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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

ADAM metallopeptidase domain 10

ADAM10, Kuzbanian
Members of the ADAM family are cell surface proteins with a unique structure possessing both potential adhesion and protease domains. This gene encodes and ADAM family member that cleaves many proteins including TNF-alpha and E-cadherin. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: TACE, metalloprotease, APP, CAN, V1a
Papers using ADAM10 antibodies
The good, the bad and the ugly substrates for ADAM10 and ADAM17 in brain pathology, inflammation and cancer
Fahrenholz Falk et al., In BMC Genomics, 2007
... Additional tables including differentially regulated genes in ADAM10 and mutant ADAM10 transgenic mice.
Ectodomain shedding of L1 adhesion molecule promotes cell migration by autocrine binding to integrins.
Means Robert E., In PLoS ONE, 2000
... The ADAM10 antibody for immunofluorescence analysis was purchased from Diaclone (Besancon, France), the ADAM10 ...
Tyrosine phosphorylation of paxillin and focal adhesion kinase by activation of muscarinic m3 receptors is dependent on integrin engagement by the extracellular matrix
Slack Barbara E et al., In BMC Cell Biology, 1997
... Labs (San Francisco, CA), mouse monoclonal antibodies to dynamin I and goat polyclonal antibodies to the ADAM10 prodomain from Santa Cruz Biotechnology (Santa Cruz, CA), rabbit ...
Papers on ADAM10
Increase of α-Secretase ADAM10 in Platelets Along Cognitively Healthy Aging.
Endres et al., In J Alzheimers Dis, Feb 2016
UNASSIGNED: ADAM10 is one of the key players in ectodomain-shedding of the amyloid-β protein precursor (AβPP).
Molecular design and structural optimization of potent peptide hydroxamate inhibitors to selectively target human ADAM metallopeptidase domain 17.
Zhong et al., Shanghai, China. In Comput Biol Chem, Jan 2016
The ADAM metallopeptidase domain 17 (ADAM17 or TACE) and its close relative ADAM10 are two of the most important ADAM members that share high conservation in sequence, structure and function, but exhibit subtle difference in regulation of downstream cell signaling events.
[Effect of ADAM10 Inhibitor GI254023X on Proliferation and Apoptosis of Multiple Myeloma H929 Cells and Its Possible Mechanisms].
Li et al., Xuzhou, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, Dec 2015
OBJECTIVE: To investigate the effect of ADAM10 inhibitor GI254023X on the proliferation and apoptosis of multiple myeloma H929 cell line and its mechanisms.
The alpha secretase ADAM10: A metalloprotease with multiple functions in the brain.
Lichtenthaler et al., Kiel, Germany. In Prog Neurobiol, Dec 2015
In the central nervous system, ADAM10 has attracted the most attention, since it was described as the amyloid precursor protein α-secretase over ten years ago.
η-Secretase processing of APP inhibits neuronal activity in the hippocampus.
Haass et al., München, Germany. In Nature, Nov 2015
We identify higher molecular mass carboxy-terminal fragments (CTFs) of APP, termed CTF-η, in addition to the long-known CTF-α and CTF-β fragments generated by the α- and β-secretases ADAM10 (a disintegrin and metalloproteinase 10) and BACE1 (β-site APP cleaving enzyme 1), respectively.
The soluble leptin receptor.
Kratzsch et al., Leipzig, Germany. In Best Pract Res Clin Endocrinol Metab, Oct 2015
Lipotoxicity and apoptosis increase OB-R cleavage via ADAM10-dependent mechanisms.
Modulation of platelet and monocyte function by the chemokine fractalkine (CX3 CL1) in cardiovascular disease.
Schäfer et al., Hannover, Germany. In Eur J Clin Invest, Jun 2015
BACKGROUND: The chemokine fractalkine, CX3CL1, bears unique features within the chemokine family: it exists in a membrane bound form acting as an adhesion molecule and surface receptor; however, when cleaved by ADAM 10, it functions as a soluble chemokine.
ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets.
Ludwig et al., Aachen, Germany. In Am J Physiol Lung Cell Mol Physiol, Mar 2015
ADAM10 and ADAM17 are the most prominent members of this protease family.
