Evidence map›Paper›PMID 24100014›Full record

ArticleMolecular and cellular biology2013

Tgif1 regulates quiescence and self-renewal of hematopoietic stem cells.

Ling Yan, Bethany Womack, David Wotton, Yan Guo, Yu Shyr, Utpal Davé, Chun Li, Scott Hiebert, Stephen Brandt, Rizwan Hamid

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 30 citations in OpenAlex.

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  13. Bone Marrow-derived Cells Contribute to the Pathogenesis of Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2016
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  15. TGIF1 promoted the growth and migration of cancer cells in nonsmall cell lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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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

10 authors at 2 institutions in 1 country.

Ling YanDepartments of Pediatrics.
Bethany Womack
David Wotton
Yan Guo
Yu Shyr
Utpal Davé
Chun Li
Scott Hiebert
Stephen Brandt
Rizwan Hamid
Vanderbilt University Medical Center · USUniversity of Virginia · US

Funding

Role of BMPR2 expression in HPAH; implications for novel therapeutic approachesR01HL102020 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HAMID, RIZWAN · 2011 to 2015
$2.3M
Functions of the TG-Interacting Transcription Factor (TGIF) in HematopoiesisK08HL089903 · NHLBI · VANDERBILT UNIVERSITY · PI HAMID, RIZWAN · 2009 to 2012
$441k
Pathophysiology of Adult T-cell Leukemia/LymphomaI01BX001799 · VA · VETERANS HEALTH ADMINISTRATION · PI DAVE, UTPAL P · 2013 to 2025
–
BLRD VA I01 BX001799NHLBI NIH HHS K08 HL089903NHLBI NIH HHS R01 HL102020
6 · The paper itself

Abstract

TG-interacting factor 1 (TGIF1) is a transcriptional repressor that can modulate retinoic acid and transforming growth factor β signaling pathways. It is required for myeloid progenitor cell differentiation and survival, and mutations in the TGIF1 gene cause holoprosencephaly. Furthermore, we have previously observed that acute myelogenous leukemia (AML) patients with low TGIF1 levels had worse prognoses. Here, we explored the role of Tgif1 in murine hematopoietic stem cell (HSC) function. CFU assays showed that Tgif1(-/-) bone marrow cells produced more total colonies and had higher serial CFU potential. These effects were also observed in vivo, where Tgif1(-/-) bone marrow cells had higher repopulation potential in short- and long-term competitive repopulation assays than wild-type cells. Serial transplantation and replating studies showed that Tgif1(-/-) HSCs exhibited greater self-renewal and were less proliferative and more quiescent than wild-type cells, suggesting that Tgif1 is required for stem cells to enter the cell cycle. Furthermore, HSCs from Tgif1(+/-) mice had a phenotype similar to that of HSCs from Tgif1(-/-) mice, while bone marrow cells with overexpressing Tgif1 showed increased proliferation and lower survival in long-term transplant studies. Taken together, our data suggest that Tgif1 suppresses stem cell self-renewal and provide clues as to how reduced expression of TGIF1 may contribute to poor long-term survival in patients with AML.

Indexed as

AnimalsBone Marrow CellsCell DifferentiationCell ProliferationCells, CulturedGene Knockout TechniquesHematopoietic Stem CellsHomeodomain ProteinsMiceMice, Inbred C57BLMice, KnockoutRepressor ProteinsTranscription, GeneticHomeodomain ProteinsRepressor ProteinsTgif1 protein, mouse

Identifiers

PMID24100014
PMCPMC3889555
OpenAlexW2140760302

What OpenQuestion holds

Textmetadata
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.