antibodies) as demonstrated by cleavage of alpha2-macroglobulin (show A2M Antibodies)
ADAMTS10 plays a major role in growth and in skin, lens, and heart development in humans.
infer that folding of the complex C-terminal ancillary domain is the rate-limiting step in biosynthesis of ADAMTS10, and that it (but not catalytic domain) is sensitive to subtle changes in efficiency of signal peptide cleavage.
Mutations in ADAMTS10 gene is not responsible for microspherophakia.
Homozygous mutation in ADAMTS10 causes lenticular myopia, ectopia lentis, glaucoma, spherophakia, and short stature.
This gene belongs to the ADAMTS (a disintegrin and metalloproteinase domain with thrombospondin type-1 motifs) family of zinc-dependent proteases. ADAMTS proteases are complex secreted enzymes containing a prometalloprotease domain of the reprolysin type attached to an ancillary domain with a highly conserved structure that includes at least one thrombospondin type 1 repeat. They have been demonstrated to have important roles in connective tissue organization, coagulation, inflammation, arthritis, angiogenesis and cell migration. The product of this gene plays a major role in growth and in skin, lens, and heart development. It is also a candidate gene for autosomal recessive Weill-Marchesani syndrome.
A disintegrin and metalloproteinase with thrombospondin motifs 10
, a disintegrin-like and metalloprotease (reprolysin type) with thrombospondin type 1 motif, 10
, zinc metalloendopeptidase
, ADAM-TS 10
, ADAM metallopeptidase with thrombospondin type 1 motif 10
, a disintegrin-like and metalloprotease with thrombospondin type 1 motif, 10