Evidence map›Paper›PMID 15665074›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

A peptide inhibitor of cytochrome c/inositol 1,4,5-trisphosphate receptor binding blocks intrinsic and extrinsic cell death pathways.

Darren Boehning, Damian B van Rossum, Randen L Patterson, Solomon H Snyder

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 121 citations in OpenAlex.

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  13. Metabolomics : Official journal of the Metabolomic Society · 2017
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  20. Rapid and transient palmitoylation of the tyrosine kinase Lck mediates Fas signaling.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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

4 authors at 2 institutions in 1 country.

Darren BoehningDepartment of Neuroscience, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.
Damian B van Rossum
Randen L Patterson
Solomon H Snyder
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

UNDERSTANDING NO SIGNALING RESULTING IN NEUROPROTECTION.P50DA000266 · NIDA · JOHNS HOPKINS UNIVERSITY · PI BARABAN, JAY M · 1985 to 2017
$45.2M
NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGSR37MH018501 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1990 to 2009
$11.5M
NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGSR01MH018501 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1985 to 2019
$10.8M
NEUROTRANSMITTER RECEPTORSK05DA000074 · NIDA · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1985 to 2009
$1.3M
Mechanism Of Activation Of Heme Oxygenase-2F32NS043850 · NINDS · JOHNS HOPKINS UNIVERSITY · PI BOEHNING, DARREN F · 2002 to 2004
$115k
NIDA NIH HHS DA-000266NIDA NIH HHS DA-00074NIDA NIH HHS K05 DA000074NIDA NIH HHS P50 DA000266NIH HHS NH65090NIMH NIH HHS MH-18501NIMH NIH HHS R01 MH018501NIMH NIH HHS R37 MH018501NINDS NIH HHS F32 NS043850NINDS NIH HHS NS-043850
6 · The paper itself

Abstract

Apoptotic stimuli augment intracellular calcium concentration through inositol 1,4,5-trisphosphate receptors (IP3R) on endoplasmic reticulum calcium stores. We previously discovered an apoptotic cascade wherein cytochrome c binds to IP3R early in apoptosis, resulting in dysregulated calcium release. Here we show that cytochrome c binding to IP3R depends on a cluster of glutamic acid residues within the C terminus of the channel. A cell permeant peptide derived from this sequence displaces cytochrome c from IP3R and abrogates cell death induced by staurosporine treatment of HeLa cells and Fas ligand stimulation of Jurkat cells. Small-molecule inhibitors of cytochrome c/IP3R interactions may prove useful in treating disorders associated with inappropriate intrinsic and extrinsic apoptotic signaling.

Indexed as

Amino Acid SequenceAnimalsApoptosisCalcium ChannelsCalcium SignalingCell DeathCloning, MolecularCytochromes cEndoplasmic ReticulumHumansInositol 1,4,5-Trisphosphate ReceptorsJurkat CellsKineticsMicroscopy, ConfocalMolecular Sequence DataPeptidesCalcium ChannelsCytochromes cInositol 1,4,5-Trisphosphate ReceptorsITPR1 protein, humanPeptidesReceptors, Cytoplasmic and NuclearStaurosporine

Identifiers

PMID15665074
PMCPMC547891
OpenAlexW1965268015

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.