ArticleExperimental eye research2013
Novel compstatin family peptides inhibit complement activation by drusen-like deposits in human retinal pigmented epithelial cell cultures.
Article in Experimental eye research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 28 citations in OpenAlex.
- Mechanistic studies on HNRNPA2B1 suggest binding but not selective recognition of mRNA biology · 2026Article
- The Complement System as a Therapeutic Target in Retinal Disease.Medicina (Kaunas, Lithuania) · 2024Review
- Understanding the Impact of Polyunsaturated Fatty Acids on Age-Related Macular Degeneration: A Review.International journal of molecular sciences · 2024Review
- Computational analysis of complement inhibitor compstatin using molecular dynamics.Journal of molecular modeling · 2020Article
- Complement system and age-related macular degeneration: drugs and challenges.Drug design, development and therapy · 2019Review
- Article
- A computational model for the evaluation of complement system regulation under homeostasis, disease, and drug intervention.PloS one · 2018Article
- Signaling of the Complement Cleavage Product Anaphylatoxin C5a Through C5aR (CD88) Contributes to Pharmacological Hematopoietic Stem Cell Mobilization.Stem cell reviews and reports · 2017Article
- Drusen in patient-derived hiPSC-RPE models of macular dystrophies.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Complement-Mediated Regulation of Apolipoprotein E in Cultured Human RPE Cells.Investigative ophthalmology & visual science · 2017Article
- Targeting the complement system for the management of retinal inflammatory and degenerative diseases.European journal of pharmacology · 2016Review
- Peptide redesign for inhibition of the complement system: Targeting age-related macular degeneration.Molecular vision · 2016Article
- Cellular models and therapies for age-related macular degeneration.Disease models & mechanisms · 2015Review
- New compstatin peptides containing N-terminal extensions and non-natural amino acids exhibit potent complement inhibition and improved solubility characteristics.Journal of medicinal chemistry · 2015Article
- Forcefield_NCAA: ab initio charge parameters to aid in the discovery and design of therapeutic proteins and peptides with unnatural amino acids and their application to complement inhibitors of the compstatin family.ACS synthetic biology · 2014Article
- Elucidating a key anti-HIV-1 and cancer-associated axis: the structure of CCL5 (Rantes) in complex with CCR5.Scientific reports · 2014Article
- Elucidating a key component of cancer metastasis: CXCL12 (SDF-1α) binding to CXCR4.Journal of chemical information and modeling · 2014Article
- Protein folding and de novo protein design for biotechnological applications.Trends in biotechnology · 2014Review
- Molecular recognition of CCR5 by an HIV-1 gp120 V3 loop.PloS one · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
We have used a novel human retinal pigmented epithelial (RPE) cell-based model that mimics drusen biogenesis and the pathobiology of age-related macular degeneration to evaluate the efficacy of newly designed peptide inhibitors of the complement system. The peptides belong to the compstatin family and, compared to existing compstatin analogs, have been optimized to promote binding to their target, complement protein C3, and to enhance solubility by improving their polarity/hydrophobicity ratios. Based on analysis of molecular dynamics simulation data of peptide-C3 complexes, novel binding features were designed by introducing intermolecular salt bridge-forming arginines at the N-terminus and at position -1 of N-terminal dipeptide extensions. Our study demonstrates that the RPE cell assay has discriminatory capability for measuring the efficacy and potency of inhibitory peptides in a macular disease environment.
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.