Evidence map›Paper›PMID 27624939›Full record

ArticleThe Journal of biological chemistry2016

Novel Insights into the PKCβ-dependent Regulation of the Oxidoreductase p66Shc.

Martina Haller, Sana Khalid, Leopold Kremser, Friedrich Fresser, Tobias Furlan, Martin Hermann, Julia Guenther, Astrid Drasche, Michael Leitges, Marco Giorgio and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Endothelin receptor A and p66Shc regulate spontaneous CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  13. Article
  14. Review
  15. Article
  16. Role of adaptor protein p66Shc in renal pathologies.American journal of physiology. Renal physiology · 2018
    Review
  17. 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

13 authors at 2 institutions in 2 countries.

Martina HallerFrom the Daniel Swarovski Research Laboratory, Department of Visceral, Transplant, and Thoracic Surgery.
Sana KhalidFrom the Daniel Swarovski Research Laboratory, Department of Visceral, Transplant, and Thoracic Surgery.
Leopold KremserDivision of Clinical Biochemistry, Protein Micro-Analysis Facility.
Friedrich FresserDepartment for Pharmacology and Genetics, Division of Translational Cell Genetics, and.
Tobias FurlanFrom the Daniel Swarovski Research Laboratory, Department of Visceral, Transplant, and Thoracic Surgery.
Martin HermannDepartment for Anesthesiology and Intensive Care, Medical University of Innsbruck, 6020 Innsbruck, Austria.
Julia GuentherFrom the Daniel Swarovski Research Laboratory, Department of Visceral, Transplant, and Thoracic Surgery.
Astrid DrascheFrom the Daniel Swarovski Research Laboratory, Department of Visceral, Transplant, and Thoracic Surgery.
Michael Leitgesthe Biotechnology Center of Oslo, 0349 Oslo, Norway, and.
Marco Giorgiothe European Institute of Oncology, 20139 Milano, Italy.
Gottfried BaierDepartment for Pharmacology and Genetics, Division of Translational Cell Genetics, and.
Herbert LindnerDivision of Clinical Biochemistry, Protein Micro-Analysis Facility.
Jakob TroppmairFrom the Daniel Swarovski Research Laboratory, Department of Visceral, Transplant, and Thoracic Surgery, jakob.troppmair@i-med.ac.at.
European Institute of Oncology · ITUniversität Innsbruck · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysfunctional mitochondria contribute to the development of many diseases and pathological conditions through the excessive production of reactive oxygen species (ROS), and, where studied, ablation of p66Shc (p66) was beneficial. p66 translocates to the mitochondria and oxidizes cytochrome c to yield H

Indexed as

3T3 CellsAnimalsCell DeathGene DeletionHEK293 CellsHumansHydrogen PeroxideMiceMitochondriaModels, MolecularOxidative StressOxidoreductasesPhosphorylationPoint MutationProtein Kinase C betaReactive Oxygen SpeciesHydrogen PeroxideOxidoreductasesProtein Kinase C betaReactive Oxygen SpeciesRNA, Small InterferingSerineSHC1 protein, humanShc1 protein, mouseSrc Homology 2 Domain-Containing, Transforming Protein 1cell deathp66shcphosphorylationphosphotyrosine binding (PTB) domainPKCreactive oxygen species (ROS)redox signaling

Identifiers

PMID27624939
PMCPMC5095410
OpenAlexW2520511949

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.