anti-ADAMTSL4 antibody :: Mouse anti-Human ADAMTSL4 Polyclonal Antibody

Anti -ADAMTSL4 (ADAMTS-like Protein 4, ADAMTSL-4, Thrombospondin Repeat-containing Protein 1, TSRC1, PP1396, UNQ2803/PRO34012, DKFZP434K1772)

For Research Use Only. Not for use in diagnostic procedures.

Chromosome: 1; NC_000001.10 (150521846..150533413). Location: 1q21.3

Polyclonal

IgG

Mouse

Recognizes human ADAMTSL4.

Affinity Purified
Purified by Protein A affinity chromatography.

Supplied as a liquid in PBS, pH 7.2.

May be stored at 4 degree C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20 degree C. Aliquots are stable for at least 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Small volumes of anti-ADAMTSL4 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Positive regulation of apoptosis. May facilitate FBN1 microfibril biogenesis.

Western Blot (WB), Immunofluorescence (IF)

Suitable for use in Immunofluorescence and Western Blot.
Dilution: Immunofluorescence: 10ug/ml

116,545 Da[Similar Products]

ADAMTS-like 4

ADAMTS-like protein 4; ADAMTSL-4; thrombospondin repeat containing 1; thrombospondin repeat-containing protein 1

ADAMTS-like protein 4

TSRC1; ADAMTSL-4  [Similar Products]

ATL4_HUMAN

This gene is a member of ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs)-like gene family and encodes a protein with protein with seven thrombospondin type 1 repeats. The thrombospondin type 1 repeat domain is found in many proteins with diverse biological functions including cellular adhesion, angiogenesis, and patterning of the developing nervous system. Alternate transcriptional splice variants, encoding different isoforms, have been characterized. [provided by RefSeq, Jul 2008]

Function: Positive regulation of apoptosis. May facilitate FBN1 microfibril biogenesis. Ref.7 Ref.10

Subunit structure: Interacts with CTSB. Interacts with FBN1. Ref.7 Ref.10

Subcellular location: Secreted › extracellular space › extracellular matrix. Note: Colocalizes with FMN1 microfibrils in the eye ECM. Ref.10

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. Ref.8

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

By similarity. Ref.10

Involvement in disease: Ectopia lentis 2, isolated, autosomal recessive (ECTOL2) [MIM:225200]: An ocular abnormality characterized by partial or complete displacement of the lens from its space resulting from defective zonule formation.Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.8Ectopia lentis et pupillae (ECTOLP) [MIM:225200]: 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.Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.9

Sequence similarities: Contains 1 PLAC domain.Contains 6 TSP type-1 domains.

Caution: Although similar to members of the ADAMTS family, it lacks the metalloprotease and disintegrin-like domains which are typical of that family.

Sequence caution: The sequence AAG17217.1 differs from that shown. Reason: Frameshift at position 719.

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