Evidence map›Paper›PMID 22031102›Full record

ArticleCell cycle (Georgetown, Tex.)2011

MG132 inhibition of proteasome blocks apoptosis induced by severe DNA damage.

Ling Zhang, Jennifer J Hu, Feng Gong

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-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

13 citing papers in PubMed, 24 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Ling ZhangDepartment of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, Miami, FL, USA.
Jennifer J Hu
Feng Gong
University of Miami · USMiller College · US

Funding

SWI/SNF chromatin remodeling in nucleotide excision repairR01ES017784 · NIEHS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI GONG, FENG · 2010 to 2014
$1.7M
NIEHS NIH HHS R01 ES017784NIEHS NIH HHS R01ES017784
6 · The paper itself

Abstract

The 26S proteasome, a multicatalytic enzyme complex, is the main intracellular proteolytic system involved in the degradation of ubiquitinated proteins. The ability of proteasome inhibitors to induce apoptosis has been exploited in the recent development of chemotherapeutic agents. Here, we show that inhibition of proteasome by MG132 blocks DNA damage-induced apoptosis. Blockage of apoptosis by MG132 correlates with p53 stabilization and upregulation of p21/WAF1, a p53 transcriptional target. Surprisingly, in the absence of MG132, robust apoptosis induced by a high dose of UV irradiation correlate with rapid p53 degradation. This is in sharp contrast to p53 stabilization when cells were exposed to lower levels of UV irradiation. Our findings highlight a scenario in which severe UV damage can induce rapid p53 degradation by the proteasome. Importantly, these data suggest that the 26S proteasome plays a key role in promoting apoptosis induced by high doses of UV irradiation.

Indexed as

DNA DamageProteasome InhibitorsUltraviolet RaysApoptosisCyclin-Dependent Kinase Inhibitor p21HeLa CellsHumansIn Situ Nick-End LabelingLeupeptinsModels, BiologicalPoly(ADP-ribose) PolymerasesProteasome Endopeptidase ComplexProtein StabilityTumor Suppressor Protein p53ATP dependent 26S proteasebenzyloxycarbonylleucyl-leucyl-leucine aldehydeCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21LeupeptinsPoly(ADP-ribose) PolymerasesProteasome Endopeptidase ComplexProteasome InhibitorsTumor Suppressor Protein p53

Identifiers

PMID22031102
PMCPMC3266179
OpenAlexW1867960014

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.