Evidence map›Paper›PMID 31919096›Full record

ArticleThe Journal of biological chemistry2020

The MNT transcription factor autoregulates its expression and supports proliferation in MYC-associated factor X (MAX)-deficient cells.

M Carmen Lafita-Navarro, Judit Liaño-Pons, Andrea Quintanilla, Ignacio Varela, Rosa Blanco, Fabiana Ourique, Gabriel Bretones, Julia Aresti, Ester Molina, Patrick Carroll and 6 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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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

16 authors at 4 institutions in 2 countries.

M Carmen Lafita-NavarroInstituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC, and Department of Molecular Biology, Universidad de Cantabria, 39005 Santander, Spain.
Judit Liaño-PonsInstituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC, and Department of Molecular Biology, Universidad de Cantabria, 39005 Santander, Spain.
Andrea QuintanillaInstituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC, and Department of Molecular Biology, Universidad de Cantabria, 39005 Santander, Spain.
Ignacio VarelaInstituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC, and Department of Molecular Biology, Universidad de Cantabria, 39005 Santander, Spain.
Rosa BlancoInstituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC, and Department of Molecular Biology, Universidad de Cantabria, 39005 Santander, Spain.
Fabiana OuriqueInstituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC, and Department of Molecular Biology, Universidad de Cantabria, 39005 Santander, Spain.
Gabriel BretonesInstituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC, and Department of Molecular Biology, Universidad de Cantabria, 39005 Santander, Spain.
Julia ArestiInstituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC, and Department of Molecular Biology, Universidad de Cantabria, 39005 Santander, Spain.
Ester MolinaInstituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC, and Department of Molecular Biology, Universidad de Cantabria, 39005 Santander, Spain.
Patrick CarrollDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109.
Peter HurlinShriners Hospitals for Children Research Center, and Department of Cell, Developmental and Cancer Biology, Knight Cancer Institute, Oregon Health and Science University, Portland, Oregon 97239.
Octavio A RomeroGenes and Cancer Group, Cancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute-IDIBELL, 08908 Barcelona, Spain.
Montse Sanchez-CéspedesGenes and Cancer Group, Cancer Epigenetics and Biology Program (PEBC), Bellvitge Biomedical Research Institute-IDIBELL, 08908 Barcelona, Spain.
Robert N EisenmanDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109.
M Dolores DelgadoInstituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC, and Department of Molecular Biology, Universidad de Cantabria, 39005 Santander, Spain.
Javier LeónInstituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC, and Department of Molecular Biology, Universidad de Cantabria, 39005 Santander, Spain. Electronic address: leonj@unican.es.
Universidad de Cantabria · ESFred Hutch Cancer Center · USInstitut d'Investigació Biomédica de Bellvitge · ESOregon Health & Science University · US

Funding

MYC ONCOPROTEIN FUNCTIONR37CA057138 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EISENMAN, ROBERT NEIL · 2003 to 2013
$8.0M
The MYC Transcription Factor Network and the Path to CancerR35CA231989 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EISENMAN, ROBERT NEIL · 2018 to 2024
$6.3M
MYC ONCOPROTEIN FUNCTIONR01CA057138 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EISENMAN, ROBERT NEIL · 1991 to 2018
$4.9M
NCI NIH HHS R01 CA057138NCI NIH HHS R35 CA231989NCI NIH HHS R37 CA057138
6 · The paper itself

Abstract

The MAX network transcriptional repressor (MNT) is an MXD family transcription factor of the basic helix-loop-helix (bHLH) family. MNT dimerizes with another transcriptional regulator, MYC-associated factor X (MAX), and down-regulates genes by binding to E-boxes. MAX also dimerizes with MYC, an oncogenic bHLH transcription factor. Upon E-box binding, the MYC-MAX dimer activates gene expression. MNT also binds to the MAX dimerization protein MLX (MLX), and MNT-MLX and MNT-MAX dimers co-exist. However, all MNT functions have been attributed to MNT-MAX dimers, and no functions of the MNT-MLX dimer have been described. MNT's biological role has been linked to its function as a

Indexed as

Transcription, GeneticAmino Acid SequenceAnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell ProliferationGene Expression RegulationGene Regulatory NetworksHelix-Loop-Helix MotifsHumansPromoter Regions, GeneticProtein MultimerizationProto-Oncogene Proteins c-mycRepressor ProteinsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMAX protein, humanMLX protein, humanMNT protein, humanProto-Oncogene Proteins c-mycRepressor Proteinsbasic helix-loop-helix leucine zipper proteingene regulationMAX dimerization protein MLXMAX network transcriptional repressor (MNT)MXD familyMYC-associated factor X (MAX)Myc (c-Myc)proliferationpromotertranscription

Identifiers

PMID31919096
PMCPMC7029127
OpenAlexW3000538449

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.