Evidence map›Paper›PMID 28486555›Full record

ArticlePloS one2017

Autophagy is a signature of a signaling network that maintains hematopoietic stem cells.

Michelle Nguyen-McCarty, Peter S Klein

Abstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. A mitochondrial surveillance mechanism activated bybioRxiv : the preprint server for biology · 2024
    Article
  2. Expansion of human hematopoietic stem cells by inhibiting translation.bioRxiv : the preprint server for biology · 2023
    Article
  3. The Tumor SuppressorJournal of developmental biology · 2023
    Article
  4. Article
  5. Article
  6. An Overview of Autophagy in Hematopoietic Stem Cell Transplantation.Frontiers in bioengineering and biotechnology · 2022
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. The clinicopathological significance of ZNF10 in invasive ductal carcinoma of the breast.International journal of clinical and experimental pathology · 2018
    Article
  13. Review
  14. Review
  15. Article
  16. Multifaceted Roles of GSK-3 in Cancer and Autophagy-Related Diseases.Oxidative medicine and cellular longevity · 2017
    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

2 authors.

Michelle Nguyen-McCartyCell and Molecular Biology Graduate Group, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States of America.
Peter S KleinCell and Molecular Biology Graduate Group, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States of America.ORCID http://orcid.org/0000-0002-2011-8538

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SHELLEY L BERGER · 1985 to 2026
$222.3M
HEMATOPOIESIS TRAINING GRANTT32DK007780 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI TONG, WEI · 1999 to 2023
$6.7M
Regulating Hematopoietic Stem Cell Homeostasis through GSK-3R01HL110806 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI KLEIN, PETER S, TONG, WEI · 2011 to 2014
$2.1M
Towards Precision Medicine in Childhood Acquired Aplastic AnemiaR24DK103001 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI CHOU, STELLA T, KLEIN, PETER S · 2014 to 2016
$1.7M
An unexpected signaling output for the tumor suppressor APCR01GM115517 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI KLEIN, PETER S · 2016 to 2019
$1.3M
Targeting Wnt and mTOR to expand hematopoietic stem cellsR21HL107968 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI KLEIN, PETER S · 2011 to 2012
$440k
NCI NIH HHS P30 CA016520NHLBI NIH HHS R01 HL110806NHLBI NIH HHS R21 HL107968NIDDK NIH HHS R24 DK103001NIDDK NIH HHS T32 DK007780NIGMS NIH HHS R01 GM115517
6 · The paper itself

Abstract

Hematopoietic stem cells (HSCs) are able to self-renew and to differentiate into all blood cells. HSCs reside in a low-perfusion niche and depend on local signals to survive and to maintain the capacity for self-renewal. HSCs removed from the niche are unable to survive without addition of hematopoietic cytokines and rapidly lose their ability to self-renew. We reported previously that inhibition of both GSK-3 and mTORC1 is essential to maintain long-term HSCs ex vivo. Although Wnt/β-catenin signaling downstream of GSK-3 is required for this response, the downstream effectors of mTORC1 remain undefined. We now report that HSCs express a pro-autophagic gene signature and accumulate LC3 puncta only when both mTORC1 and GSK-3 are inhibited, identifying autophagy as a signature for a signaling network that maintains HSCs ex vivo. In addition, these conditions sustain HSC repopulating function despite an increased rate of global translation. Together, these findings provide new insight into the relative contributions of various mTORC1 outputs toward the maintenance of HSC function and build upon the growing body of literature implicating autophagy and tightly controlled protein synthesis as important modulators of diverse stem cell populations.

Indexed as

AutophagySignal TransductionHematopoietic Stem CellsHumans

Identifiers

PMID28486555
PMCPMC5423627

What OpenQuestion holds

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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.