Evidence map›Paper›PMID 16331266›Full record

ArticleOncogene2006

A peptide aptamer to antagonize BCL-6 function.

A Chattopadhyay, S A Tate, R W Beswick, S D Wagner, P Ko Ferrigno

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. The Expanding Role of the BCL6 Oncoprotein as a Cancer Therapeutic Target.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Review
  3. Article
  4. Peptide aptamers: tools to negatively or positively modulate HSPB1(27) function.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013
    Review
  5. Promising personalized therapeutic options for diffuse large B-cell Lymphoma Subtypes with oncogene addictions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Structure of the wild-type human BCL6 POZ domain.Acta crystallographica. Section F, Structural biology and crystallization communications · 2008
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
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

5 authors at 3 institutions in 1 country.

A ChattopadhyayMRC Cancer Cell Unit, Hutchison/MRC Research Centre, Cambridge, UK.
S A Tate
R W Beswick
S D Wagner
P Ko Ferrigno
Cancer Research UK · GBHammersmith Hospital · GBMRC Cancer Unit · GB

Funding

Medical Research Council MC_U105359876
6 · The paper itself

Abstract

BCL-6 is a transcription factor essential for germinal centre B-cell development. The BCL-6 gene is involved in diffuse large-cell lymphoma and overexpressed in other types of non-Hodgkin's lymphoma and in high-grade breast cancer. BCL-6 is a transcriptional repressor whose N-terminal POZ domain mediates protein-protein interactions to exert its effects. Reasoning that disruption of POZ domain-mediated interactions may be an effective route to antagonizing the effects of BCL-6 in lymphoma, we screened a library for peptide aptamers that specifically bind to BCL-6 POZ and not the POZ domains of related proteins and describe here the first of these reagents, Apt48. Apt48 binds BCL-6 POZ in a manner distinct from the transcriptional corepressor SMRT, yet was found to prevent BCL-6-mediated repression of a luciferase reporter gene. Apt48 also reproduced several previously validated effects of BCL-6 inhibition. Notably, expression of the differentiation markers CD69, Blimp-1 and cyclin D2 was increased in B-cell lines when Apt48 was expressed. We also show that expression of Apt48 restores cytokine-mediated growth arrest to BCL-6 overexpressing cells. Thus, we have identified a peptide aptamer that affects a function of BCL-6 that is required to prevent differentiation of proliferating B cells.

Indexed as

Antigens, CDAntigens, Differentiation, T-LymphocyteAptamers, PeptideBlotting, WesternBone NeoplasmsCD69 AntigensCell DifferentiationCell SurvivalCombinatorial Chemistry TechniquesCyclin D2CyclinsDNA-Binding ProteinsHumansImmunoprecipitationLectins, C-TypeNuclear Receptor Co-Repressor 2Antigens, CDAntigens, Differentiation, T-LymphocyteAptamers, PeptideCCND2 protein, humanCD69 AntigensCyclin D2CyclinsDNA-Binding ProteinsLectins, C-TypeNCOR2 protein, humanNuclear Receptor Co-Repressor 2Peptide LibraryPositive Regulatory Domain I-Binding Factor 1PRDM1 protein, humanProto-Oncogene Proteins c-bcl-6Repressor ProteinsTranscription Factors

Identifiers

PMID16331266
OpenAlexW2041236494

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.