Evidence map›Paper›PMID 23571214›Full record

ArticleDevelopment (Cambridge, England)2013

BEND6 is a nuclear antagonist of Notch signaling during self-renewal of neural stem cells.

Qi Dai, Celia Andreu-Agullo, Ryan Insolera, Li Chin Wong, Song-Hai Shi, Eric C Lai

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. DifferentialProceedings of the National Academy of Sciences of the United States of America · 2026
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  18. Regulation of embryonic and adult neurogenesis by Ars2.Development (Cambridge, England) · 2020
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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

6 authors at 1 institution in 1 country.

Qi DaiDepartment of Developmental Biology, Sloan-Kettering Institute, 1275 York Avenue, New York, NY 10065, USA.
Celia Andreu-Agullo
Ryan Insolera
Li Chin Wong
Song-Hai Shi
Eric C Lai
Kettering University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
BEN factors are conserved CSL co-repressors in Notch-mediated neural developmentR01NS074037 · NINDS · SLOAN-KETTERING INST CAN RESEARCH · PI LAI, ERIC C · 2011 to 2015
$2.1M
NCI NIH HHS P30 CA008748NINDS NIH HHS 1R01-NS074037NINDS NIH HHS R01 NS074037
6 · The paper itself

Abstract

The activity of the Notch pathway revolves around a CSL-class transcription factor, which recruits distinct complexes that activate or repress target gene expression. The co-activator complex is deeply conserved and includes the cleaved Notch intracellular domain (NICD) and Mastermind. By contrast, numerous CSL co-repressor proteins have been identified, and these are mostly different between invertebrate and vertebrate systems. In this study, we demonstrate that mammalian BEND6 is a neural BEN-solo factor that shares many functional attributes with Drosophila Insensitive, a co-repressor for the Drosophila CSL factor. BEND6 binds the mammalian CSL protein CBF1 and antagonizes Notch-dependent target activation. In addition, its association with Notch- and CBF1-regulated enhancers is promoted by CBF1 and antagonized by activated Notch. In utero electroporation experiments showed that ectopic BEND6 inhibited Notch-mediated self-renewal of neocortical neural stem cells and promoted neurogenesis. Conversely, knockdown of BEND6 increased NSC self-renewal in wild-type neocortex, and exhibited genetic interactions with gain and loss of Notch pathway activity. We recapitulated all of these findings in cultured neurospheres, in which overexpression and depletion of BEND6 caused reciprocal effects on neural stem cell renewal and neurogenesis. These data reveal a novel mammalian CSL co-repressor in the nervous system, and show that the Notch-inhibitory activity of certain BEN-solo proteins is conserved between flies and mammals.

Indexed as

Signal TransductionAnimalsCell NucleusCloning, MolecularCo-Repressor ProteinsElectroporationFemaleHEK293 CellsHeLa CellsHumansImmunoglobulin J Recombination Signal Sequence-Binding ProteinMiceNeocortexNeural Stem CellsNeurogenesisNeuronsCo-Repressor ProteinsImmunoglobulin J Recombination Signal Sequence-Binding ProteinRBPJ protein, humanRbpj protein, mouseReceptors, NotchRecombinant Fusion ProteinsRNA, Small Interfering

Identifiers

PMID23571214
PMCPMC3631965
OpenAlexW2036100227

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.