Evidence map›Paper›PMID 10688671›Full record

ArticleMolecular and cellular biology2000

mSin3A regulates murine erythroleukemia cell differentiation through association with the TAL1 (or SCL) transcription factor.

S Huang, S J Brandt

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
1.3field-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

54 citing papers in PubMed, 99 citations in OpenAlex.

  1. Noncoding RNA,Molecular and cellular biology · 2025
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  12. Histone deacetylase 1 activates PU.1 gene transcription through regulating TAF9 deacetylation and transcription factor IID assembly.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
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  13. Article
  14. Review
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  16. SCL/TAL1-mediated transcriptional network enhances megakaryocytic specification of human embryonic stem cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2015
    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

2 authors at 1 institution in 1 country.

S HuangDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA.
S J Brandt
Vanderbilt University Medical Center · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
REGULATION AND FUNCTION OF THE TAL1/SCL GENER01HL049118 · NHLBI · VANDERBILT UNIVERSITY · PI BRANDT, STEPHEN J. · 1998 to 2011
$2.4M
NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NHLBI NIH HHS R01 HL049118NHLBI NIH HHS R01 HL49118NIDDK NIH HHS DK20593NIDDK NIH HHS P30 DK020593
6 · The paper itself

Abstract

Activation of the TAL1 (or SCL) gene is the most frequent gain-of-function mutation in T-cell acute lymphoblastic leukemia (T-ALL). TAL1 belongs to the basic helix-loop-helix (HLH) family of transcription factors that bind as heterodimers with the E2A and HEB/HTF4 gene products to a nucleotide sequence motif termed the E-box. Reported to act both as an activator and as a repressor of transcription, the mechanisms underlying TAL1-regulated gene expression are poorly understood. We report here that the corepressor mSin3A is associated with TAL1 in murine erythroleukemia (MEL) and human T-ALL cells. Interaction mapping showed that the basic-HLH domain of TAL1 was both necessary and sufficient for TAL1-mSin3A interaction. TAL1 was found, in addition, to interact with the histone deacetylase HDAC1 in vitro and in vivo, and a specific histone deacetylase inhibitor, trichostatin A (TSA), relieved TAL1-mediated repression of an E-box-containing promoter and a GAL4 reporter linked to a thymidine kinase minimal promoter. Further, TAL1 association with mSin3A and HDAC1 declined during dimethyl sulfoxide-induced differentiation of MEL cells in parallel with a decrease in mSin3A abundance. Finally, TSA had a synergistic effect with enforced TAL1 expression in stimulating MEL cells to differentiate, while constitutive expression of mSin3A inhibited MEL cell differentiation. These results demonstrate that a corepressor complex containing mSin3A and HDAC1 interacts with TAL1 and restricts its function in erythroid differentiation. This also has implications for this transcription factor's actions in leukemogenesis.

Indexed as

Proto-Oncogene ProteinsAnimalsBasic Helix-Loop-Helix ProteinsCell DifferentiationDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansLeukemia, Erythroblastic, AcuteMiceRepressor ProteinsSignal TransductionSin3 Histone Deacetylase and Corepressor ComplexT-Cell Acute Lymphocytic Leukemia Protein 1Transcription FactorsTumor Cells, CulturedBasic Helix-Loop-Helix ProteinsDNA-Binding ProteinsProto-Oncogene ProteinsRepressor ProteinsSIN3A transcription factorSin3 Histone Deacetylase and Corepressor ComplexTAL1 protein, humanTal1 protein, mouseT-Cell Acute Lymphocytic Leukemia Protein 1Transcription Factors

Identifiers

PMID10688671
PMCPMC110841
OpenAlexW2124732783

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.