Evidence map›Paper›PMID 31349190›Full record

ArticleiScience2019

Myosin 1b Regulates Nuclear AKT Activation by Preventing Localization of PTEN in the Nucleus.

Yi Yu, Yuyan Xiong, Diogo Ladeiras, Zhihong Yang, Xiu-Fen Ming

Open access · goldAbstract read
In one paragraph

Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Prenylcysteine Oxidase 1 Deficiency Protects the Cardiac Muscle Cell Line HL-1 Against Ischaemic/Hypoxic Stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Oncogenic role and potential mechanisms of MYO1B in breast cancer.In vitro cellular & developmental biology. Animal · 2026
    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

5 authors at 1 institution in 1 country.

Yi YuCardiovascular and Aging Research, Department of Endocrinology, Metabolism and Cardiovascular System, Medicine Section, Faculty of Science and Medicine, University of Fribourg, Chemin du Musée 5, 1700 Fribourg, Switzerland.
Yuyan XiongCardiovascular and Aging Research, Department of Endocrinology, Metabolism and Cardiovascular System, Medicine Section, Faculty of Science and Medicine, University of Fribourg, Chemin du Musée 5, 1700 Fribourg, Switzerland.
Diogo LadeirasCardiovascular and Aging Research, Department of Endocrinology, Metabolism and Cardiovascular System, Medicine Section, Faculty of Science and Medicine, University of Fribourg, Chemin du Musée 5, 1700 Fribourg, Switzerland.
Zhihong YangCardiovascular and Aging Research, Department of Endocrinology, Metabolism and Cardiovascular System, Medicine Section, Faculty of Science and Medicine, University of Fribourg, Chemin du Musée 5, 1700 Fribourg, Switzerland. Electronic address: zhihong.yang@unifr.ch.
Xiu-Fen MingCardiovascular and Aging Research, Department of Endocrinology, Metabolism and Cardiovascular System, Medicine Section, Faculty of Science and Medicine, University of Fribourg, Chemin du Musée 5, 1700 Fribourg, Switzerland. Electronic address: xiu-fen.ming@unifr.ch.
University of Fribourg · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin-induced AKT activation is dependent on phosphoinositide 3-kinase and opposed by tumor suppressor phosphatase and tensin homolog (PTEN). Our previous study demonstrates that myosin 1b (MYO1B) mediates arginase-II-induced activation of mechanistic target of rapamycin complex 1 that is regulated by AKT. However, the role of MYO1B in AKT activation is unknown. Here we show that silencing MYO1B in mouse embryonic fibroblasts (MEF) inhibits insulin-induced nuclear but not cytoplasmic AKT activation accompanied by elevated nuclear PTEN level. Co-immunoprecipitation, co-immunostaining, and proximity ligation assay show an interaction of MYO1B and PTEN resulting in reduced nuclear PTEN. Moreover, the elevated nuclear PTEN upon silencing MYO1B promotes apoptosis of MEFs and melanoma B16F10 cells. Taken together, we demonstrate that MYO1B, by interacting with PTEN, prevents nuclear localization of PTEN contributing to nuclear AKT activation and suppression of cell apoptosis. This may present a therapeutic approach for cancer treatment such as melanoma.

Indexed as

BiochemistryBiological SciencesCell BiologyMolecular Biology

Identifiers

PMID31349190
PMCPMC6660601
OpenAlexW2959810235

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.