Evidence map›Paper›PMID 31787758›Full record

ReviewCell death & disease2019

The many substrates and functions of NEDD4-1.

Xi Huang, Jing Chen, Wen Cao, Li Yang, Qingxiao Chen, Jingsong He, Qing Yi, He Huang, Enfan Zhang, Zhen Cai

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

71 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
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  8. Review
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  10. Notch2-expressing CD4Cellular & molecular immunology · 2025
    Article
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11 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Xi HuangBone Marrow Transplantation Center, Department of Hematology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Jing ChenBone Marrow Transplantation Center, Department of Hematology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Wen CaoBone Marrow Transplantation Center, Department of Hematology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Li YangBone Marrow Transplantation Center, Department of Hematology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Qingxiao ChenBone Marrow Transplantation Center, Department of Hematology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Jingsong HeBone Marrow Transplantation Center, Department of Hematology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Qing YiCenter for Hematologic Malignancy Research Institute, Houston Methodist, Houston, TX, USA.
He HuangBone Marrow Transplantation Center, Department of Hematology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Enfan ZhangBone Marrow Transplantation Center, Department of Hematology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China. efzhang@zju.edu.cn.
Zhen CaiBone Marrow Transplantation Center, Department of Hematology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China. caiz@zju.edu.cn.ORCID http://orcid.org/0000-0002-6327-5066
Zhejiang University · CNFirst Affiliated Hospital Zhejiang University · CNHouston Methodist · USZhejiang University-University of Edinburgh Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumorigenesis, tumor growth, and prognosis are highly related to gene alterations and post-translational modifications (PTMs). Ubiquitination is a critical PTM that governs practically all aspects of cellular function. An increasing number of studies show that E3 ubiquitin ligases (E3s) are important enzymes in the process of ubiquitination that primarily determine substrate specificity and thus need to be tightly controlled. Among E3s, neural precursor cell expressed developmentally downregulated 4-1 (NEDD4-1) has been shown to play a critical role in modulating the proliferation, migration, and invasion of cancer cells and the sensitivity of cancer cells to anticancer therapies via regulating multiple substrates. This review discusses some significant discoveries on NEDD4-1 substrates and the signaling pathways in which NEDD4-1 participates. In addition, we introduce the latest potential therapeutic strategies that inhibit or activate NEDD4-1 activity using small molecules. NEDD4-1 likely acts as a novel drug target or diagnostic marker in the battle against cancer.

Indexed as

AnimalsAutophagyHumansModels, BiologicalNedd4 Ubiquitin Protein LigasesOncogenesSubstrate SpecificityUbiquitinationNedd4 Ubiquitin Protein Ligases

Identifiers

PMID31787758
PMCPMC6885513
OpenAlexW2991640319

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.