ArticleThe pharmacogenomics journal2010
Upregulating CD59: a new strategy for protection of neurons from complement-mediated degeneration.
Article in The pharmacogenomics journal, 2010. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Predictive value of soluble CD59 for poor 28-day neurological prognosis and all-cause mortality in patients after cardiopulmonary resuscitation: a prospective observatory study.Journal of intensive care · 2023Article
- Contribution of proteases to the hallmarks of aging and to age-related neurodegeneration.Aging cell · 2022Review
- Transcriptome and Translatome Regulation of Pathogenesis in Alzheimer's Disease Model Mice.Journal of Alzheimer's disease : JAD · 2022Article
- Proteome Profile of Myelin in the Zebrafish Brain.Frontiers in cell and developmental biology · 2021Article
- Increased Macrophages and C1qA, C3, C4 Transcripts in the Midbrain of People With Schizophrenia.Frontiers in immunology · 2020Article
- Complement, a Therapeutic Target in Diabetic Kidney Disease.Frontiers in medicine · 2020Review
- Complement-dependent bystander injury to neurons in AQP4-IgG seropositive neuromyelitis optica.Journal of neuroinflammation · 2018Article
- Brain injury with systemic inflammation in newborns with congenital heart disease undergoing heart surgery.Experimental and therapeutic medicine · 2017Article
- CD59 mediates cartilage patterning during spontaneous tail regeneration.Scientific reports · 2015Article
- What does complement do in Alzheimer's disease? Old molecules with new insights.Translational neurodegeneration · 2013Article
- A shift in microglial β-amyloid binding in Alzheimer's disease is associated with cerebral amyloid angiopathy.Brain pathology (Zurich, Switzerland) · 2013Article
- Adenovirus serotype 26 utilizes CD46 as a primary cellular receptor and only transiently activates T lymphocytes following vaccination of rhesus monkeys.Journal of virology · 2012Article
- Membrane attack complex inhibitor CD59a protects against focal cerebral ischemia in mice.Journal of neuroinflammation · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
An increasing number of studies have shown a critical role for the membrane attack complex, synthesized on activation of the terminal pathway of the complement system, in causing demyelination and neuronal death in neurodegeneration. The aim of this study was to develop a strategy to increase the resistance of neurons to complement damage by modulating the expression of membrane complement regulatory protein CD59, the only inhibitor of the terminal pathway of the complement cascade. We exploited our recent finding that CD59 expression is regulated by the neural-restrictive silencer factor (REST) and designed a novel REST-derived peptide (REST5) containing the nuclear localization domain of the wild-type protein. The effect of REST5 and the mechanism by which it modulates CD59 expression were modelled in neuroblastoma cells transfected with expression constructs, and then confirmed in human neurons differentiated from neural progenitor cells. REST5 increased the expression of CD59 in neurons by fivefold and protected them from complement-mediated lysis spontaneously triggered by neurons. As a source of complement, we used either human serum or conditioned medium from primary human oligodendroglia. This study brings new insight into immunopharmacological research that may serve to inhibit neuronal death triggered by the terminal pathway of complement activation.
Indexed as
Identifiers
What OpenQuestion holds
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.