Evidence map›Paper›PMID 22745813›Full record

ArticlePloS one2012

Differential developmental deficits in retinal function in the absence of either protein tyrosine sulfotransferase-1 or -2.

David M Sherry, Yogita Kanan, Robert Hamilton, Adam Hoffhines, Kelsey L Arbogast, Steven J Fliesler, Muna I Naash, Kevin L Moore, Muayyad R Al-Ubaidi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. 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

9 authors at 4 institutions in 1 country.

David M SherryDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Yogita Kanan
Robert Hamilton
Adam Hoffhines
Kelsey L Arbogast
Steven J Fliesler
Muna I Naash
Kevin L Moore
Muayyad R Al-Ubaidi
University of Oklahoma Health Sciences Center · USCenter for Neurosciences · USOklahoma Medical Research Foundation · USUniversity at Buffalo, State University of New York · US

Funding

UNDERSTANDING THE ROLE OF RETINOL DEHYDROGENASES RDH11 AND RDH12 IN VISIONP20RR017703 · NCRR · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI MANDAL, NAWAJES · 2002 to 2011
$23.6M
ZEBRAFISH INTERNATIONAL RESOURCE CENTERP40RR012546 · NCRR · UNIVERSITY OF OREGON · PI WESTERFIELD, MONTE · 1998 to 2011
$21.9M
Supplement for: Mechanism of Photoreceptor Cell Degeneration in Animal Models of Retinal DiseasesR01EY010609 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI MUAYYAD R AL-UBAIDI, Muna I. Naash · 1995 to 2026
$11.0M
CORE--MOLECULAR BIOLOGYP30EY012190 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ANDERSON, ROBERT E · 1999 to 2009
$5.2M
ISOPRENOID METABOLISM IN THE RETINAR01EY007361 · NEI · UNIVERSITY OF SOUTH FLORIDA · PI FLIESLER, STEVEN J. · 1988 to 2015
$4.4M
Identification of Tyrosine-Sulfated Proteins in the Male Genital TractR01HD056022 · NICHD · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI MOORE, KEVIN L · 2008 to 2012
$1.6M
Retinal degeneration caused by alterations in protein tyrosine O-sulfationR01EY018137 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI AL-UBAIDI, MUAYYAD R · 2009 to 2013
$1.1M
NCRR NIH HHS P20 RR017703NCRR NIH HHS P20RR017703NCRR NIH HHS P40 RR012546NEI NIH HHS P30 EY012190NEI NIH HHS P30EY12190NEI NIH HHS R01 EY007361NEI NIH HHS R01 EY010609NEI NIH HHS R01 EY018137NEI NIH HHS R01 EY10609NICHD NIH HHS R01 HD056022
6 · The paper itself

Abstract

To investigate the role(s) of protein-tyrosine sulfation in the retina and to determine the differential role(s) of tyrosylprotein sulfotransferases (TPST) 1 and 2 in vision, retinal function and structure were examined in mice lacking TPST-1 or TPST-2. Despite the normal histologic retinal appearance in both Tpst1(-/-) and Tpst2(-/-) mice, retinal function was compromised during early development. However, Tpst1(-/-) retinas became electrophysiologically normal by postnatal day 90 while Tpst2(-/-) mice did not functionally normalize with age. Ultrastructurally, the absence of TPST-1 or TPST-2 caused minor reductions in neuronal plexus. These results demonstrate the functional importance of protein-tyrosine sulfation for proper development of the retina and suggest that the different phenotypes resulting from elimination of either TPST-1 or -2 may reflect differential expression patterns or levels of the enzymes. Furthermore, single knock-out mice of either TPST-1 or -2 did not phenocopy mice with double-knockout of both TPSTs, suggesting that the functions of the TPSTs are at least partially redundant, which points to the functional importance of these enzymes in the retina.

Indexed as

AnimalsElectroretinographyImmunoblottingMiceMice, KnockoutMicroscopy, ElectronRetinaSulfotransferasesprotein-tyrosine sulfotransferaseSulfotransferasesTPST2 protein, mouse

Identifiers

PMID22745813
PMCPMC3382163
OpenAlexW1974444731

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.