Evidence map›Paper›PMID 20354168›Full record

ArticleBlood2010

AKT1 and AKT2 maintain hematopoietic stem cell function by regulating reactive oxygen species.

Marisa M Juntilla, Vineet D Patil, Marco Calamito, Rohan P Joshi, Morris J Birnbaum, Gary A Koretzky

Abstract read
In one paragraph

Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers.

0numbers the graph read from it
0cells of the map it votes in
163citing papers in PubMed
12.3field-weighted citation impact, top 1% 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

163 citing papers in PubMed, 277 citations in OpenAlex.

  1. Article
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  15. Review
  16. Role of mitochondrial reactive oxygen species in homeostasis regulation.Redox report : communications in free radical research · 2022
    Review
  17. Mechanisms involved in hematopoietic stem cell aging.Cellular and molecular life sciences : CMLS · 2022
    Review
  18. Article
  19. Bone Marrow Niches of Hematopoietic Stem and Progenitor Cells.International journal of molecular sciences · 2022
    Review
  20. Molecular regulation of hematopoietic stem cell quiescence.Cellular and molecular life sciences : CMLS · 2022
    Review

103 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

6 authors at 2 institutions in 1 country.

Marisa M JuntillaAbramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia 19104, USA.
Vineet D Patil
Marco Calamito
Rohan P Joshi
Morris J Birnbaum
Gary A Koretzky
University of Pennsylvania · USCancer Research Institute · US

Funding

The Function of Tribbles in the Pathogenesis of AMLP01CA093615 · NCI · UNIVERSITY OF PENNSYLVANIA · PI BURKHARDT, JANIS K. · 2002 to 2011
$16.2M
THE ROLE OF THE AKT/PKB SIGNALING IN INSULIN ACTIONR01DK056886 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI BIRNBAUM, MORRIS J · 2000 to 2014
$5.3M
Predoctoral Program for Minority StudentsF31AI056671 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI JUNTILLA, MARISA · 2003 to 2007
$238k
NCI NIH HHS P01 CA093615NCI NIH HHS P01-CA093615NIAID NIH HHS F31 AI056671NIAID NIH HHS F31-AI056671NIDDK NIH HHS R01 DK056886NIDDK NIH HHS R01-DK56886NIGMS NIH HHS R37-GM053526
6 · The paper itself

Abstract

Although AKT is essential for multiple cellular functions, the role of this kinase family in hematopoietic stem cells (HSCs) is unknown. Thus, we analyzed HSC function in mice deficient in the 2 isoforms most highly expressed in the hematopoietic compartment, AKT1 and AKT2. Although loss of either isoform had only a minimal effect on HSC function, AKT1/2 double-deficient HSCs competed poorly against wild-type cells in the development of myeloid and lymphoid cells in in vivo reconstitution assays. Serial transplantations revealed an essential role for AKT1 and AKT2 in the maintenance of long-term HSCs (LT-HSCs). AKT1/2 double-deficient LT-HSCs were found to persist in the G(0) phase of the cell cycle, suggesting that the long-term functional defects are caused by increased quiescence. Furthermore, we found that the intracellular content of reactive oxygen species (ROS) is dependent on AKT because double-deficient HSCs demonstrate decreased ROS. The importance of maintaining ROS for HSC differentiation was shown by a rescue of the differentiation defect after pharmacologically increasing ROS levels in double-deficient HSCs. These data implicate AKT1 and AKT2 as critical regulators of LT-HSC function and suggest that defective ROS homeostasis may contribute to failed hematopoiesis.

Indexed as

Cell DifferentiationAnimalsAntigens, CDCD48 AntigenCell LineageFlow CytometryHematopoiesisHematopoietic Stem CellsMiceMice, Inbred C57BLMice, KnockoutProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptors, Cell SurfaceReverse Transcriptase Polymerase Chain ReactionRNA, MessengerAkt1 protein, mouseAkt2 protein, mouseAntigens, CDCD48 AntigenProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptors, Cell SurfaceRNA, MessengerSignaling Lymphocytic Activation Molecule Family Member 1

Identifiers

PMID20354168
PMCPMC2875090
OpenAlexW2040595174

What OpenQuestion holds

Textmetadata
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.