Evidence map›Paper›PMID 26124274›Full record

ArticleThe Journal of biological chemistry2015

cGMP/Protein Kinase G Signaling Suppresses Inositol 1,4,5-Trisphosphate Receptor Phosphorylation and Promotes Endoplasmic Reticulum Stress in Photoreceptors of Cyclic Nucleotide-gated Channel-deficient Mice.

Hongwei Ma, Michael R Butler, Arjun Thapa, Josh Belcher, Fan Yang, Wolfgang Baehr, Martin Biel, Stylianos Michalakis, Xi-Qin Ding

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. cGMP Signaling in Photoreceptor Degeneration.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Preservation of endoplasmic reticulum (ER) CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  12. Article
  13. Review
  14. Potential contribution of ryanodine receptor 2 upregulation to cGMP/PKG signaling-induced cone degeneration in cyclic nucleotide-gated channel deficiency.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Involvement of natriuretic peptide system in C2C12 myocytes.Molecular and cellular biochemistry · 2019
    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

9 authors at 3 institutions in 2 countries.

Hongwei MaDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.
Michael R ButlerDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.
Arjun ThapaDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.
Josh BelcherDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.
Fan YangDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.
Wolfgang BaehrJohn A. Moran Eye Center, University of Utah, Salt Lake City, Utah 84132.
Martin BielCenter for Integrated Protein Science Munich and Department of Pharmacy, Center for Drug Research, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.
Stylianos MichalakisCenter for Integrated Protein Science Munich and Department of Pharmacy, Center for Drug Research, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.
Xi-Qin DingDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104. Electronic address: xi-qin-ding@ouhsc.edu.
University of Oklahoma Health Sciences Center · USCenter for Integrated Protein Science Munich · DEUniversity of Utah · US

Funding

P30-CENTER CORE GRANT FOR VISION RESEARCHP30EY021725 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Michelle C Callegan, MICHAEL H ELLIOTT · 2011 to 2026
$10.5M
RETINAL PHOTORECEPTOR CYCLIC GMP PHOSPHODIESTERASER01EY008123 · NEI · UNIVERSITY OF UTAH · PI BAEHR, WOLFGANG · 1990 to 2019
$7.8M
Membrane Protein Transport in PhotoreceptorsR01EY019298 · NEI · UNIVERSITY OF UTAH · PI BAEHR, WOLFGANG · 2009 to 2018
$3.7M
Mechanism of Cone Degeneration Resulting from CNG Channel DeficiencyR01EY019490 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI DING, XI-QIN · 2010 to 2014
$1.8M
Vision Science Training ProgramT32EY023202 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CALLEGAN, MICHELLE C · 2014 to 2025
$952k
NEI NIH HHS P30 EY021725NEI NIH HHS P30EY021725NEI NIH HHS R01 EY008123NEI NIH HHS R01 EY019298NEI NIH HHS R01EY019298NEI NIH HHS R01 EY019490NEI NIH HHS R01EY019490NEI NIH HHS R01EY08123NEI NIH HHS T32 EY023202NEI NIH HHS T32EY023202
6 · The paper itself

Abstract

Photoreceptor cyclic nucleotide-gated (CNG) channels play a pivotal role in phototransduction. Mutations in the cone CNG channel subunits CNGA3 and CNGB3 are associated with achromatopsia and cone dystrophies. We have shown endoplasmic reticulum (ER) stress-associated apoptotic cone death and increased phosphorylation of the ER Ca(2+) channel inositol 1,4,5-trisphosphate receptor 1 (IP3R1) in CNG channel-deficient mice. We also presented a remarkable elevation of cGMP and an increased activity of the cGMP-dependent protein kinase (protein kinase G, PKG) in CNG channel deficiency. This work investigated whether cGMP/PKG signaling regulates ER stress and IP3R1 phosphorylation in CNG channel-deficient cones. Treatment with PKG inhibitor and deletion of guanylate cyclase-1 (GC1), the enzyme producing cGMP in cones, were used to suppress cGMP/PKG signaling in cone-dominant Cnga3(-/-)/Nrl(-/-) mice. We found that treatment with PKG inhibitor or deletion of GC1 effectively reduced apoptotic cone death, increased expression levels of cone proteins, and decreased activation of Müller glial cells. Furthermore, we observed significantly increased phosphorylation of IP3R1 and reduced ER stress. Our findings demonstrate a role of cGMP/PKG signaling in ER stress and ER Ca(2+) channel regulation and provide insights into the mechanism of cone degeneration in CNG channel deficiency.

Indexed as

AnimalsApoptosisBasic-Leucine Zipper Transcription FactorsCarbazolesCyclic GMPCyclic GMP-Dependent Protein KinasesCyclic Nucleotide-Gated Cation ChannelsEndoplasmic Reticulum StressEpendymoglial CellsEye ProteinsGene Expression RegulationGuanylate CyclaseInositol 1,4,5-Trisphosphate ReceptorsMiceMice, KnockoutPhosphorylation8-bromoguanosino-3',5'-cyclic monophosphorothioateBasic-Leucine Zipper Transcription FactorsCarbazolesCnga3 protein, mouseCyclic GMPCyclic GMP-Dependent Protein KinasesCyclic Nucleotide-Gated Cation ChannelsEye ProteinsGuanylate Cyclaseguanylate cyclase 1Inositol 1,4,5-Trisphosphate ReceptorsItpr1 protein, mouseKT 5823Nrl protein, mouseProtein Kinase InhibitorsReceptors, Cell SurfaceThionucleotidescalcium channelcyclic GMP (cGMP)endoplasmic reticulum stress (ER stress)photoreceptorprotein kinase G (PKG)

Identifiers

PMID26124274
PMCPMC4543649
OpenAlexW2261169281

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.