Novel receptors for bacterial protein toxins.
Aktories et al., Freiburg, Germany. In Curr Opin Microbiol, Feb 2015
Using optimized protocols and new methods novel toxin receptors have been identified, including metalloprotease ADAM 10 for Staphylococcus aureus α-toxin, laminin receptor Lu/BCAM for Escherichia coli cytotoxic necrotizing factor CNF1, lipolysis stimulated lipoprotein receptor (LSR) for Clostridium difficile transferase CDT and low-density lipoprotein receptor-related protein (LRP) 1 for Clostridium perfringens TpeL toxin.
Association of a BACE1 Gene Polymorphism with Parkinson's Disease in a Norwegian Population.
Maple-Grødem et al., Stavanger, Norway. In Parkinsons Dis, 2014
The aim of this study was to investigate whether candidate polymorphisms in five genes (ADAM10, BACE1, BACE2, PSEN2, and CLU) involved in the APP processing pathway affect PD risk in a population-based cohort of patients with incident PD and control subjects from the Norwegian ParkWest study.
Expression of MICA in oral squamous carcinoma cells and its effect on NK cells.
Liu et al., Fuzhou, China. In Int J Clin Exp Med, 2014
ADAM10 and ADAM17 were detected by ELISA method.
Loss of the Timp gene family is sufficient for the acquisition of the CAF-like cell state.
Khokha et al., Toronto, Canada. In Nat Cell Biol, 2014
The proteome of these exosomes is enriched in extracellular matrix proteins and the metalloproteinase ADAM10.
ADAM10 promotes pituitary adenoma cell migration by regulating cleavage of CD44 and L1.
Ding et al., Shanghai, China. In J Mol Endocrinol, 2012
ADAM10 facilitated cell migration through modulation of CD44 and L1 cleavage.
Self-control of HGF regulation on human trophoblast cell invasion via enhancing c-Met receptor shedding by ADAM10 and ADAM17.
Wang et al., Beijing, China. In J Clin Endocrinol Metab, 2012
HGF down-regulated c-Met receptor expression, whereas it up-regulated pro- and active/mature forms of ADAM10 and ADAM17 expression, which resulted in enhanced sMet production
siRNA knockdown of ADAM-10, but not ADAM-17, significantly reduces fractalkine shedding following pro-inflammatory cytokine treatment in a human adult brain endothelial cell line.
Woodroofe et al., Sheffield, United Kingdom. In Neurosci Lett, 2012
ADAM-10 is the major protease involved in fractalkine release under pro-inflammatory conditions in this human adult brain endothelial cell model.
Melittin modulates keratinocyte function through P2 receptor-dependent ADAM activation.
Reiss et al., Kiel, Germany. In J Biol Chem, 2012
Data indicate that melittin induced keratinocyte cell function through activation of purinergic P2 receptor P2X7R, ADAM10 and ADAM17.
Role of ADAM10 and ADAM17 in CD16b shedding mediated by different stimulators.
Zhang et al., Beijing, China. In Chin Med Sci J, 2012
Both ADAM10 and ADAM17 could shed CD16b, but they possess differed preferences. ADAM10 is the main sheddase under stimulation of ionomycin, while ADAM17 is the main sheddase under stimulation of PMA.
A Staphylococcus aureus pore-forming toxin subverts the activity of ADAM10 to cause lethal infection in mice.
Bubeck Wardenburg et al., Chicago, United States. In Nat Med, 2011
ADAM10 is the cellular receptor for alpha-hemolysin.
Cleavage of E-cadherin by ADAM10 mediates epithelial cell sorting downstream of EphB signalling.
Batlle et al., Barcelona, Spain. In Nat Cell Biol, 2011
Data show that EphB receptors interact with E-cadherin and with the metalloproteinase ADAM10 at sites of adhesion.
The sirtuin pathway in ageing and Alzheimer disease: mechanistic and therapeutic considerations.
Zhu et al., Cleveland, United States. In Lancet Neurol, 2011
Mechanistically, SIRT1 increases α-secretase production and activity through activation of the α-secretase gene ADAM10.
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