Anti-ADAM10 polyclonal antibody

Name: Anti-ADAM10 polyclonal antibody
SKU: DPABH-18550
Rating: 5 (1 reviews)

Rabbit Anti-Human ADAM10 polyclonal antibody for IP, WB

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COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Mouse; Rat; Human

Immunogen

Synthetic peptide conjugated to KLH derived from within residues 700 to the C-terminus of Human ADAM10.

Conjugate

Unconjugated

Applications

Application Notes

IP: 5 μg/ml; WB: 1 μg/ml.

Target

Alternative Names

ADAM10; ADAM metallopeptidase domain 10; a disintegrin and metalloproteinase domain 10; disintegrin and metalloproteinase domain-containing protein 10; CD156c; HsT18717; kuz; MADM; CDw156; ADAM 10; kuzbanian protein homolog; mammalian disintegrin-metallop

Entrez Gene ID

102

UniProt ID

A0A024R5U5

Product Background

Antigen Description

Cleaves the membrane-bound precursor of TNF-alpha at 76-Ala--Val-77 to its mature soluble form. Responsible for the proteolytical release of soluble JAM3 from endothelial cells surface. Responsible for the proteolytic release of several other cell-surface proteins, including heparin-binding epidermal growth-like factor, ephrin-A2 and for constitutive and regulated alpha-secretase cleavage of amyloid precursor protein (APP). Contributes to the normal cleavage of the cellular prion protein. Involved in the cleavage of the adhesion molecule L1 at the cell surface and in released membrane vesicles, suggesting a vesicle-based protease activity. Controls also the proteolytic processing of Notch and mediates lateral inhibition during neurogenesis.

Pathway

Activated NOTCH1 Transmits Signal to the Nucleus; Alzheimers disease; Delta-Notch Signaling Pathway; Disease; Epithelial cell signaling in Helicobacter pylori infection;

Citations

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Documents

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References

Dissecting the interaction between tissue inhibitor of metalloproteinases-3 (TIMP-3) and low density lipoprotein receptor-related protein-1 (LRP-1): Development of a "TRAP" to increase levels of TIMP-3 in the tissue

MATRIX BIOLOGY

Authors: Scilabra, Simone D.; Yamamoto, Kazuhiro; Pigoni, Martina; Sakamoto, Kazuma; Mueller, Stephan A.; Papadopoulou, Alkmini; Lichtenthaler, Stefan F.; Troeberg, Linda; Nagase, Hideaki; Kadomatsu, Kenji

Abstract

Tissue inhibitor of metalloproteinases 3 (TIMP-3) is a key regulator of extracellular matrix turnover for its ability to inhibit matrix metalloproteinases (MMPs), adamalysin-like metalloproteinases (ADAMs) and ADAMs with thrombospondin motifs (ADAMTSs). TIMP-3 is a secreted protein whose extracellular levels are regulated by endocytosis via the low-density-lipoprotein receptor-related protein-1 (LRP-1). In this study we developed a molecule able to "trap" TIMP-3 extracellularly, thereby increasing its tissue bioavailability. LRP-1 contains four ligand-binding clusters. In order to investigate the TIMP-3 binding site on LRP-1, we generated soluble minireceptors (sLRPs) containing the four distinct binding clusters or part of each cluster. We used an array of biochemical methods to investigate the binding of TIMP-3 to different sLRPs. We found that TIMP-3 binds to the ligand-binding cluster II of the receptor with the highest affinity and a soluble minireceptor containing the N-terminal half of cluster II specifically blocked TIMP-3 internalization, without affecting the turnover of metalloproteinases. Mass spectrometry-based secretome analysis showed that this minireceptor, named T3TRAP, selectively increased TIMP-3 levels in the extracellular space and inhibited constitutive shedding of a number of cell surface proteins. In conclusion, T3TRAP represents a biological tool that can be used to modulate TIMP-3 levels in the tissue and could be potentially developed as a therapy for diseases characterized by a deficit of TIMP-3, including arthritis. (C) 2016 Elsevier B.V. All rights reserved.

Correlations Between Single Nucleotide Polymorphisms, Cognitive Dysfunction, and Postmortem Brain Pathology in Alzheimer's Disease Among Han Chinese

NEUROSCIENCE BULLETIN

Authors: Yang, Qian; Chen, Kang; Zhang, Hanlin; Zhang, Wanying; Gong, Changlin; Zhang, Qing; Liu, Pan; Sun, Tianyi; Xu, Yuanyuan; Qian, Xiaojing; Qiu, Wenying; Ma, Chao

Abstract

In this study, the distribution of five Alzheimer's disease (AD)-related single nucleotide polymorphisms (SNPs) in the Han population was examined in combination with the evaluation of clinical cognition and brain pathological analysis. The associations among SNPs, clinical daily cognitive states, and postmortem neuropathological changes were analyzed in 110 human brains from the Chinese Academy of Medical Sciences/Peking Union Medical College (CAMS/PUMC) Human Brain Bank. APOE epsilon 4 (OR=4.482, P=0.004), the RS2305421 GG genotype (adjusted OR=4.397, P=0.015), and the RS10498633 GT genotype (adjusted OR=2.375, P=0.028) were associated with a higher score on the ABC (A plaque score, Braak NFT stage, and CERAD neuritic plaque score) dementia scale. These results advance our understanding of the pathogenesis of AD, the relationship between pathological diagnosis and clinical diagnosis, and the SNPs in the Han population for future research.