Evidence map›Paper›PMID 27277682›Full record

ArticleCell death & disease2016

Mysm1 is required for interferon regulatory factor expression in maintaining HSC quiescence and thymocyte development.

X F Huang, V Nandakumar, G Tumurkhuu, T Wang, X Jiang, B Hong, L Jones, H Won, H Yoshii, K Ozato and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2016. 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
0.9field-weighted citation impact, top 24% 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, 22 citations in OpenAlex.

  1. Article
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  7. A lncRNA identifieseLife · 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

12 authors at 4 institutions in 2 countries.

X F HuangDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
V NandakumarDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
G TumurkhuuDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
T WangDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
X JiangDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
B HongDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
L JonesDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
H WonDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
H YoshiiLaboratory of Molecular Growth Regulation, Program in Genomics of Differentiation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
K OzatoLaboratory of Molecular Growth Regulation, Program in Genomics of Differentiation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
A MasumiDepartment of Safety Research on Blood and Biological Products, National Institute of Infectious Diseases, Tokyo, Japan.
S-Y ChenDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
University of Southern California · USEunice Kennedy Shriver National Institute of Child Health and Human Development · USNational Institute of Infectious Diseases · JPNational Institutes of Health · US

Funding

Chromatin and epigenetic memory ZIAHD008815 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI OZATO, KEIKO · 2009 to 2025
$16.2M
Overcoming Immune Suppression to Enhance Tumor Vaccine EfficacyR01CA090427 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHEN, SI-YI · 2002 to 2013
$3.1M
Developing novel adjuvants for HIV vaccinationR01AI084811 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHEN, SI-YI · 2009 to 2013
$2.2M
Novel adjuvants of activating RIG-I and inhibiting immune inhibitors for HIV vaccR21AI087185 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HUANG, XUE F · 2010 to 2011
$444k
NCI NIH HHS R01 CA090427NIAID NIH HHS R01 AI084811NIAID NIH HHS R21 AI087185
6 · The paper itself

Abstract

Mysm1(-/-) mice have severely decreased cellularity in hematopoietic organs. We previously revealed that Mysm1 knockout impairs self-renewal and lineage reconstitution of HSCs by abolishing the recruitment of key transcriptional factors to the Gfi-1 locus, an intrinsic regulator of HSC function. The present study further defines a large LSKs in >8-week-old Mysm1(-/-) mice that exhibit increased proliferation and reduced cell lineage differentiation compared with those of WT LSKs. We found that IRF2 and IRF8, which are important for HSC homeostasis and commitment as transcription repressors, were expressed at lower levels in Mysm1(-/-) HSCs, and Mysm1 enhanced function of the IRF2 and IRF8 promoters, suggesting that Mysm1 governs the IRFs for HSC homeostasis. We further found that the lower expressions of IRF2 and IRF8 led to an enhanced transcription of p53 in Mysm1(-/-) HSCs, which was recently defined to have an important role in mediating Mysm1(-/-)-associated defects. The study also revealed that Mysm1(-/-) thymocytes exhibited lower IRF2 expression, but had higher Sca1 expression, which has a role in mediating thymocyte death. Furthermore, we found that the thymocytes from B16 melanoma-bearing mice, which display severe thymus atrophy at late tumor stages, exhibited reduced Mysm1 and IRF2 expression but enhanced Sca1 expression, suggesting that tumors may downregulate Mysm1 and IRF2 for thymic T-cell elimination.

Indexed as

Cell CycleAnimalsCell DifferentiationEndopeptidasesHematopoietic Stem CellsInterferon Regulatory Factor-2Interferon Regulatory Factor-8Interferon Regulatory FactorsLymphopoiesisMelanoma, ExperimentalMice, Inbred C57BLPromoter Regions, GeneticProtein BindingThymocytesTrans-ActivatorsTranscription, GeneticEndopeptidasesInterferon Regulatory Factor-2Interferon Regulatory Factor-8Interferon Regulatory FactorsIrf2 protein, mouseMYSM1 protein, mouseTrans-ActivatorsTumor Suppressor Protein p53Ubiquitin-Specific Proteases

Identifiers

PMID27277682
PMCPMC5143390
OpenAlexW2413123002

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.