Evidence map›Paper›PMID 29570858›Full record

ArticleImmunology and cell biology2018

Metabolic control of cell fate bifurcations in a hematopoietic progenitor population.

Radomir Kratchmarov, Sara Viragova, Min Jung Kim, Nyanza J Rothman, Kang Liu, Boris Reizis, Steven L Reiner

Abstract read
In one paragraph

Article in Immunology and cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

31 citing papers in PubMed, 48 citations in OpenAlex.

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  16. Lipid metabolism in dendritic cell biology.Immunological reviews · 2023
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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

7 authors at 2 institutions in 1 country.

Radomir KratchmarovDepartment of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
Sara ViragovaDepartment of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
Min Jung KimDepartment of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
Nyanza J RothmanDepartment of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
Kang LiuDepartment of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
Boris ReizisDepartment of Pathology, NYU Langone Medical Center, New York, NY, 10016, USA.
Steven L ReinerDepartment of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.ORCID 0000-0002-1635-8619
Columbia University · USNYU Langone Health · US

Funding

Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Parisa Tehranifar · 1985 to 2026
$115.3M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007367 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI REINER, STEVEN L · 1985 to 2021
$25.1M
Asymmetric Lymphocyte Division in the Immune ResponseR01AI076458 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI REINER, STEVEN L · 2008 to 2019
$3.7M
Columbia University Graduate Training Program in Microbiology and ImmunologyT32AI106711 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Nicholas Arpaia, Uttiya Basu · 2014 to 2026
$2.1M
Diversifying and Regenerating T Cell FunctionR01AI113365 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REINER, STEVEN L · 2014 to 2018
$2.0M
Self-renewing Lymphocyte Division in The Immune ResponseR56AI076458 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REINER, STEVEN L · 2014 to 2021
$802k
NCI NIH HHS P30 CA013696NIAID NIH HHS R01 AI076458NIAID NIH HHS R01 AI113365NIAID NIH HHS R56 AI076458NIAID NIH HHS T32 AI106711NIGMS NIH HHS T32 GM007367
6 · The paper itself

Abstract

Growth signals drive hematopoietic progenitor cells to proliferate and branch into divergent cell fates, but how unequal outcomes arise from a common progenitor is not fully understood. We used steady-state analysis of in vivo hematopoiesis and Fms-related tyrosine kinase 3 ligand (Flt3L)-induced in vitro differentiation of dendritic cells (DCs) to determine how growth signals regulate lineage bias. We found that Flt3L signaling induced anabolic activation and proliferation of DC progenitors, which was associated with DC differentiation. Perturbation of processes associated with quiescence and catabolism, including AMP-activated protein kinase signaling, fatty acid oxidation, or mitochondrial clearance increased development of cDC2 cells at the expense of cDC1 cells. Conversely, scavenging anabolism-associated reactive oxygen species skewed differentiation toward cDC1 cells. Sibling daughter cells of dividing DC progenitors exhibited unequal expression of the transcription factor interferon regulatory factor 8, which correlated with clonal divergence in FoxO3a signaling and population-level bifurcation of cell fate. We propose that unequal transmission of growth signals during cell division might support fate branches during proliferative expansion of progenitors.

Indexed as

AnimalsCell DifferentiationCell LineageCell ProliferationCells, CulturedCytokinesDendritic CellsFatty AcidsHematopoiesisHematopoietic Stem CellsInterferon Regulatory Factor-8Interferon Regulatory FactorsLipid MetabolismMembrane ProteinsMetabolismMiceCytokinesFatty Acidsflt3 ligand proteinInterferon Regulatory Factor-8Interferon Regulatory FactorsMembrane ProteinsReactive Oxygen SpeciesAMPKasymmetric divisiondendritic cellFlt3LPI3K

Identifiers

PMID29570858
PMCPMC6146018
OpenAlexW2793330342

What OpenQuestion holds

Textmetadata
LicenceTDM
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.