Evidence map›Paper›PMID 26462035›Full record

ReviewThe FEBS journal2016

Inhibitor of apoptosis proteins as intracellular signaling intermediates.

Andrew J Kocab, Colin S Duckett

Open access · bronzeAbstract readReview
In one paragraph

Review in The FEBS journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 81 citations in OpenAlex.

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  14. cIAP1/2 Antagonism Induces Antigen-Specific T Cell-Dependent Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
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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

2 authors at 1 institution in 1 country.

Andrew J KocabGraduate Program in Immunology, The University of Michigan, Ann Arbor, MI, USA.
Colin S DuckettDepartment of Pathology, The University of Michigan, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
RESEARCH TRAINING IN EXPERIMENTAL IMMUNOPATHOLOGYT32AI007413 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Bethany B. Moore · 1993 to 2026
$9.8M
Signal Transduction Pathways in CD30-positive LymphomasR01CA142809 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DUCKETT, COLIN S. · 2010 to 2014
$1.3M
NCI NIH HHS 5P30CA46592NCI NIH HHS P30 CA046592NCI NIH HHS R01 CA142809NCI NIH HHS R01CA142809NIAID NIH HHS T32 AI007413NIAID NIH HHS T32AI007413
6 · The paper itself

Abstract

Inhibitor of apoptosis (IAP) proteins have often been considered inhibitors of cell death due to early reports that described their ability to directly bind and inhibit caspases, the primary factors that implement apoptosis. However, a greater understanding is evolving regarding the vital roles played by IAPs as transduction intermediates in a diverse set of signaling cascades associated with functions ranging from the innate immune response to cell migration to cell-cycle regulation. In this review, we discuss the functions of IAPs in signaling, focusing primarily on the cellular IAP (c-IAP) proteins. The c-IAPs are important components in tumor necrosis factor receptor superfamily signaling cascades, which include activation of the NF-κB transcription factor family. As these receptors modulate cell proliferation and cell death, the involvement of the c-IAPs in these pathways provides an additional means of controlling cellular fate beyond simply inhibiting caspase activity. Additionally, IAP-binding proteins, such as Smac and caspases, which have been described as having cell death-independent roles, may affect c-IAP activity in intracellular signaling. Collectively, the multi-faceted functions and complex regulation of the c-IAPs illustrate their importance as intracellular signaling intermediates.

Indexed as

AnimalsApoptosis Regulatory ProteinsCaspasesHumansInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsMitochondrial ProteinsMolecular MimicryReceptors, Tumor Necrosis FactorSignal TransductionSmall Molecule LibrariesApoptosis Regulatory ProteinsCaspasesDIABLO protein, humanInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsMitochondrial ProteinsReceptors, Tumor Necrosis FactorSmall Molecule Librariesapoptosiscaspasescd30cell signalinginhibitor of apoptosis protein (IAP)NF-κBSmacSmac mimetictumor necrosis factor (TNF)ubiquitin-mediated signaling

Identifiers

PMID26462035
PMCPMC4767650
OpenAlexW2141918040

What OpenQuestion holds

Textmetadata
LicenceTDM
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.