Evidence map›Paper›PMID 30858178›Full record

ArticleThe Journal of biological chemistry2019

UVB-induced inactivation of manganese-containing superoxide dismutase promotes mitophagy via ROS-mediated mTORC2 pathway activation.

Sanjit K Dhar, Ines Batinic-Haberle, Daret K St Clair

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. TIMP3 deficiency accelerates UVB-induced HaCaT cell senescence by regulating ferroptosis.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Photochemical reactions between 1,4-benzoquinone and OEnvironmental science and pollution research international · 2020
    Article
  11. Article
  12. Review
  13. 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

3 authors at 2 institutions in 1 country.

Sanjit K DharFrom the Department of Toxicology and Cancer Biology, University of Kentucky, Lexington, Kentucky 40536 and.ORCID 0000-0003-3193-2778
Ines Batinic-Haberlethe Department of Radiation Oncology, Duke University Medical Center, Durham, North Carolina 27710.
Daret K St ClairFrom the Department of Toxicology and Cancer Biology, University of Kentucky, Lexington, Kentucky 40536 and dstcl00@uky.edu.
University of Kentucky · USDuke Medical Center · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
A redox-mediated mechanism of UVB-induced metabolic switch in skin carcinogenesisR01CA214638 · NCI · UNIVERSITY OF KENTUCKY · PI ST CLAIR, DARET K · 2018 to 2022
$2.0M
NCI NIH HHS P30 CA177558NCI NIH HHS R01 CA214638
6 · The paper itself

Abstract

Mitochondria are major sites of energy metabolism that influence numerous cellular events, including immunity and cancer development. Previously, we reported that the mitochondrion-specific antioxidant enzyme, manganese-containing superoxide dismutase (MnSOD), has dual roles in early- and late-carcinogenesis stages. However, how defective MnSOD impacts the chain of events that lead to cell transformation in pathologically normal epidermal cells that have been exposed to carcinogens is unknown. Here, we show that UVB radiation causes nitration and inactivation of MnSOD leading to mitochondrial injury and mitophagy. In keratinocytes, exposure to UVB radiation decreased mitochondrial oxidative phosphorylation, increased glycolysis and the expression of autophagy-related genes, and enhanced AKT Ser/Thr kinase (AKT) phosphorylation and cell growth. Interestingly, UVB initiated a prosurvival mitophagy response by mitochondria-mediated reactive oxygen species (ROS) signaling via the mammalian target of the mTOR complex 2 (mTORC2) pathway. Knockdown of rictor but not raptor abrogated UVB-induced mitophagy responses. Furthermore, fractionation and proximity-ligation assays reveal that ROS-mediated mTOC2 activation in mitochondria is necessary for UVB-induced mitophagy. Importantly, pretreatment with the MnSOD mimic MnTnBuOE-2-PyP

Indexed as

Ultraviolet RaysAnimalsAutophagyCell LineMechanistic Target of Rapamycin Complex 2MiceMitochondriaMitophagyNitratesOxidation-ReductionRapamycin-Insensitive Companion of mTOR ProteinReactive Oxygen SpeciesRegulatory-Associated Protein of mTORSuperoxide DismutaseMechanistic Target of Rapamycin Complex 2NitratesRapamycin-Insensitive Companion of mTOR ProteinReactive Oxygen SpeciesRegulatory-Associated Protein of mTORrictor protein, mouseRptor protein, mouseSuperoxide DismutaseautophagycancermetabolismmitophagyMnSODmTORmTOR complex 2 (mTOR C2)oxidative stressreactive oxygen species (ROS)rictor

Identifiers

PMID30858178
PMCPMC6497943
OpenAlexW2922263232

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.