Recombinant Human ADAMTS-L2 His-tag Protein, CF

When Recombinant Human ADAMTSL2 His-tag (Catalog# 10950-AD) is immobilized at 2.00 μg/mL, 100 μL/well, the concentration of Recombinant Human Lysyl Oxidase Homolog 2 Protein (2639-AO) that produces 50% of the optimal binding response is approximately 0.60-3.00 μg/mL.

2 μg/lane of Recombinant Human ADAMTS-L2 His-tag Protein (Catalog # 10950-AD) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue staining, showing bands at 130-144 kDa.

• Reactivity: Hu
• Applications: Bioactivity
• Format: Carrier-Free

Recombinant Human ADAMTS-L2 His-tag Protein, CF Summary

• Details of Functionality: Measured by its binding ability in a functional ELISA. When Recombinant Human ADAMTSL2 His-tag (Catalog# 10950-AD) immobilized at 2.00 μg/mL, 100 μL/well, the concentration of Recombinant Human Lysyl Oxidase Homolog 2 Protein (Catalog # 2639-AO) that produces 50% of the optimal binding response is approximately 0.60-3.00 μg/mL.
• Source: Chinese Hamster Ovary cell line, CHO-derived human ADAMTSL2 protein Asp23-Ser951 with a C-terminal 6-His tag
• Accession #: Q86TH1.1
• N-terminal Sequence: Asp23
• Protein/Peptide Type: Recombinant Enzymes
• Purity: >95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
• Endotoxin Note: <0.10 EU per 1 μg of the protein by the LAL method.

Applications/Dilutions

• Dilutions:
  • Bioactivity
• Theoretical MW: 103 kDa.
  Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
• SDS-PAGE: 130-144 kDa, under reducing conditions

Packaging, Storage & Formulations

• Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  12 months from date of receipt, -20 to -70 degreesC as supplied. 1 month, 2 to 8 degreesC under sterile conditions after reconstitution. 3 months, -20 to -70 degreesC under sterile conditions after reconstitution.
• Buffer: Lyophilized from a 0.2 μm filtered solution in HEPES and NaCl with Trehalose.
• Purity: >95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
• Reconstitution Instructions: Reconstitute at 100 μg/mL in PBS.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for Recombinant Human ADAMTS-L2 His-tag Protein, CF

• ADAMTSL2 ADAMTS-like 2
• ADAMTSL2
• GPHYSD1

Background

ADAMTSL2 (a disintegrin and metalloproteinase with thrombospondin motifs like 2), is one protein from a seven-member family of ADAMTS-like secreted proteins that are related to ADAMTS zinc metalloproteases but do not contain a metalloprotease domain. ADAMTSL2 contains a multidomain structure that includes an N-terminal signal sequence, C-terminal thrombospondin repeats, ADAMTS cysteine-rich and spacer modules, a PLAC domain and an N-glycan rich module unique amongst ADAMTSL family members (1). These domains play a substantial role in ADAMTS specificity and ADAMTSLs are also expected to have specific extracellular ligands. ADAMTSL2 is abundantly expressed in liver, lung, and spleen and resides in the extracellular matrix (ECM) (2). It has been shown to interact with many ECM proteins including fibrillin microfibrils (3), members of the lysyl oxidase family such as LOXL2 (4), and latent transforming growth factor beta binding protein 1 (LTBP1) (5). The interaction between ADAMTSL2 and LTBP1 and fibrillin indicates ADAMTSL2 may have a role in modulation of microfibrillar formation and function (3,5) and ADAMTSL2 has been found upregulated in cardiac fibrosis (6). Through its interaction with the LTBP1 protein and lysyl oxidase family members, ADAMTSL2 protein has been suggested to regulate the availability of TGF-beta and consequent TGF-beta signaling (1,5). Several mutations of ADAMTSL2 lead to a heterogeneous autosomal recessive disease, Geleophysic dysplasia 1 (7, 8). Geleophysic dysplasia 1 may be specifically caused by impaired secretion of ADAMTSL2 due to glycosylation differences (9). A variant of ADAMTSL2 has also been shown to result in an autosomal dominant inherited connective tissue disorder consistent with Ehlers-Danlos syndrome (10).

1. Mead, T.J. and S.S. Apte. (2018) Matrix Biol. 71:225.
2. Koo, B. et al. (2007) Matrix Biol. 26:431.
3. Hubmacher, D. and S. S. Apte. (2015) Matrix Biol. 47:34.
4. Aviram, R. et al. (2019) Matrix Biol. 75-76:114-125.
5. Le Goff, C. et al. (2008) Nat. Genet. 9:1119-23.
6. Trenson, S. et al. (2021) Circ. Heart Fail. 14:e006979.
7. Allali, S. et al. (2011) J. Med. Genet. 48:417.
8. Marzin, P. et al. (2009) Gene Reviews. Internet:1993-2020.
9. Zhang, A. et al. (2020) J. Biol. Chem. 295:15742.  
10. Steinle, J. et al. (2021) Am. J. Med. Genet. A. 185:743.

Bioinformatics

• Uniprot:
  • Q86TH1.1()