Evidence map›Paper›PMID 33328510›Full record

ArticleScientific reports2020

LncRNA HOTAIRM1 promotes MDSC expansion and suppressive functions through the HOXA1-miR124 axis during HCV infection.

Bal Krishna Chand Thakuri, Jinyu Zhang, Juan Zhao, Lam N Nguyen, Lam N T Nguyen, Sushant Khanal, Dechao Cao, Xindi Dang, Madison Schank, Xiao Y Wu and 8 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

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  11. A conservedRNA biology · 2023
    Article
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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

18 authors at 2 institutions in 1 country.

Bal Krishna Chand ThakuriCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Jinyu ZhangCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Juan ZhaoCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Lam N NguyenCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Lam N T NguyenCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Sushant KhanalCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Dechao CaoCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Xindi DangCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Madison SchankCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Xiao Y WuCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Zheng D MorrisonCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Mohamed El GazzarCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Zhengke LiCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Yong JiangCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Shunbin NingCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Ling WangCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Jonathan P MoormanCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Zhi Q YaoCenter of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA. yao@etsu.edu.
East Tennessee State University · USJames H. Quillen VA Medical Center · US

Funding

miRNA-mediated premature T cell aging in vaccine failure during viral infectionR01AI114748 · NIAID · EAST TENNESSEE STATE UNIVERSITY · PI YAO, ZHI Q. · 2015 to 2019
$1.9M
Multiuser Advanced Biosafe Flow CytometerS10OD021572 · OD · EAST TENNESSEE STATE UNIVERSITY · PI MOORMAN, JONATHAN P · 2017 to 2017
$553k
Telomere loss and T cell aging in HBV vaccine response in HIV-infected individualR21AI138598 · NIAID · EAST TENNESSEE STATE UNIVERSITY · PI YAO, ZHI Q. · 2018 to 2019
$407k
BLRD VA I01 BX002670BLRD VA I01 BX004281NIAID NIH HHS R01 AI114748NIAID NIH HHS R01AI114748NIAID NIH HHS R21 AI138598NIH HHS S10 OD021572VA 1I01BX002670
6 · The paper itself

Abstract

HOXA transcript antisense RNA myeloid-specific 1 (HOTAIRM1) is a long non-coding RNA (lncRNA) that plays a pivotal role in regulating myeloid cell development via targeting HOXA1 gene expression. We and others have previously shown that myeloid-derived suppressor cells (MDSCs), a heterogeneous population of immature myeloid cells, expand during chronic viral (HCV, HIV) infections. However, the role of HOTAIRM1 in the development and suppression of MDSCs during viral infection remains unknown. In this study, we demonstrate that the expressions of HOTAIRM1 and its target HOXA1 are substantially upregulated to promote the expressions of immunosuppressive molecules, including arginase 1, inducible nitric oxide synthase, signal transducer and activator of transcription 3, and reactive oxygen species, in CD33

Indexed as

CD4-Positive T-LymphocytesCell DifferentiationCell ProliferationGene SilencingHepacivirusHepatitis C, ChronicHomeobox A1 ProteinHomeodomain ProteinsHumansImmunosuppression TherapyMicroRNAsMyeloid-Derived Suppressor CellsRNA, MessengerTranscription FactorsUp-RegulationHomeobox A1 ProteinHomeodomain Proteinslong non-coding RNA HOTAIRM1, humanMicroRNAsMIRN124 microRNA, humanRNA, MessengerTranscription Factors

Identifiers

PMID33328510
PMCPMC7745042
OpenAlexW3111130740

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.