Evidence map›Paper›PMID 31289326›Full record

ArticleScientific reports2019

Mitochondrial Akt Signaling Modulated Reprogramming of Somatic Cells.

Yu-Han Chen, Ching-Chieh Su, Wu Deng, Leslie F Lock, Peter J Donovan, Matthew A Kayala, Pierre Baldi, Hsiao-Chen Lee, Yumay Chen, Ping H Wang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 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
1.2field-weighted citation impact, top 21% 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, 21 citations in OpenAlex.

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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

10 authors at 3 institutions in 2 countries.

Yu-Han ChenUC Irvine Diabetes Center, University of California, Irvine, California, USA.ORCID http://orcid.org/0000-0002-3307-2903
Ching-Chieh SuUC Irvine Diabetes Center, University of California, Irvine, California, USA.
Wu DengUC Irvine Diabetes Center, University of California, Irvine, California, USA.
Leslie F LockSue & Bill Gross Stem Cell Research Center, University of California, Irvine, California, USA.
Peter J DonovanUC Irvine Diabetes Center, University of California, Irvine, California, USA.
Matthew A KayalaDepartment of Computer Science, University of California, Irvine, California, USA.
Pierre BaldiDepartment of Computer Science, University of California, Irvine, California, USA.ORCID http://orcid.org/0000-0001-8752-4664
Hsiao-Chen LeeUC Irvine Diabetes Center, University of California, Irvine, California, USA.ORCID http://orcid.org/0000-0001-5261-0773
Yumay ChenUC Irvine Diabetes Center, University of California, Irvine, California, USA.
Ping H WangUC Irvine Diabetes Center, University of California, Irvine, California, USA. phwang@uci.edu.ORCID http://orcid.org/0000-0002-7847-7752
University of California, Irvine · USFu Jen Catholic University · TWKaohsiung Medical University · TW

Funding

Insulin's Control of Myocardial Mitochondria Bioenergetics and BiogenesisR01HL096987 · NHLBI · UNIVERSITY OF CALIFORNIA-IRVINE · PI WANG, PING H · 2010 to 2013
$1.5M
NHLBI NIH HHS R01 HL096987
6 · The paper itself

Abstract

The signaling mechanisms controlling somatic cell reprogramming are not fully understood. In this study, we report a novel role for mitochondrial Akt1 signaling that enhanced somatic cell reprogramming efficiency. The role of mitochondrial Akt1 in somatic cell reprogramming was investigated by transducing fibroblasts with the four reprogramming factors (Oct4, Sox2, Klf4, c-Myc) in conjunction with Mito-Akt1, Mito-dnAkt1, or control virus. Mito-Akt1 enhanced reprogramming efficiency whereas Mito-dnAkt1 inhibited reprogramming. The resulting iPSCs formed embryoid bodies in vitro and teratomas in vivo. Moreover, Oct4 and Nanog promoter methylation was reduced in the iPSCs generated in the presence of Mito-Akt1. Akt1 was activated and translocated into mitochondria after growth factor stimulation in embryonic stem cells (ESCs). To study the effect of mitochondrial Akt in ESCs, a mitochondria-targeting constitutively active Akt1 (Mito-Akt1) was expressed in ESCs. Gene expression profiling showed upregulation of genes that promote stem cell proliferation and survival and down-regulation of genes that promote differentiation. Analysis of cellular respiration indicated similar metabolic profile in the resulting iPSCs and ESCs, suggesting comparable bioenergetics. These findings showed that activation of mitochondrial Akt1 signaling was required during somatic cell reprogramming.

Indexed as

Cell DifferentiationCellular ReprogrammingAnimalsCells, CulturedEmbryonic Stem CellsHumansInduced Pluripotent Stem CellsKruppel-Like Factor 4MiceMice, Inbred C57BLProto-Oncogene Proteins c-aktSignal TransductionTranscriptional ActivationKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Proto-Oncogene Proteins c-akt

Identifiers

PMID31289326
PMCPMC6616364
OpenAlexW2961311147

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.