Evidence map›Paper›PMID 30109811›Full record

ArticleAutophagy2018

The pro-oxidant adaptor p66SHC promotes B cell mitophagy by disrupting mitochondrial integrity and recruiting LC3-II.

Anna Onnis, Valentina Cianfanelli, Chiara Cassioli, Dijana Samardzic, Pier Giuseppe Pelicci, Francesco Cecconi, Cosima T Baldari

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Guideline
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  6. p66shc deficiency attenuates high glucose-induced autophagy dysfunction in Schwann cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  7. Article
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  12. The E3 ubiquitin ligase SOCS-7 reverses immunosuppression via Shc1 signaling in hepatocellular carcinoma.Laboratory investigation; a journal of technical methods and pathology · 2022
    Article
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  19. Editorial: Molecular Mechanisms of Selective Autophagy in Human Disease.Frontiers in cell and developmental biology · 2020
    Article
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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

7 authors at 5 institutions in 2 countries.

Anna Onnisa Department of Life Sciences , University of Siena , Siena , Italy.ORCID 0000-0003-3199-9868
Valentina Cianfanellib Cell Stress and Survival Unit , Danish Cancer Society Research Center , Copenhagen , Denmark.ORCID 0000-0002-3857-9463
Chiara Cassiolia Department of Life Sciences , University of Siena , Siena , Italy.ORCID 0000-0002-4853-2298
Dijana Samardzicc Venetian Institute of Molecular Medicine , University of Padova , Padova , Italy.ORCID 0000-0002-0232-7686
Pier Giuseppe Peliccid Department of Experimental Oncology , European Institute of of Oncology , Milan , Italy.ORCID 0000-0002-5076-2316
Francesco Cecconib Cell Stress and Survival Unit , Danish Cancer Society Research Center , Copenhagen , Denmark.ORCID 0000-0002-5614-4359
Cosima T Baldaria Department of Life Sciences , University of Siena , Siena , Italy.ORCID 0000-0002-4414-6744
University of Siena · ITDanish Cancer Society · DKEuropean Institute of Oncology · ITUniversity of Rome Tor Vergata · ITVeneto Institute of Molecular Medicine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy/autophagy has emerged as a central process in lymphocyte homeostasis, activation and differentiation. Based on our finding that the p66 isoform of SHC1 (p66SHC) pro-apoptotic ROS-elevating SHC family adaptor inhibits MTOR signaling in these cells, here we investigated the role of p66SHC in B-cell autophagy. We show that p66SHC disrupts mitochondrial function through its CYCS (cytochrome c, somatic) binding domain, thereby impairing ATP production, which results in AMPK activation and enhanced autophagic flux. While p66SHC binding to CYCS is sufficient for triggering apoptosis, p66SHC-mediated autophagy additionally depends on its ability to interact with membrane-associated LC3-II through a specific binding motif within its N terminus. Importantly, p66SHC also has an impact on mitochondria homeostasis by inducing mitochondrial depolarization, protein ubiquitination at the outer mitochondrial membrane, and local recruitment of active AMPK. These events initiate mitophagy, whose full execution relies on the role of p66SHC as an LC3-II receptor which brings phagophore membranes to mitochondria. Importantly, p66SHC also promotes hypoxia-induced mitophagy in B cells. Moreover, p66SHC deficiency enhances B cell differentiation to plasma cells, which is controlled by intracellular ROS levels and the hypoxic germinal center environment. The results identify mitochondrial p66SHC as a novel regulator of autophagy and mitophagy in B cells and implicate p66SHC-mediated coordination of autophagy and apoptosis in B cell survival and differentiation. Abbreviations: ACTB: actin beta; AMPK: AMP-activated protein kinase; ATP: adenosine triphosphate; ATG: autophagy-related; CYCS: cytochrome c, somatic; CLQ: chloroquine; COX: cyclooxygenase; CTR: control; GFP: green fluorescent protein; HIFIA/Hif alpha: hypoxia inducible factor 1 subunit alpha; IMS: intermembrane space; LIR: LC3 interacting region; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MTOR/mTOR: mechanistic target of rapamycin kinase; OA: oligomycin and antimycin A; OMM: outer mitochondrial membrane; PHB: prohibitin; PBS: phosphate-buffered saline; PINK1: PTEN induced putative kinase 1; RFP: red fluorescent protein; ROS: reactive oxygen species; SHC: src Homology 2 domain-containing transforming protein; TMRM: tetramethylrhodamine, methyl ester; TOMM: translocase of outer mitochondrial membrane; ULK1: unc-51 like autophagy activating kinase 1; WT: wild-type.

Indexed as

AnimalsB-LymphocytesCell DifferentiationCells, CulturedCell SurvivalHEK293 CellsHeLa CellsHumansMiceMice, 129 StrainMice, KnockoutMicrotubule-Associated ProteinsMitochondriaMitochondrial MembranesMitophagyOxidantsMAP1LC3B protein, humanMicrotubule-Associated ProteinsOxidantsPHB protein, humanProhibitinsReactive Oxygen SpeciesSHC1 protein, humanShc1 protein, mouseSrc Homology 2 Domain-Containing, Transforming Protein 1AutophagyB lymphocytesLC3 adaptormitochondriamitophagyp66SHC

Identifiers

PMID30109811
PMCPMC6984773
OpenAlexW2887990863

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.