Evidence map›Paper›PMID 35717902›Full record

ArticleBlood cells, molecules & diseases2022

Liver kinase B1 (LKB1) in murine erythroid progenitors modulates erythropoietin setpoint in association with maturation control.

Zollie White, Kamaleldin E Elagib, Alejandro A Gru, Adam N Goldfarb

Open access · greenAbstract read
In one paragraph

Article in Blood cells, molecules & diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 95% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

4 authors at 1 institution in 1 country.

Zollie WhiteDepartment of Pathology, University of Virginia School of Medicine, USA.
Kamaleldin E ElagibDepartment of Pathology, University of Virginia School of Medicine, USA.
Alejandro A GruDepartment of Pathology, University of Virginia School of Medicine, USA.
Adam N GoldfarbDepartment of Pathology, University of Virginia School of Medicine, USA. Electronic address: ang3x@virginia.edu.
University of Virginia · US

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Jay William FOX · 1987 to 2026
$72.1M
Cancer Research Training Program: From Molecular Mechanisms to Therapeutic StrategiesT32CA009109 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Andrew Carl Dudley, Melanie R Rutkowski · 1985 to 2026
$13.9M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007267 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI GARCIA-BLANCO, MARIANO A. · 1985 to 2024
$13.4M
Iron Deficiency: Molecular and Cellular ConsequencesR01DK079924 · NIDDK · UNIVERSITY OF VIRGINIA · PI GOLDFARB, ADAM N. · 2008 to 2023
$5.2M
Targeting Dyrk1a to Promote Donor-independent Platelet ProductionR01HL149667 · NHLBI · UNIVERSITY OF VIRGINIA · PI GOLDFARB, ADAM N. · 2020 to 2023
$2.8M
NCI NIH HHS P30 CA044579NCI NIH HHS T32 CA009109NHLBI NIH HHS R01 HL149667NIDDK NIH HHS R01 DK079924NIGMS NIH HHS T32 GM007267
6 · The paper itself

Abstract

Erythropoiesis is a tightly regulated process. It is stimulated by decreased oxygen in circulation, which leads to the secretion of the hormone erythropoietin (Epo) by the kidneys. An additional layer of control involves the coordinated sensing and use of nutrients. Much cellular machinery contributes to sensing and responding to nutrient status in cells, and one key participant is the kinase LKB1. The current study examines the role of LKB1 in erythropoiesis using a murine in vivo and ex vivo conditional knockout system. In vivo analysis showed erythroid loss of LKB1 to be associated with a robust increase in serum Epo and mild reticulocytosis. Despite these abnormalities, no evidence of anemia or hemolysis was found. Further characterization using an ex vivo progenitor culture assay demonstrated accelerated erythroid maturation in the LKB1-deficient cells. Based on pharmacologic evidence, this phenotype appeared to result from impaired AMP-activated protein kinase (AMPK) signaling downstream of LKB1. These findings reveal a role for LKB1 in fine-tuning Epo-driven erythropoiesis in association with maturational control.

Indexed as

AMP-Activated Protein KinasesErythroid Precursor CellsErythropoiesisErythropoietinAnimalsHumansLiverMiceReceptors, ErythropoietinAMP-Activated Protein KinasesErythropoietinReceptors, ErythropoietinStk11 protein, mouseAMPKErythropoiesisLKB1Maturation

Identifiers

PMID35717902
PMCPMC9436178
OpenAlexW4281882121

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Registered trials

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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.