Evidence map›Paper›PMID 23563689›Full record

ArticleNature immunology2013

Satb1 regulates the self-renewal of hematopoietic stem cells by promoting quiescence and repressing differentiation commitment.

Britta Will, Thomas O Vogler, Boris Bartholdy, Francine Garrett-Bakelman, Jillian Mayer, Laura Barreyro, Ashley Pandolfi, Tihomira I Todorova, Ujunwa C Okoye-Okafor, Robert F Stanley and 6 more

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

72 citing papers in PubMed, 104 citations in OpenAlex.

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12 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Britta WillDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, New York, USA.
Thomas O Vogler
Boris Bartholdy
Francine Garrett-Bakelman
Jillian Mayer
Laura Barreyro
Ashley Pandolfi
Tihomira I Todorova
Ujunwa C Okoye-Okafor
Robert F Stanley
Tushar D Bhagat
Amit Verma
Maria E Figueroa
Ari Melnick
Michael Roth
Ulrich Steidl
Albert Einstein College of Medicine · USCornell University · USUniversity of Michigan–Ann Arbor · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
Role of a Novel Homeobox Transcription Factor (HLX) in Acute Myeloid LeukemiaR01CA166429 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STEIDL, ULRICH · 2013 to 2017
$1.9M
Genetic and epigenetic basis of relapse in acute myeloid leukemiaK08CA169055 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI GARRETT-BAKELMAN, FRANCINE EVALINA · 2012 to 2016
$742k
Transcriptional regulation of leukemic stem cells in acute myeloid leukemiaR00CA131503 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI STEIDL, ULRICH · 2009 to 2011
$740k
The role of c-Maf in Stem cells in LeukemiaF31CA162770 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI OKOYE-OKAFOR, UJUNWA CYNTHIA · 2011 to 2015
$212k
Unraveling crucial roles of homeobox gene Hlx in hematopoiesis and leukemogenesisF30HL117545 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI ECKEL, ASHLEY MARIE · 2013 to 2015
$143k
NCI NIH HHS (1K08CA169055-01NCI NIH HHS F31 CA162770NCI NIH HHS F31CA162770NCI NIH HHS K08 CA169055NCI NIH HHS R00 CA131503NCI NIH HHS R00CA131503NCI NIH HHS R01 CA166429NHLBI NIH HHS F30 HL117545NHLBI NIH HHS F30HL117545NIGMS NIH HHS T32 GM007288
6 · The paper itself

Abstract

How hematopoietic stem cells (HSCs) coordinate the regulation of opposing cellular mechanisms such as self-renewal and differentiation commitment remains unclear. Here we identified the transcription factor and chromatin remodeler Satb1 as a critical regulator of HSC fate. HSCs lacking Satb1 had defective self-renewal, were less quiescent and showed accelerated lineage commitment, which resulted in progressive depletion of functional HSCs. The enhanced commitment was caused by less symmetric self-renewal and more symmetric differentiation divisions of Satb1-deficient HSCs. Satb1 simultaneously repressed sets of genes encoding molecules involved in HSC activation and cellular polarity, including Numb and Myc, which encode two key factors for the specification of stem-cell fate. Thus, Satb1 is a regulator that promotes HSC quiescence and represses lineage commitment.

Indexed as

AnimalsCell DifferentiationCell LineageCell PolarityCells, CulturedCell SurvivalChromatin Assembly and DisassemblyGene Expression Regulation, DevelopmentalHematopoietic Stem CellsMatrix Attachment Region Binding ProteinsMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsProto-Oncogene Proteins c-mycMatrix Attachment Region Binding ProteinsMembrane ProteinsMyc protein, mouseNerve Tissue ProteinsNumb protein, mouseProto-Oncogene Proteins c-mycSatb1 protein, mouse

Identifiers

PMID23563689
PMCPMC3633104
OpenAlexW2012774087

What OpenQuestion holds

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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.