Evidence map›Paper›PMID 19502560›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2009

THAP5 is a human cardiac-specific inhibitor of cell cycle that is cleaved by the proapoptotic Omi/HtrA2 protease during cell death.

Meenakshi P Balakrishnan, Lucia Cilenti, Zineb Mashak, Paiyal Popat, Emad S Alnemri, Antonis S Zervos

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 48 citations in OpenAlex.

  1. From Thanatos to transcription: the emerging biology of THAP proteins.Cellular and molecular life sciences : CMLS · 2026
    Review
  2. Article
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  5. Review
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  7. Transposon-derived transcription factors across metazoans.Frontiers in cell and developmental biology · 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

6 authors at 1 institution in 1 country.

Meenakshi P BalakrishnanBiomolecular Science Center, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida 32826, USA.
Lucia Cilenti
Zineb Mashak
Paiyal Popat
Emad S Alnemri
Antonis S Zervos
University of Central Florida · US

Funding

Function of Omi/HtrA2 in Renal Tubular Cell DeathR01DK055734 · NIDDK · UNIVERSITY OF CENTRAL FLORIDA · PI ZERVOS, ANTONIS S · 1999 to 2009
$2.1M
The Omi/HtrA2 Signal Transduction PathwayR01GM076176 · NIGMS · THOMAS JEFFERSON UNIVERSITY · PI ALNEMRI, EMAD S · 2006 to 2009
$1.2M
NIDDK NIH HHS 5R01 DK55734NIGMS NIH HHS GM076176
6 · The paper itself

Abstract

Omi/HtrA2 is a mitochondrial serine protease that has a dual function: while confined in the mitochondria, it promotes cell survival, but when released into the cytoplasm, it participates in caspase-dependent as well as caspase-independent cell death. To investigate the mechanism of Omi/HtrA2's function, we set out to isolate and characterize novel substrates for this protease. We have identified Thanatos-associated protein 5 (THAP5) as a specific interactor and substrate of Omi/HtrA2 in cells undergoing apoptosis. This protein is an uncharacterized member of the THAP family of proteins. THAP5 has a unique pattern of expression and is found predominantly in the human heart, although a very low expression is also seen in the human brain and muscle. THAP5 protein is localized in the nucleus and, when ectopically expressed, induces cell cycle arrest. During apoptosis, THAP5 protein is degraded, and this process can be blocked using a specific Omi/HtrA2 inhibitor, leading to reduced cell death. In patients with coronary artery disease, THAP5 protein levels substantially decrease in the myocardial infarction area, suggesting a potential role of this protein in human heart disease. This work identifies human THAP5 as a cardiac-specific nuclear protein that controls cell cycle progression. Furthermore, during apoptosis, THAP5 is cleaved and removed by the proapoptotic Omi/HtrA2 protease. Taken together, we provide evidence to support that THAP5 and its regulation by Omi/HtrA2 provide a new link between cell cycle control and apoptosis in cardiomyocytes.

Indexed as

Antineoplastic AgentsApoptosisCell CycleCell NucleusCisplatinCoronary Artery DiseaseDNA-Binding ProteinsGene Expression Regulation, EnzymologicHeLa CellsHigh-Temperature Requirement A Serine Peptidase 2HomeostasisHumansHydrogen PeroxideKidneyMitochondria, HeartMitochondrial ProteinsAntineoplastic AgentsCisplatinDNA-Binding ProteinsHigh-Temperature Requirement A Serine Peptidase 2HTRA2 protein, humanHydrogen PeroxideMitochondrial ProteinsNuclear ProteinsOxidantsPyrimidinonesRNA, MessengerSerine EndopeptidasesTHAP5 protein, humanThionesUCF 101

Identifiers

PMID19502560
PMCPMC2724199
OpenAlexW2094946788

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.