Evidence map›Paper›PMID 26563995›Full record

ReviewNeurotoxicity research2016

Bcl11b: A New Piece to the Complex Puzzle of Amyotrophic Lateral Sclerosis Neuropathogenesis?

Matthew J Lennon, Simon P Jones, Michael D Lovelace, Gilles J Guillemin, Bruce J Brew

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 31% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Retroviral Elements in Pathophysiology and as Therapeutic Targets for Amyotrophic Lateral Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
  7. Case report: A novel truncating variant ofFrontiers in pediatrics · 2022
    Article
  8. Identification of two novel variants of theFrontiers in molecular neuroscience · 2022
    Article
  9. Review
  10. Review
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 2 institutions in 1 country.

Matthew J LennonPeter Duncan Neurosciences Research Unit, St Vincent's Centre for Applied Medical Research, Sydney, Australia.
Simon P JonesPeter Duncan Neurosciences Research Unit, St Vincent's Centre for Applied Medical Research, Sydney, Australia.
Michael D LovelacePeter Duncan Neurosciences Research Unit, St Vincent's Centre for Applied Medical Research, Sydney, Australia.
Gilles J GuilleminFaculty of Medicine and Health Sciences, MND Research Centre, Macquarie University, Sydney, Australia.
Bruce J BrewPeter Duncan Neurosciences Research Unit, St Vincent's Centre for Applied Medical Research, Sydney, Australia. B.Brew@unsw.edu.au.
UNSW Sydney · AUMacquarie University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is an idiopathic, fatal, neurodegenerative disease of the human motor system. The pathogenesis of ALS is a topic of fascinating speculation and experimentation, with theories revolving around intracellular protein inclusions, mitochondrial structural issues, glutamate excitotoxicity and free radical formation. This review explores the rationale for the involvement of a novel protein, B-cell lymphoma/leukaemia 11b (Bcl11b) in ALS. Bcl11b is a multifunctional zinc finger protein transcription factor. It functions as both a transactivator and genetic suppressor, acting both directly, binding to promoter regions, and indirectly, binding to promoter-bound transcription factors. It has essential roles in the differentiation and growth of various cells in the central nervous system, immune system, integumentary system and cardiovascular system, to the extent that Bcl11b knockout mice are incompatible with extra-uterine life. It also has various roles in pathology including the suppression of latent retroviruses, thymic tumourigenesis and neurodegeneration. In particular its functions in neurodevelopment, viral latency and T-cell development suggest potential roles in ALS pathology.

Indexed as

Amyotrophic Lateral SclerosisAnimalsBrainEncephalitisEndogenous RetrovirusesHumansMiceMotor NeuronsNerve RegenerationNeuronsRepressor ProteinsT-LymphocytesTumor Suppressor ProteinsBCL11B protein, humanRepressor ProteinsTumor Suppressor ProteinsAmyotrophic lateral sclerosisBcl11bMotor neurone diseaseNeurodegenerationNeuroinflammationTranscription factorViral latency

Identifiers

PMID26563995
OpenAlexW2257923196

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.