Evidence map›Paper›PMID 29425509›Full record

ArticleCell reports2018

Polycomb Group Protein YY1 Is an Essential Regulator of Hematopoietic Stem Cell Quiescence.

Zhanping Lu, Courtney C Hong, Guangyao Kong, Anna L F V Assumpção, Irene M Ong, Emery H Bresnick, Jing Zhang, Xuan Pan

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  17. Molecular regulation of hematopoietic stem cell quiescence.Cellular and molecular life sciences : CMLS · 2022
    Review
  18. Dual Role of YY1 in HPV Life Cycle and Cervical Cancer Development.International journal of molecular sciences · 2022
    Review
  19. Article
  20. Review
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

8 authors at 2 institutions in 2 countries.

Zhanping LuDepartment of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, 2015 Linden Dr., Madison, WI 57306, USA; Carbone Cancer Center, UW-Madison Blood Research Program, Madison, WI 53706, USA.
Courtney C HongDepartment of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, 2015 Linden Dr., Madison, WI 57306, USA; Carbone Cancer Center, UW-Madison Blood Research Program, Madison, WI 53706, USA.
Guangyao KongMcArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, 1111 Highland Ave., Madison, WI 53705, USA; National Local Joint Engineering Research Center of Biodiagnostics and Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, PRC; Carbone Cancer Center, UW-Madison Blood Research Program, Madison, WI 53706, USA.
Anna L F V AssumpçãoDepartment of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, 2015 Linden Dr., Madison, WI 57306, USA; Carbone Cancer Center, UW-Madison Blood Research Program, Madison, WI 53706, USA.
Irene M OngDepartment of Biostatistics and Medical Informatics, University of Wisconsin School of Medicine and Public Health, 1111 Highland Ave., Madison, WI 53705, USA; Carbone Cancer Center, UW-Madison Blood Research Program, Madison, WI 53706, USA.
Emery H BresnickDepartment of Cell and Regenerative Biology, University of Wisconsin School of Medicine and Public Health, 1111 Highland Ave., Madison, WI 53705, USA; Carbone Cancer Center, UW-Madison Blood Research Program, Madison, WI 53706, USA.
Jing ZhangMcArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, 1111 Highland Ave., Madison, WI 53705, USA; Carbone Cancer Center, UW-Madison Blood Research Program, Madison, WI 53706, USA.
Xuan PanDepartment of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, 2015 Linden Dr., Madison, WI 57306, USA; Carbone Cancer Center, UW-Madison Blood Research Program, Madison, WI 53706, USA. Electronic address: xpan24@wisc.edu.
University of Wisconsin Carbone Cancer Center · USUniversity of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
Hematopoietic Regulation via GATA SwitchesR01DK068634 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI Emery H. Bresnick · 2006 to 2026
$7.5M
The role of TCOF1 in germline predisposition to and in leukemic transformation of chronic myelomonocytic leukemiaR01CA152108 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Jing Zhang · 2011 to 2026
$5.4M
Dose-dependent Activation of the MEK/ERK Pathway in HematopoiesisR01HL113066 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI ZHANG, JING · 2013 to 2016
$1.5M
PcG protein YY1 functions in HSC self-renewal and differentiationK01OD020153 · OD · UNIVERSITY OF WISCONSIN-MADISON · PI PAN, XUAN · 2015 to 2019
$657k
Hematopoietic Regulation Via GATA SwitchesR56DK068634 · NIDDK · UNIVERSITY OF WISCONSIN MADISON · PI BRESNICK, EMERY H. · 2005 to 2005
$109k
NCI NIH HHS P30 CA014520NCI NIH HHS R01 CA152108NHLBI NIH HHS R01 HL113066NIDDK NIH HHS R01 DK068634NIDDK NIH HHS R56 DK068634NIH HHS K01 OD020153
6 · The paper itself

Abstract

Yin yang 1 (YY1) is a ubiquitous transcription factor and mammalian polycomb group protein (PcG) with important functions to regulate embryonic development, lineage differentiation, and cell proliferation. YY1 mediates stable PcG-dependent transcriptional repression via recruitment of PcG proteins that catalyze histone modifications. Many questions remain unanswered regarding how cell- and tissue-specificity is achieved by PcG proteins. Here, we demonstrate that a conditional knockout of Yy1 in hematopoietic stem cells (HSCs) decreases long-term repopulating activity and ectopic YY1 expression expands HSCs. Although the YY1 PcG domain is required for Igκ chain rearrangement in B cells, the YY1 mutant lacking the PcG domain retained the capacity to stimulate HSC self-renewal. YY1 deficiency deregulated the genetic network governing HSC cell proliferation and impaired stem cell factor/c-Kit signaling, disrupting mechanisms conferring HSC quiescence. These results reveal a mechanism for how a ubiquitously expressed transcriptional repressor mediates lineage-specific functions to control adult hematopoiesis.

Indexed as

AnimalsCell Self RenewalGene Knockout TechniquesHematopoiesisHematopoietic Stem CellsMiceYY1 Transcription FactorYy1 protein, mouseYY1 Transcription Factorcell cyclec-Kithematopoietic stem cellpolycomb group proteinquiescenceYY1

Identifiers

PMID29425509
PMCPMC6140794
OpenAlexW2786464181

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.