Evidence map›Paper›PMID 14657037›Full record

ArticleThe EMBO journal2003

The crucial role of caspase-9 in the disease progression of a transgenic ALS mouse model.

Haruhisa Inoue, Kayoko Tsukita, Takuji Iwasato, Yasuyuki Suzuki, Masanori Tomioka, Minako Tateno, Masahiro Nagao, Akihiro Kawata, Takaomi C Saido, Masayuki Miura and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 105 citations in OpenAlex.

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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

13 authors at 1 institution in 1 country.

Haruhisa InoueLaboratory for Motor System Neurodegeneration, RIKEN Brain Science Institute (BSI), Saitama, PRESTO, Japan.
Kayoko Tsukita
Takuji Iwasato
Yasuyuki Suzuki
Masanori Tomioka
Minako Tateno
Masahiro Nagao
Akihiro Kawata
Takaomi C Saido
Masayuki Miura
Hidemi Misawa
Shigeyoshi Itohara
Ryosuke Takahashi
RIKEN Center for Brain Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutant copper/zinc superoxide dismutase (SOD1)-overexpressing transgenic mice, a mouse model for familial amyotrophic lateral sclerosis (ALS), provides an excellent resource for developing novel therapies for ALS. Several observations suggest that mitochondria-dependent apoptotic signaling, including caspase-9 activation, may play an important role in mutant SOD1-related neurodegeneration. To elucidate the role of caspase-9 in ALS, we examined the effects of an inhibitor of X chromosome-linked inhibitor of apoptosis (XIAP), a mammalian inhibitor of caspase-3, -7 and -9, and p35, a baculoviral broad caspase inhibitor that does not inhibit caspase-9. When expressed in spinal motor neurons of mutant SOD1 mice using transgenic techniques, XIAP attenuated disease progression without delaying onset. In contrast, p35 delayed onset without slowing disease progression. Moreover, caspase-9 was activated in spinal motor neurons of human ALS subjects. These data strongly suggest that caspase-9 plays a crucial role in disease progression of ALS and constitutes a promising therapeutic target.

Indexed as

Amyotrophic Lateral SclerosisAnimalsBase SequenceCysteine Proteinase InhibitorsDisease Models, AnimalDNA PrimersGenotypeImmunohistochemistryMiceMice, Inbred C57BLMice, TransgenicProteinsReverse Transcriptase Polymerase Chain ReactionSpinal CordSuperoxide DismutaseSuperoxide Dismutase-1Cysteine Proteinase InhibitorsDNA PrimersProteinsSOD1 protein, humanSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1X-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID14657037
PMCPMC291829
OpenAlexW2162978926

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.