Evidence map›Paper›PMID 31110240›Full record

ReviewGenes and immunity2019

Inhibitor of apoptosis proteins in human health and disease.

Matous Hrdinka, Monica Yabal

Abstract readReview
PubMed Publisher
In one paragraph

Review in Genes and immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Endothelial c-IAP2 loss amplifies P2X7 receptor-driven inflammation and worsens schistosomiasis-associated pulmonary hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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 2 institutions in 2 countries.

Matous HrdinkaDepartment of Haematooncology, University Hospital Ostrava, 17. listopadu 1790, 70800, Ostrava, Czech Republic.
Monica YabalInstitute of Molecular Immunology and Experimental Oncology, School of Medicine, Technical University of Munich, Ismaninger Straße 22, 81675, Munich, Germany. monica.yabal@tum.de.
Technical University of Munich · DEUniversity Hospital Ostrava · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inhibitor of apoptosis proteins (IAPs) are best known for their ability to regulate cell survival and death processes. However, in addition to cell death, IAPs also act as innate immune sensors and modulate multiple pathways, such as autophagy and cell division. Many of these IAP functions are non-redundant even though they are based on the same molecular mechanism of action. These distinct functions of IAPs derive from their capacity to target specific substrates for ubiquitination and/or proteolytic cleavage. The unique functions of IAPs also derives from their unique cellular localizations, cell type and tissue-specific expression patterns. The diverse roles of IAPs are reflected by the fact that in humans the IAP family comprises eight distinct members. Genetic evidence from human pathologies also attests to the non-redundant functions of the IAPs since very diverse diseases arise upon aberrant IAP expression. In this review, we give an overview of the known mechanisms of action of the various IAPs, and focus on their specific roles in mediating innate immunity. We also look at the distinct phenotypes related to the dysregulation of the IAPs, and the human pathologies associated with each human IAP.

Indexed as

Cell SurvivalAnimalsAutoimmune DiseasesCell DeathHumansInfectionsInflammasomesInhibitor of Apoptosis ProteinsSignal TransductionInflammasomesInhibitor of Apoptosis Proteins

Identifiers

PMID31110240
OpenAlexW2946370603

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.