Evidence map›Paper›PMID 17656371›Full record

ArticleHuman molecular genetics2007

Crx activates opsin transcription by recruiting HAT-containing co-activators and promoting histone acetylation.

Guang-Hua Peng, Shiming Chen

Open access · greenAbstract read
In one paragraph

Article in Human molecular genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Pathogenic variants inGenome research · 2024
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  3. Review
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  5. Article
  6. International journal of molecular sciences · 2023
    Review
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  14. Review
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  16. Article
  17. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Guang-Hua PengDepartment of Ophthalmology and Visual Sciences, Washington University School of Medicine, St Louis, MO 63110, USA.
Shiming Chen
Washington University in St. Louis · US

Funding

WASHINGTON UNIVERSITY CENTER VISION RESEARCHP30EY002687 · NEI · WASHINGTON UNIVERSITY · PI Philip Andrew Ruzycki · 1985 to 2026
$18.4M
Vulnerable and Resilient Cells in Retinal DegenerationR01EY012543 · NEI · WASHINGTON UNIVERSITY · PI SHIMING CHEN, Philip Raymond Williams · 2000 to 2026
$12.2M
NEI NIH HHS EY02687NEI NIH HHS EY12543NEI NIH HHS P30 EY002687NEI NIH HHS R01 EY012543
6 · The paper itself

Abstract

The homeodomain transcription factor Crx is required for expression of many photoreceptor genes in the mammalian retina. The mechanism by which Crx activates transcription remains to be determined. Using protein-protein interaction assays, Crx was found to interact with three co-activator proteins (complexes): STAGA, Cbp and p300, all of which possess histone acetyl-transferase (HAT) activity. To determine the role of Crx-HAT interactions in target gene chromatin modification and transcriptional activation, quantitative RT-PCR and chromatin immunoprecipitation were performed on Crx target genes, rod and cone opsins, in developing mouse retina. Although cone opsins are transcribed earlier than rhodopsin during development, the transcription of each gene is preceded by the same sequence of events in their promoter and enhancer regions: (i) binding of Crx, followed by (ii) binding of HATs, (iii) the acetylation of histone H3, then (iv) binding of other photoreceptor transcription factors (Nrl and Nr2e3) and RNA polymerase II. In Crx knockout mice (Crx(-/-)), the association of HATs and AcH3 with target promoter/enhancer regions was significantly decreased, which correlates with aberrant opsin transcription and photoreceptor dysfunction in these mice. Similar changes to the opsin chromatin were seen in Y79 retinoblastoma cells, where opsin genes are barely transcribed. These defects in Y79 cells can be reversed by expressing a recombinant Crx or applying histone deacetylase inhibitors. Altogether, these results suggest that one mechanism for Crx-mediated transcriptional activation is to recruit HATs to photoreceptor gene chromatin for histone acetylation, thereby inducing and maintaining appropriate chromatin configurations for transcription.

Indexed as

Transcriptional ActivationAcetylationAnimalsAnimals, NewbornCells, CulturedHistone AcetyltransferasesHistonesHomeodomain ProteinsMiceMice, Inbred C57BLMice, KnockoutModels, Biologicalp300-CBP-Associated Factorp300-CBP Transcription FactorsPromoter Regions, GeneticProtein Bindingcone rod homeobox proteinHistone AcetyltransferasesHistonesHomeodomain Proteinsp300-CBP-Associated Factorp300-CBP Transcription FactorsRod OpsinsTrans-Activators

Identifiers

PMID17656371
PMCPMC2276662
OpenAlexW2170466740

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.