Evidence map›Paper›PMID 34211088›Full record

ArticleOncogene2021

TRIM44 mediated p62 deubiquitination enhances DNA damage repair by increasing nuclear FLNA and 53BP1 expression.

Lin Lyu, Tsung-Chin Lin, Nami McCarty

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 48 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 1 institution in 1 country.

Lin Lyu *Center for Stem Cell and Regenerative Disease, Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases (IMM), the University of Texas-Health Science Center at Houston, Houston, TX, 77030, USA.ORCID 0000-0001-9771-0110
Tsung-Chin Lin *Center for Stem Cell and Regenerative Disease, Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases (IMM), the University of Texas-Health Science Center at Houston, Houston, TX, 77030, USA.
Nami McCartyCenter for Stem Cell and Regenerative Disease, Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases (IMM), the University of Texas-Health Science Center at Houston, Houston, TX, 77030, USA. nami.mccarty@uth.tmc.edu.ORCID 0000-0002-7384-5165
Brown Foundation · US

Funding

Targeting Stem-Cell Dependent Drug Resistance in Human MCLR01CA181319 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MCCARTY, NAMI · 2014 to 2025
$3.4M
NCI NIH HHS R01 CA181319U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA181319
6 · The paper itself

Abstract

Cancer cells show increases in protein degradation pathways, including autophagy, during progression to meet the increased protein degradation demand and support cell survival. On the other hand, reduced autophagy activity during aging is associated with a reduced DNA damage response and increased genomic instability. Therefore, it is a puzzling how DNA repair can be increased in cancer cells that are resistant to chemotherapies or during progression when autophagy activity is intact or increased. We discovered that tripartite motif containing 44 (TRIM44) is a pivotal element regulating the DNA damage response in cancer cells with intact autophagy. TRIM44 deubiquitinates p62, an autophagy substrate, which leads to its oligomerization. This prevents p62 localization to the nucleus upon irradiation. Increased cytoplasmic retention of p62 by TRIM44 prevents the degradation of FLNA and 53BP1, which increases DNA damage repair. Together, our data support TRIM44 a potential therapeutic target for therapy-resistant tumor cells with intact autophagy.

Indexed as

DNA DamageDNA RepairGene Expression RegulationAutophagyCell Line, TumorCell SurvivalDNA End-Joining RepairFilaminsGenomic InstabilityHumansIntracellular Signaling Peptides and ProteinsMultiple MyelomaProtein BindingProtein MultimerizationProtein TransportRadiation, IonizingFilaminsFLNA protein, humanIntracellular Signaling Peptides and ProteinsSequestosome-1 ProteinSQSTM1 protein, humanTP53BP1 protein, humanTRIM44 protein, humanTripartite Motif ProteinsTumor Suppressor p53-Binding Protein 1

Identifiers

PMID34211088
PMCPMC9744239
OpenAlexW3177035356

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.