Evidence map›Paper›PMID 23926104›Full record

ArticleThe Journal of biological chemistry2013

Tripartite Motif-containing 33 (TRIM33) protein functions in the poly(ADP-ribose) polymerase (PARP)-dependent DNA damage response through interaction with Amplified in Liver Cancer 1 (ALC1) protein.

Atul Kulkarni, Jay Oza, Ming Yao, Honeah Sohail, Vasudeva Ginjala, Antonia Tomas-Loba, Zuzana Horejsi, Antoinette R Tan, Simon J Boulton, Shridar Ganesan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.8field-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

39 citing papers in PubMed, 68 citations in OpenAlex.

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  14. Dermatomyositis autoantibodies: how can we maximize utility?Annals of translational medicine · 2021
    Review
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  20. The Roles of TIF1γ in Cancer.Frontiers in oncology · 2019
    Review
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

10 authors at 1 institution in 1 country.

Atul KulkarniFrom the Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, New Jersey 08903.
Jay OzaFrom the Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, New Jersey 08903.
Ming YaoFrom the Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, New Jersey 08903.
Honeah SohailFrom the Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, New Jersey 08903.
Vasudeva GinjalaFrom the Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, New Jersey 08903.
Antonia Tomas-Lobathe DNA Damage Response Laboratory, London Research Institute, Clare Hall, South Mimms, EN6 3LD Herts, United Kingdom.
Zuzana Horejsithe DNA Damage Response Laboratory, London Research Institute, Clare Hall, South Mimms, EN6 3LD Herts, United Kingdom.
Antoinette R TanFrom the Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, New Jersey 08903.
Simon J Boultonthe DNA Damage Response Laboratory, London Research Institute, Clare Hall, South Mimms, EN6 3LD Herts, United Kingdom.
Shridar GanesanFrom the Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, New Jersey 08903. Electronic address: ganesash@umdnj.edu.
Rutgers, The State University of New Jersey · US

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
Cancer Research UK 11581NCI NIH HHS P30 CA072720
6 · The paper itself

Abstract

Activation of poly(ADP-ribose) polymerase (PARP) near sites of DNA breaks facilitates recruitment of DNA repair proteins and promotes chromatin relaxation in part through the action of chromatin-remodeling enzyme Amplified in Liver Cancer 1 (ALC1). Through proteomic analysis we find that ALC1 interacts after DNA damage with Tripartite Motif-containing 33 (TRIM33), a multifunctional protein implicated in transcriptional regulation, TGF-β signaling, and tumorigenesis. We demonstrate that TRIM33 is dynamically recruited to DNA damage sites in a PARP1- and ALC1-dependent manner. TRIM33-deficient cells show enhanced sensitivity to DNA damage and prolonged retention of ALC1 at sites of DNA breaks. Conversely, overexpression of TRIM33 alleviates the DNA repair defects conferred by ALC1 overexpression. Thus, TRIM33 plays a role in PARP-dependent DNA damage response and regulates ALC1 activity by promoting its timely removal from sites of DNA damage.

Indexed as

DNA BreaksAnimalsDNA-Binding ProteinsDNA HelicasesDNA RepairHEK293 CellsHumansMiceMice, KnockoutPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesProteomicsTranscription FactorsTransforming Growth Factor betaCHD1L protein, humanChd1l protein, mouseDNA-Binding ProteinsDNA HelicasesParp1 protein, mousePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesTranscription FactorsTransforming Growth Factor betaTRIM33 protein, humanTrim33 protein, mouseALC1ATPasesCancer BiologyCell SignalingChromatinDNA Damage ResponsePARPTRIM33

Identifiers

PMID23926104
PMCPMC3820871
OpenAlexW2077676934

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.