Evidence map›Paper›PMID 18758483›Full record

ReviewOncogene2008

Mastermind-like transcriptional co-activators: emerging roles in regulating cross talk among multiple signaling pathways.

A S McElhinny, J-L Li, L Wu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

84 citing papers in PubMed, 153 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Apoptotic proteins with non-apoptotic activity: expression and function in cancer.Apoptosis : an international journal on programmed cell death · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Targeting Notch and EGFR signaling in human mucoepidermoid carcinoma.Signal transduction and targeted therapy · 2021
    Article
  18. Two classes of active transcription sites and their roles in developmental regulation.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  19. MAML1/2 promote YAP/TAZ nuclear localization and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  20. Article

24 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

3 authors at 2 institutions in 1 country.

A S McElhinnyVentana Medical Systems Inc., Tucson, AZ, USA.
J-L Li
L Wu
University of Florida · USVentana Research Corporation (United States) · US

Funding

Transformation of Epithelial Cell by E6 OncogeneR01CA097148 · NCI · UNIVERSITY OF FLORIDA · PI WU, LIZI · 2003 to 2007
$1.3M
6 · The paper itself

Abstract

A family of Mastermind-like (MAML) genes encodes critical transcriptional co-activators for Notch signaling, an evolutionarily conserved pathway with numerous roles in both development and human diseases. Notch receptors are cleaved upon ligand engagement and the intracellular domain of Notch shuttles to the nucleus. MAMLs form a functional DNA-binding complex with the cleaved Notch receptor and the transcription factor CSL, thereby regulating transcriptional events that are specific to the Notch pathway. Here, we review recent studies that have utilized molecular, cellular and physiological model system strategies to reveal the pivotal roles of the MAML proteins in Notch signaling. Unexpectedly, however, emerging evidence implicate MAML proteins as exciting key transcriptional co-activators in other signal transduction pathways including: muscle differentiation and myopathies (MEF2C), tumor suppressor pathway (p53) and colon carcinoma survival (beta-catenin). Thus, the MAML family appears to function in transcriptional co-activation in a multitude of cellular processes. It is hypothesized that MAML proteins mediate cross-talk among the various signaling pathways and the diverse activities of the MAML proteins converge to impact normal biological processes and human diseases, including cancers.

Indexed as

AdenocarcinomaAnimalsbeta CateninCell CommunicationCell DifferentiationColonic NeoplasmsDNA-Binding ProteinsHumansMADS Domain ProteinsMEF2 Transcription FactorsMiceMice, KnockoutMultiprotein ComplexesMuscular DiseasesMyogenic Regulatory FactorsOrgan Specificitybeta CateninDNA-Binding ProteinsMADS Domain ProteinsMAML1 protein, humanMEF2C protein, humanMEF2 Transcription FactorsMultiprotein ComplexesMyogenic Regulatory FactorsReceptors, NotchTrans-ActivatorsTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID18758483
OpenAlexW2000145238

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.