Evidence map›Paper›PMID 26828436›Full record

ReviewSeminars in cell & developmental biology2016

Mitochondria in human pluripotent stem cell apoptosis.

Tara TeSlaa, Kiyoko Setoguchi, Michael A Teitell

Abstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
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  5. Strategies to Improve the Safety of iPSC-Derived β Cells for β Cell Replacement in Diabetes.Transplant international : official journal of the European Society for Organ Transplantation · 2022
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. A single-cell Raman-based platform to identify developmental stages of human pluripotent stem cell-derived neurons.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Mitochondrial functions and melatonin: a tour of the reproductive cancers.Cellular and molecular life sciences : CMLS · 2019
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
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

3 authors.

Tara TeSlaaMolecular Biology Institute, University of California, Los Angeles, CA 90095, USA.
Kiyoko SetoguchiDepartment of Pathology and Laboratory Medicine, University of California, Los Angeles, CA 90095, USA.
Michael A TeitellMolecular Biology Institute, University of California, Los Angeles, CA 90095, USA; Department of Pathology and Laboratory Medicine, University of California, Los Angeles, CA 90095, USA; Department of Bioengineering, Department of Pediatrics, California NanoSystems Institute, Jonsson Comprehensive Cancer Center, and Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, CA 90095, USA. Electronic address: mteitell@mednet.ucla.edu.

Funding

UCLA NIGMS T32 Program AssessmentT32GM007185 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TORRES, JORGE · 1985 to 2020
$21.7M
RNA trafficking in mitochondriaR01GM073981 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Carla M Koehler, MICHAEL A TEITELL · 2006 to 2026
$5.1M
TCL1 ONCOGENE IN B LYMPHOCYTE DEVELOPMENT AND NEOPLASIAR01CA090571 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TEITELL, MICHAEL A · 2002 to 2015
$3.8M
(PQD5) Mass Profiling Melanoma Responses to Improve Therapy Choices and PrognosisR01CA185189 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI REED, JASON C, TEITELL, MICHAEL A · 2014 to 2017
$1.9M
Reverse Mitochondrial Genetics Enabled by BlastR01GM114188 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHIOU, PEI-YU, TEITELL, MICHAEL A · 2015 to 2018
$1.9M
A Fourth Outcome: DNA Damage and the Differentiation of B CellsR01CA156674 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TEITELL, MICHAEL A · 2011 to 2015
$1.5M
NCI NIH HHS CA156674NCI NIH HHS CA185189NCI NIH HHS CA90571NCI NIH HHS R01 CA090571NCI NIH HHS R01 CA156674NCI NIH HHS R01 CA185189NIGMS NIH HHS GM007185NIGMS NIH HHS GM073981NIGMS NIH HHS GM114188NIGMS NIH HHS R01 GM073981NIGMS NIH HHS R01 GM114188NIGMS NIH HHS T32 GM007185
6 · The paper itself

Abstract

Human pluripotent stem cells (hPSCs) have great potential in regenerative medicine because they can differentiate into any cell type in the body. Genome integrity is vital for human development and for high fidelity passage of genetic information across generations through the germ line. To ensure genome stability, hPSCs maintain a lower rate of mutation than somatic cells and undergo rapid apoptosis in response to DNA damage and additional cell stresses. Furthermore, cellular metabolism and the cell cycle are also differentially regulated between cells in pluripotent and differentiated states and can aid in protecting hPSCs against DNA damage and damaged cell propagation. Despite these safeguards, clinical use of hPSC derivatives could be compromised by tumorigenic potential and possible malignant transformation from failed to differentiate cells. Since hPSCs and mature cells differentially respond to cell stress, it may be possible to specifically target undifferentiated cells for rapid apoptosis in mixed cell populations to enable safer use of hPSC-differentiated cells in patients.

Indexed as

AnimalsApoptosisCellular ReprogrammingHumansInduced Pluripotent Stem CellsMitochondriaApoptosisHuman pluripotent stem cellsp53Tumorigenicity

Identifiers

PMID26828436
PMCPMC4805448

What OpenQuestion holds

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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.