Evidence map›Paper›PMID 19751724›Full record

ArticleExperimental neurology2009

Calpain 1 and Calpastatin expression is developmentally regulated in rat brain.

Yanzhang Li, Vimala Bondada, Aashish Joshi, James W Geddes

Abstract read
In one paragraph

Article in Experimental neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

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  15. Conditional disruption of calpain in the CNS alters dendrite morphology, impairs LTP, and promotes neuronal survival following injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
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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

4 authors at 1 institution in 1 country.

Yanzhang LiSpinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY 40536-0509, USA.
Vimala Bondada
Aashish Joshi
James W Geddes
University of Kentucky · US

Funding

ROLE OF CALCIUM, CALPAINS, AND CASPASES IN NEURODEGENERATIONP01AG010836 · NIA · UNIVERSITY OF KENTUCKY · PI LANDFIELD, PHILIP W. · 1992 to 2008
$12.4M
UK Spinal Cord &Brain Injury Research Center Core GrantP30NS051220 · NINDS · UNIVERSITY OF KENTUCKY · PI HALL, EDWARD D. · 2005 to 2015
$6.4M
Role of calpastatin in modulating function following TBIP01NS058484 · NINDS · UNIVERSITY OF KENTUCKY · PI GEDDES, JAMES W. · 2007 to 2011
$4.8M
NIA NIH HHS P01 AG010836NIA NIH HHS P01AG10836NINDS NIH HHS P01 NS058484NINDS NIH HHS P01NS058484NINDS NIH HHS P30 NS051220NINDS NIH HHS P30NS051220
6 · The paper itself

Abstract

Calpains and caspases are cysteine endopeptidases which share many similar substrates. Caspases are essential for caspase-dependent apoptotic death where calpains may play an augmentive role, while calpains are strongly implicated in necrotic cell death morphologies. Previous studies have demonstrated a down-regulation in the expression of many components of the caspase-dependent cell death pathway during CNS development. We therefore sought to determine if there is a corresponding upregulation of calpains. The major CNS calpains are the mu-and m-isoforms, composed of the unique 80 kDa calpain 1 and 2 subunits, respectively, and the shared 28 kDa small subunit. In rat brain, relative protein and mRNA levels of calpain 1, calpain 2, caspase 3, and the endogenous calpain inhibitor-calpastatin, were evaluated using western blot and real-time RT-PCR. The developmental time points examined ranged from embryonic day 18 until postnatal day 90. Calpain 1 and calpastatin protein and mRNA levels were low at early developmental time points and increased dramatically by P30. Conversely, caspase-3 expression was greatest at E18, and was rapidly downregulated by P30. Calpain 2 protein and mRNA levels were relatively constant throughout the E18-P90 age range examined. The inverse relationship of calpain 1 and caspase 3 levels during CNS development is consistent with the shift from caspase-dependent to caspase-independent cell death mechanisms following CNS injury in neonatal vs. adult rat brain.

Indexed as

AgingAnimalsAnimals, NewbornBlotting, WesternBrainBrain ChemistryCalcium-Binding ProteinsCalpainCaspase 3MitochondriaRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionRNA, MessengerCalcium-Binding ProteinsCalpaincalpastatinCaspase 3RNA, Messenger

Identifiers

PMID19751724
PMCPMC2796375
OpenAlexW2094403434

What OpenQuestion holds

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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.