Evidence map›Paper›PMID 29931788›Full record

ArticleCancer science2018

UNC119 is a binding partner of tumor suppressor Ras-association domain family 6 and induces apoptosis and cell cycle arrest by MDM2 and p53.

Hiroaki Iwasa, Aradhan Sarkar, Takanobu Shimizu, Takeru Sawada, Shakhawoat Hossain, Xiaoyin Xu, Junichi Maruyama, Kyoko Arimoto-Matsuzaki, Kanchanamala Withanage, Kentaro Nakagawa and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

5 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
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

13 authors at 2 institutions in 3 countries.

Hiroaki IwasaDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Aradhan SarkarDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Takanobu ShimizuDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Takeru SawadaDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Shakhawoat HossainDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Xiaoyin XuDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Junichi MaruyamaDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Kyoko Arimoto-MatsuzakiDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Kanchanamala WithanageDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Kentaro NakagawaDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Hidetake KuriharaDepartment of Physical Therapy, Faculty of Health Science, Aino University, Osaka, Japan.
Hidehito KuroyanagiLaboratory of Gene Expression, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Yutaka HataDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.ORCID http://orcid.org/0000-0003-1304-5286
Tokyo Medical and Dental University · JPAino University · JP

Funding

Japan Society for the Promotion of Science 26293061Japan Society for the Promotion of Science 26460359
6 · The paper itself

Abstract

Ras-association domain family 6 (RASSF6) is a tumor suppressor that interacts with MDM2 and stabilizes p53. Caenorhabditis elegans unc-119 encodes a protein that is required for normal development of the nervous system. Humans have 2 unc-119 homologues, UNC119 and UNC119B. We have identified UNC119 as a RASSF6-interacting protein. UNC119 promotes the interaction between RASSF6 and MDM2 and stabilizes p53. Thus, UNC119 induces apoptosis by RASSF6 and p53. UNC119 depletion impairs DNA repair after DNA damage and results in polyploid cell generation. These findings support that UNC119 is a regulator of the RASSF6-MDM2-p53 axis and functions as a tumor suppressor.

Indexed as

Adaptor Proteins, Signal TransducingApoptosisApoptosis Regulatory ProteinsCell Cycle CheckpointsCell Line, TumorDNA DamageDNA RepairHCT116 CellsHEK293 CellsHeLa CellsHumansMonomeric GTP-Binding ProteinsNeoplasmsPolyploidyProtein BindingProto-Oncogene Proteins c-mdm2Adaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsMDM2 protein, humanMonomeric GTP-Binding ProteinsProto-Oncogene Proteins c-mdm2RASSF6 protein, humanTP53 protein, humanTumor Suppressor Protein p53Tumor Suppressor ProteinsUNC119 protein, humanapoptosisMDM2p53RASSFtumor suppressor

Identifiers

PMID29931788
PMCPMC6125449
OpenAlexW2808884075

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.