Evidence map›Paper›PMID 19255249›Full record

ArticleThe Journal of cell biology2009

Bcl-x L increases mitochondrial fission, fusion, and biomass in neurons.

Sarah B Berman, Ying-bei Chen, Bing Qi, J Michael McCaffery, Edmund B Rucker, Sandra Goebbels, Klaus-Armin Nave, Beth A Arnold, Elizabeth A Jonas, Fernando J Pineda and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

137 citing papers in PubMed, 228 citations in OpenAlex.

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  20. BCLXCell death & disease · 2021
    Article

77 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

11 authors at 8 institutions in 2 countries.

Sarah B BermanW. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA.
Ying-bei Chen
Bing Qi
J Michael McCaffery
Edmund B Rucker
Sandra Goebbels
Klaus-Armin Nave
Beth A Arnold
Elizabeth A Jonas
Fernando J Pineda
J Marie Hardwick
Johns Hopkins University · USMax Planck Institute of Experimental Medicine · DEImaging Center · USInstitute for Neurodegenerative Disorders · USJohns Hopkins Medicine · USUniversity of Missouri · USUniversity of Pittsburgh · USYale University · US

Funding

Mitochondrial Ion Channels in Hypoxic NeuronsR37NS045876 · NINDS · YALE UNIVERSITY · PI Elizabeth Ann Jonas · 2014 to 2026
$4.9M
REGULATION OF BCL XL BY CASPASESR01NS037402 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HARDWICK, J. MARIE · 1999 to 2014
$4.5M
Mitochondrial ion channels in hypoxic neuronsR01NS045876 · NINDS · YALE UNIVERSITY · PI JONAS, ELIZABETH ANN · 2004 to 2013
$3.3M
REGULATION OF VIRAL INFECTIONS BY CELLULAR GENESR01NS034175 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HARDWICK, J. MARIE · 1995 to 2009
$2.5M
Mitochondrial Dynamics in NeurodegenerationK08NS059576 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BERMAN, SARAH B · 2007 to 2011
$822k
NINDS NIH HHS K08 NS059576NINDS NIH HHS KO8 NS059576NINDS NIH HHS NS034175NINDS NIH HHS NS037402NINDS NIH HHS NS045876NINDS NIH HHS R01 NS034175NINDS NIH HHS R01 NS037402NINDS NIH HHS R01 NS045876NINDS NIH HHS R37 NS045876
6 · The paper itself

Abstract

Mitochondrial fission and fusion are linked to synaptic activity in healthy neurons and are implicated in the regulation of apoptotic cell death in many cell types. We developed fluorescence microscopy and computational strategies to directly measure mitochondrial fission and fusion frequencies and their effects on mitochondrial morphology in cultured neurons. We found that the rate of fission exceeds the rate of fusion in healthy neuronal processes, and, therefore, the fission/fusion ratio alone is insufficient to explain mitochondrial morphology at steady state. This imbalance between fission and fusion is compensated by growth of mitochondrial organelles. Bcl-x(L) increases the rates of both fusion and fission, but more important for explaining the longer organelle morphology induced by Bcl-x(L) is its ability to increase mitochondrial biomass. Deficits in these Bcl-x(L)-dependent mechanisms may be critical in neuronal dysfunction during the earliest phases of neurodegeneration, long before commitment to cell death.

Indexed as

AnimalsApoptosisbcl-X ProteinEnergy MetabolismMembrane FusionMiceMice, KnockoutMicroscopy, FluorescenceMitochondriaNerve DegenerationNeuronsRatsBcl2l1 protein, mousebcl-X Protein

Identifiers

PMID19255249
PMCPMC2686401
OpenAlexW1991994507

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.