ArticleNeuroscience2008
Human membrane metallo-endopeptidase-like protein degrades both beta-amyloid 42 and beta-amyloid 40.
Article in Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Identification of genetic variants for blood insulin level in sex-stratified Korean population and evaluation of the causal relationship between blood insulin level and polycystic ovary syndrome.Genes & genomics · 2021Article
- Amyloid beta: structure, biology and structure-based therapeutic development.Acta pharmacologica Sinica · 2017Review
- Monitoring proteolytic processing events by quantitative mass spectrometry.Expert review of proteomics · 2017Review
- Replication of GWAS Coding SNPs Implicates MMEL1 as a Potential Susceptibility Locus among Saudi Arabian Celiac Disease Patients.Disease markers · 2015Article
- Amyloid-beta and Alzheimer's disease: the role of neprilysin-2 in amyloid-beta clearance.Frontiers in aging neuroscience · 2014Review
- Identification and characterization of Aβ peptide interactors in Alzheimer's disease by structural approaches.Frontiers in aging neuroscience · 2014Article
- Proteolytic degradation of amyloid β-protein.Cold Spring Harbor perspectives in medicine · 2012Review
- Altered NEP2 expression and activity in mild cognitive impairment and Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2012Article
- The Alzheimer's amyloid-degrading peptidase, neprilysin: can we control it?International journal of Alzheimer's disease · 2012Article
- Intranasal phosphoramidon increases beta-amyloid levels in wild-type and NEP/NEP2-deficient mice.Journal of molecular neuroscience : MN · 2011Article
- Neprilysin-2 is an important β-amyloid degrading enzyme.The American journal of pathology · 2011Article
- A non-synonymous SNP within membrane metalloendopeptidase-like 1 (MMEL1) is associated with multiple sclerosis.Genes and immunity · 2010Article
- Distinctive RNA expression profiles in blood associated with Alzheimer disease after accounting for white matter hyperintensities.Alzheimer disease and associated disordersArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Beta-amyloid (Abeta) degrading endopeptidases are thought to protect against Alzheimer's disease (AD) and are potentially therapeutic. Of particular interest are endopeptidases that are blocked by thiorphan and phosphoramidon (T/P), as these inhibitors rapidly induce Abeta deposition in rodents. Neprilysin (NEP) is the best known target of T/P; however neprilysin knockout results in only modest Abeta increases insufficient to induce deposition. Therefore, other endopeptidases targeted by T/P must be critical for Abeta catabolism. Another candidate is the T/P sensitive membrane metallo-endopeptidase-like protein (MMEL), a close homolog of neprilysin. The endopeptidase properties of beta and gamma splice forms of human MMEL were determined in HEK293T cells transduced with the human cDNAs for the two splice forms; this showed degradation of both Abeta(42) and Abeta(40) by hMMEL-beta but not hMMEL-gamma. hMMEL-beta activity was found at the extracellular surface with no significant secreted activity. hMMEL-gamma was not expressed at the extracellular surface. Finally, it was found that hMMEL cleaves Abeta near the alpha-secretase site (producing Abeta(1-17)>>Abeta(1-16)). These data establish hMMEL as a mediator of Abeta catabolism and raise the possibility of its involvement in the etiology of AD and as a target for intervention.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.