Evidence map›Paper›PMID 28330618›Full record

ArticleStem cell reports2017

Latexin Inactivation Enhances Survival and Long-Term Engraftment of Hematopoietic Stem Cells and Expands the Entire Hematopoietic System in Mice.

Yi Liu, Cuiping Zhang, Zhenyu Li, Chi Wang, Jianhang Jia, Tianyan Gao, Gerhard Hildebrandt, Daohong Zhou, Subbarao Bondada, Peng Ji and 6 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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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

16 authors at 4 institutions in 2 countries.

Yi LiuDepartment of Physiology, University of Kentucky, Lexington, KY 40536, USA.
Cuiping ZhangDepartment of Toxicology and Cancer Biology, University of Kentucky, Health Sciences Research Building Room 340, 1095 V.A. Drive, Lexington, KY 40536, USA.
Zhenyu LiDepartment of Internal Medicine, University of Kentucky, Lexington, KY 40536, USA.
Chi WangDepartment of Cancer Biostatistics, University of Kentucky, Lexington, KY 40536, USA.
Jianhang JiaDepartment of Molecular & Cellular Biochemistry, University of Kentucky, Lexington, KY 40536, USA.
Tianyan GaoDepartment of Molecular & Cellular Biochemistry, University of Kentucky, Lexington, KY 40536, USA.
Gerhard HildebrandtDepartment of Internal Medicine, University of Kentucky, Lexington, KY 40536, USA.
Daohong ZhouDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Subbarao BondadaDepartment of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, KY 40536, USA.
Peng JiDepartment of Pathology, Northwestern University, Chicago, IL 60611, USA.
Daret St ClairDepartment of Toxicology and Cancer Biology, University of Kentucky, Health Sciences Research Building Room 340, 1095 V.A. Drive, Lexington, KY 40536, USA.
Jinze LiuDepartment of Computer Science, University of Kentucky, Lexington, KY 40536, USA.
Changguo ZhanDepartment of Pharmaceutical Sciences, University of Kentucky, Lexington, KY 40536, USA.
Hartmut GeigerCincinnati Children's Hospital Medical Center, Experimental Hematology and Cancer Biology, Cincinnati, OH 45229, USA; Institute for Molecular Medicine, University of Ulm, 89081 Ulm, Germany.
Shuxia WangDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY 40536, USA.
Ying LiangDepartment of Toxicology and Cancer Biology, University of Kentucky, Health Sciences Research Building Room 340, 1095 V.A. Drive, Lexington, KY 40536, USA. Electronic address: ying.liang@uky.edu.
University of Kentucky · USCincinnati Children's Hospital Medical Center · USNorthwestern University · USUniversity of Arkansas for Medical Sciences · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
Institutional Career Development CoreKL2TR001996 · NCATS · UNIVERSITY OF KENTUCKY · PI BUSH, MATTHEW LEE, KELLY, THOMAS H. · 2016 to 2025
$7.1M
The Role of PHLPP in Colon CancerR01CA133429 · NCI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI GAO, TIANYAN · 2009 to 2024
$5.6M
Latexin function in the maintenance and regeneration of the hematopoietic systemR01HL124015 · NHLBI · UNIVERSITY OF KENTUCKY · PI LIANG, YING · 2016 to 2024
$3.6M
The Regulation of Smoothened in Hedgehog SignalingR01GM079684 · NIGMS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI JIA, JIANHANG · 2008 to 2018
$3.0M
Thrombospondin 1 in obesity associated inflammation and insulin resistanceR01DK098176 · NIDDK · UNIVERSITY OF KENTUCKY · PI WANG, SHUXIA · 2014 to 2017
$1.2M
Increasing PKG activity protects aging kidney from ischemic-reperfusion induced injuryR03AG047452 · NIA · UNIVERSITY OF KENTUCKY · PI WANG, SHUXIA · 2015 to 2016
$150k
NCATS NIH HHS KL2 TR001996NCI NIH HHS P30 CA060553NCI NIH HHS P30 CA177558NCI NIH HHS R01 CA133429NHLBI NIH HHS R01 HL124015NIA NIH HHS R03 AG047452NIDDK NIH HHS R01 DK098176NIGMS NIH HHS R01 GM079684
6 · The paper itself

Abstract

Natural genetic diversity offers an important yet largely untapped resource to decipher the molecular mechanisms regulating hematopoietic stem cell (HSC) function. Latexin (Lxn) is a negative stem cell regulatory gene identified on the basis of genetic diversity. By using an Lxn knockout mouse model, we found that Lxn inactivation in vivo led to the physiological expansion of the entire hematopoietic hierarchy. Loss of Lxn enhanced the competitive repopulation capacity and survival of HSCs in a cell-intrinsic manner. Gene profiling of Lxn-null HSCs showed altered expression of genes enriched in cell-matrix and cell-cell interactions. Thrombospondin 1 (Thbs1) was a potential downstream target with a dramatic downregulation in Lxn-null HSCs. Enforced expression of Thbs1 restored the Lxn inactivation-mediated HSC phenotypes. This study reveals that Lxn plays an important role in the maintenance of homeostatic hematopoiesis, and it may lead to development of safe and effective approaches to manipulate HSCs for clinical benefit.

Indexed as

Hematopoietic Stem Cell TransplantationAnimalsCell ProliferationCell SurvivalGene DeletionHematopoiesisHematopoietic Stem CellsMiceMice, Inbred C57BLMice, KnockoutNerve Tissue Proteinslatexin protein, mouseNerve Tissue Proteinsexpansionhematopoietic stem celllatexinrepopulating advantagesurvivalthrombospondin 1

Identifiers

PMID28330618
PMCPMC5390104
OpenAlexW2597293566

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.