ArticleProteome science2007
Identification of differentially regulated proteins in a patient with Leber's Congenital Amaurosis--a proteomic study.
Article in Proteome science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Alterations in energy metabolism, neuroprotection and visual signal transduction in the retina of Parkinsonian, MPTP-treated monkeys.PloS one · 2013Article
- Novel roles for α-crystallins in retinal function and disease.Progress in retinal and eye research · 2012Review
- Ocular proteomics with emphasis on two-dimensional gel electrophoresis and mass spectrometry.Biological procedures online · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo identify the pattern of protein expression in the retina from a patient with Leber's Congenital Amaurosis (LCA) secondary to a mutation in the AIPL1 gene. The retina from one eye of a patient with LCA and 7 control eyes were studied. The tissue was subjected to high resolution two-dimensional gel electrophoresis, image analysis and mass spectrometry, in an effort to identify differentially regulated proteins.
resultsIn the LCA retina seven protein spots were differentially expressed. Six proteins were significantly up-regulated of which three could be identified as: alphaA-crystallin, triosephophate isomerase, and an N-terminal fragment of the beta-chain of ATP synthase. One protein spot that was down-regulated in the LCA retina was identified as a C-terminal fragment of beta-tubulin.
conclusionRetinal tissue in LCA is characterised by an up-regulation of alphaA-crystallin, triosephosphate isomerase, and ATP synthase (beta-chain fragment) and down-regulation of a fragment of beta-tubulin. These proteins/protein fragments may play a crucial role for the retinal degeneration processes in LCA and other retinal dystrophies.
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Registered trials
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