Use at an assay dependent concentration. PubMed: 19836009
Tissue specificityIsoform 1 and isoform 2 are expressed at high levels in the lung, brain, whole eye and retina. Isoform 1 shows a weaker expression in the heart, kidney and skeletal muscle. Isoform 2 shows a weaker expression in the kidney, bone marrow and skeletal muscle. Isoform 1 and isoform 2 are expressed at high levels in the fetal heart, kidney, and whole eye, whereas a weak expression is seen in the fetal liver.
Involvement in diseaseDefects in ADAMTS17 are the cause of Weill-Marchesani-like syndrome (WMLS) [MIM:613195]. It is a disorder characterized by many of the key features of Weill-Marchesani syndrome, including lenticular myopia, ectopia lentis, glaucoma, spherophakia and short stature. However, the characteristic brachydactyly or decreased joint flexibility of Weill-Marchesani syndrome are absent.
DomainThe conserved cysteine present in the cysteine-switch motif binds the catalytic zinc ion, thus inhibiting the enzyme. The dissociation of the cysteine from the zinc ion upon the activation-peptide release activates the enzyme.
Post-translational modificationsThe precursor is cleaved by a furin endopeptidase.
Cellular localizationSecreted > extracellular space > extracellular matrix.
A disintegrin and metalloproteinase with thrombospondin motifs 17 antibody
A disintegrin-like and metalloprotease (reprolysin type) with thrombospondin type 1 motif, 17 antibody
ADAM metallopeptidase with thrombospondin type 1 motif, 17 antibody
ADAM-TS 17 antibody
ADAMTS 17 antibody
EC 3.4.24. antibody
Anti-ADAMTS17 antibody images
Western blot - ADAMTS17 antibody (ab58099)
Predicted band size : 121 kDa ADAMTS17 antibody (ab58099) at 1ug/lane + A-431 cell lysate at 25ug/lane.
References for Anti-ADAMTS17 antibody (ab58099)
This product has been referenced in:
Morales J et al. Homozygous mutations in ADAMTS10 and ADAMTS17 cause lenticular myopia, ectopia lentis, glaucoma, spherophakia, and short stature. Am J Hum Genet85:558-68 (2009).
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