Evidence map›Paper›PMID 27308891›Full record

ArticleAutophagy2016

MARCH2 regulates autophagy by promoting CFTR ubiquitination and degradation and PIK3CA-AKT-MTOR signaling.

Dan Xia, Liujing Qu, Ge Li, Beiqi Hongdu, Chentong Xu, Xin Lin, Yaxin Lou, Qihua He, Dalong Ma, Yingyu Chen

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. MARCH E3 Ligases: Understudied Regulators of Pulmonary Immune Function.Journal of respiratory biology and translational medicine · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
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  16. Article
  17. Targeting ubiquitination machinery in cystic fibrosis: Where do we stand?Cellular and molecular life sciences : CMLS · 2024
    Review
  18. Article
  19. 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

10 authors at 1 institution in 1 country.

Dan Xiaa Department of Immunology , Peking University School of Basic Medical Sciences , Beijing , China.
Liujing Qua Department of Immunology , Peking University School of Basic Medical Sciences , Beijing , China.
Ge Lia Department of Immunology , Peking University School of Basic Medical Sciences , Beijing , China.
Beiqi Hongdua Department of Immunology , Peking University School of Basic Medical Sciences , Beijing , China.
Chentong Xua Department of Immunology , Peking University School of Basic Medical Sciences , Beijing , China.
Xin Lina Department of Immunology , Peking University School of Basic Medical Sciences , Beijing , China.
Yaxin Loud Medical and Healthy Analytical Center, Peking University , Beijing , China.
Qihua Hed Medical and Healthy Analytical Center, Peking University , Beijing , China.
Dalong Maa Department of Immunology , Peking University School of Basic Medical Sciences , Beijing , China.
Yingyu Chena Department of Immunology , Peking University School of Basic Medical Sciences , Beijing , China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MARCH2 (membrane-associated RING-CH protein 2), an E3 ubiquitin ligase, is mainly associated with the vesicle trafficking. In the present study, for the first time, we demonstrated that MARCH2 negatively regulates autophagy. Our data indicated that overexpression of MARCH2 impaired autophagy, as evidenced by attenuated levels of LC3B-II and impaired degradation of endogenous and exogenous autophagic substrates. By contrast, loss of MARCH2 expression had the opposite effects. In vivo experiments demonstrate that MARCH2 knockout mediated autophagy results in an inhibition of tumorigenicity. Further investigation revealed that the induction of autophagy by MARCH2 deficiency was mediated through the PIK3CA-AKT-MTOR signaling pathway. Additionally, we found that MARCH2 interacts with CFTR (cystic fibrosis transmembrane conductance regulator), promotes the ubiquitination and degradation of CFTR, and inhibits CFTR-mediated autophagy in tumor cells. The functional PDZ domain of MARCH2 is required for the association with CFTR. Thus, our study identified a novel negative regulator of autophagy and suggested that the physical and functional connection between the MARCH2 and CFTR in different conditions will be elucidated in the further experiments.

Indexed as

AutophagyGene Expression RegulationAnimalsCarrier ProteinsCell Line, TumorClass I Phosphatidylinositol 3-KinasesCystic Fibrosis Transmembrane Conductance RegulatorHumansMembrane ProteinsMiceMice, KnockoutPhenotypePhosphatidylinositol 3-KinasesProtein DomainsProto-Oncogene Proteins c-aktRNA, Small InterferingAKT1 protein, humanAkt1 protein, mouseCarrier ProteinsClass I Phosphatidylinositol 3-KinasesCystic Fibrosis Transmembrane Conductance RegulatorMARCH2 protein, mouseMARCHF2 protein, humanMembrane ProteinsMTOR protein, humanmTOR protein, mousePhosphatidylinositol 3-KinasesPIK3CA protein, humanPik3ca protein, mouseProto-Oncogene Proteins c-aktRNA, Small InterferingTOR Serine-Threonine KinasesUbiquitin-Protein LigasesautophagyCFTRMARCH2MTORprotein degradation

Identifiers

PMID27308891
PMCPMC5082784
OpenAlexW2435227038

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.