Anti-ADAMTSL4 antibody (AA32825)


Alternative names ADAMTS-like protein 4, ADAMTSL-4, Thrombospondin repeat-containing protein 1, ADAMTSL4, TSRC1, PP1396, UNQ2803/PRO34012, ATL4_HUMAN, Q6UY14, 54507
Source 1074
Species Reactivity Human, Mouse, Rat
Applications IHC, WB
Host Rabbit
Class Polyclonal
Conjugated Unconjugated


Product name Anti-ADAMTSL4 antibody (AA32825)
Catalog number AA32825
Brand family Ango
Product type Primary Antibody
Antibody Alternative Names ADAMTS-like protein 4 antibody, ADAMTSL-4 antibody, Thrombospondin repeat-containing protein 1 antibody, ADAMTSL4 antibody, TSRC1 antibody, PP1396 antibody, UNQ2803/PRO34012 antibody, ATL4_HUMAN antibody

Biological Information

Immunogen Recombinant protein of human ADAMTSL4
Concentration 1 mg/ml
Isotype IgG
Application Notes WB 1:500-1:2000 IHC 1:50-1:200
Purification method Purified by affinity chromatography


Target Name ADAMTSL4
SwissProt ID Link Q6UY14
Function Positive regulation of apoptosis. May facilitate FBN1 microfibril biogenesis.
Subcellular Location Secreted, extracellular space, extracellular matrix. Colocalizes with FMN1 microfibrils in the eye ECM.
Involvement in Disease Ectopia lentis 2, isolated, autosomal recessive: An ocular abnormality characterized by partial or complete displacement of the lens from its space resulting from defective zonule formation. The disease is caused by mutations affecting the gene represented in this entry. Ectopia lentis et pupillae: An ocular abnormality characterized by displacement of the lenses and the pupils, associated with other ocular anomalies, but without systemic manifestations. The condition is usually bilateral, with the lenses and pupils displaced in opposite directions. Additional signs include enlarged corneal diameter, increased corneal astigmatism, increased anterior chamber depth, thinning and flattening of the iris with loss of crypts, angle malformation caused by enlarged iris processes, persistent pupillary membrane, loss of zonular fibers, tilted disk, and increased axial length. Secondary manifestations include refractive errors, glaucoma, early cataract development, and retinal detachment. Membrane formation on the posterior aspect of the iris has been observed both in histologic sections and on ultrasound biomicroscopy. The disease is caused by mutations affecting the gene represented in this entry.
Post-Translational Modification N-glycosylated. Can be O-fucosylated by POFUT2 on a serine or a threonine residue found within the consensus sequence C1-X(2)-(S/T)-C2-G of the TSP type-1 repeat domains where C1 and C2 are the first and second cysteine residue of the repeat, respectively. Fucosylated repeats can then be further glycosylated by the addition of a beta-1,3-glucose residue by the glucosyltransferase, B3GALTL. Fucosylation mediates the efficient secretion of ADAMTS family members. Also can be C-glycosylated with one or two mannose molecules on tryptophan residues within the consensus sequence W-X-X-W of the TPRs. N- and C-glycosylations can also facilitate secretion.
Tissue Specificity Expressed in colon, heart, leukocyte, liver, lung, skeletal muscle, spleen, testis and placenta. Weaker expression in bone marrow, brain tissue, kidney and pancreas. Expression studies in fetal tissues reveal strong expression in heart, kidney, liver, lung and skeletal muscle, but weaker expression in fetal brain and skin.
Subunit Structure Interacts with CTSB. Interacts with FBN1.
Sequence Similarities Contains 1 PLAC domain. Contains 6 TSP type-1 domains.

Poduct Presentation

Form Liquid
Preservative 0.02% (w/v) sodium azide
Storage buffer PBS with 50% glycerol, pH 7.3

Storage and Shipping Information

Storage Store at -20 or -80 C. Avoid multiple freeze/thaw cycles.