Evidence map›Paper›PMID 10460238›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

A neuronal-specific mammalian homolog of the Drosophila retinal degeneration B gene with expression restricted to the retina and dentate gyrus.

C Lu, T S Vihtelic, D R Hyde, T Li

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 44 citations in OpenAlex.

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  14. Nir2, a novel regulator of cell morphogenesis.Molecular and cellular biology · 2002
    Article
  15. Molecular aspects of retinal degenerative diseases.Cellular and molecular neurobiology · 2001
    Review
  16. Review
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

4 authors at 2 institutions in 1 country.

C LuBerman-Gund Laboratory for the Study of Retinal Degenerations, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts 02114, USA.
T S Vihtelic
D R Hyde
T Li
Massachusetts Eye and Ear Infirmary · USUniversity of Notre Dame · US

Funding

MODELS OF PHOTORECEPTOR DISEASER01EY010309 · NEI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI SANDBERG, MICHAEL A · 1994 to 2008
$2.6M
MOLECULAR ANALYSIS OF PHOTOTRANSDUCTION IN DROSOPHILAR01EY008058 · NEI · UNIVERSITY OF NOTRE DAME · PI HYDE, DAVID R · 1989 to 1997
–
NEI NIH HHS EY08058NEI NIH HHS EY10309NEI NIH HHS R01 EY010309
6 · The paper itself

Abstract

Mutations in the Drosophila retinal degeneration B (rdgB) gene cause a rapid loss of the electrophysiological light response and subsequent light-enhanced photoreceptor degeneration. The rdgB gene encodes a protein with an N-terminal phosphatidylinositol transfer protein domain, a large C-terminal segment, and several hydrophobic regions thought to multiply span the subrhabdomeric cisternal membrane. A mammalian rdgB homolog (m-rdgB1) was previously identified and shown to exhibit widespread tissue distribution and functionally rescue the Drosophila rdgB mutant phenotypes. We describe a second mammalian rdgB homolog (m-rdgB2) that possesses 46% amino acid identity to Drosophila RdgB and 56% identity to M-RdgB1. M-RdgB2 possesses a neuronal-specific expression pattern, with high levels in the retina and the dentate gyrus mossy fibers and dendritic field. Using M-RdgB2-specific antibodies and subcellular fractionation, we demonstrate that M-RdgB2 is not an integral membrane protein but is stably associated with a particulate fraction through protein-protein interactions. Although transgenic expression of M-RdgB2 in rdgB2 null mutant flies suppressed the retinal degeneration, it failed to fully restore the electrophysiological light response. Because transgenic expression of M-RdgB2 does not restore the wild-type phenotype to rdgB2 mutant flies to the same extent as M-RdgB1, functional differences likely exist between the two M-RdgB homologs.

Indexed as

Chromosome MappingDrosophila ProteinsAmino Acid SequenceAnimalsBrainCalcium-Binding ProteinsCloning, MolecularCrosses, GeneticDentate GyrusDrosophila melanogasterExonsEye ProteinsIntronsMammalsMembrane ProteinsMembrane Transport ProteinsCalcium-Binding ProteinsDrosophila ProteinsEye ProteinsMembrane ProteinsMembrane Transport ProteinsPitpnm2 protein, mouserdgB protein, DrosophilaRecombinant Proteins

Identifiers

PMID10460238
PMCPMC6782490
OpenAlexW2145417534

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.