Evidence map›Paper›PMID 17998389›Full record

ArticleThe Journal of experimental medicine2007

BCL11B is required for positive selection and survival of double-positive thymocytes.

Diana I Albu, Dongyun Feng, Debarati Bhattacharya, Nancy A Jenkins, Neal G Copeland, Pentao Liu, Dorina Avram

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

87 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Dual role ofBlood science (Baltimore, Md.) · 2024
    Review
  8. Article
  9. Article
  10. A Bcl11bFrontiers in immunology · 2024
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

27 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

7 authors at 4 institutions in 2 countries.

Diana I AlbuCenter for Cell Biology and Cancer Research, Albany Medical College, Albany, NY 12208, USA.
Dongyun Feng
Debarati Bhattacharya
Nancy A Jenkins
Neal G Copeland
Pentao Liu
Dorina Avram
Albany Medical Center Hospital · USCancer Genetics (United States) · USNational Cancer Institute · USWellcome Sanger Institute · GB

Funding

Role of Bcl11b in CD4+ T cells and innate lymphoid cellsR01AI067846 · NIAID · UNIVERSITY OF FLORIDA · PI AVRAM, DORINA · 2007 to 2023
$6.2M
TISSUE REMODELING AND CARDIOVASCULAR DISEASET32HL007194 · NHLBI · ALBANY MEDICAL COLLEGE · PI MC KEOWN-LONGO, PAULA J · 1985 to 2006
$2.9M
A Novel Zinc Finger Transcriptional Modulator Of T CellsK01AR002194 · NIAMS · OREGON STATE UNIVERSITY · PI AVRAM, DORINA · 2001 to 2005
$565k
NHLBI NIH HHS T32 HL007194NHLBI NIH HHS T32-HL-07194NIAID NIH HHS R01 AI067846NIAMS NIH HHS K01 AR002194NIAMS NIH HHS K01 AR-02194
6 · The paper itself

Abstract

Transcriptional control of gene expression in double-positive (DP) thymocytes remains poorly understood. We show that the transcription factor BCL11B plays a critical role in DP thymocytes by controlling positive selection of both CD4 and CD8 lineages. BCL11B-deficient DP thymocytes rearrange T cell receptor (TCR) alpha; however, they display impaired proximal TCR signaling and attenuated extracellular signal-regulated kinase phosphorylation and calcium flux, which are all required for initiation of positive selection. Further, provision of transgenic TCRs did not improve positive selection of BCL11B-deficient DP thymocytes. BCL11B-deficient DP thymocytes have altered expression of genes with a role in positive selection, TCR signaling, and other signaling pathways intersecting the TCR, which may account for the defect. BCL11B-deficient DP thymocytes also presented increased susceptibility to spontaneous apoptosis associated with high levels of cleaved caspase-3 and an altered balance of proapoptotic/prosurvival factors. This latter susceptibility was manifested even in the absence of TCR signaling and was only partially rescued by provision of the BCL2 transgene, indicating that control of DP thymocyte survival by BCL11B is nonredundant and, at least in part, independent of BCL2 prosurvival factors.

Indexed as

AnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell SurvivalDNA-Binding ProteinsGene Expression RegulationMiceMice, TransgenicOpen Reading FramesProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Repressor ProteinsThymus GlandT-LymphocytesTumor Suppressor ProteinsBcl11b protein, mouseBcl2 protein, mouseDNA-Binding ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Repressor ProteinsTumor Suppressor Proteins

Identifiers

PMID17998389
PMCPMC2118514
OpenAlexW2136394465

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.