Evidence map›Paper›PMID 32439806›Full record

ArticleThe Journal of biological chemistry2020

The N-terminal domain of the non-receptor tyrosine kinase ABL confers protein instability and suppresses tumorigenesis.

Zhengwei Yan, Karthigayan Shanmugasundaram, Dongwen Ma, Jiayu Luo, Shiwen Luo, Hai Rao

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

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. 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

6 authors at 2 institutions in 2 countries.

Zhengwei YanCenter for Experimental Medicine, First Affiliated Hospital, Nanchang University, Nanchang, China.
Karthigayan ShanmugasundaramDepartment of Molecular Medicine, University of Texas Health Science Center, San Antonio, Texas, USA.
Dongwen MaCenter for Experimental Medicine, First Affiliated Hospital, Nanchang University, Nanchang, China.
Jiayu LuoCenter for Experimental Medicine, First Affiliated Hospital, Nanchang University, Nanchang, China.
Shiwen LuoCenter for Experimental Medicine, First Affiliated Hospital, Nanchang University, Nanchang, China. Electronic address: shiwenluo@ncu.edu.cn.
Hai RaoDepartment of Molecular Medicine, University of Texas Health Science Center, San Antonio, Texas, USA. Electronic address: raoh@uthscsa.edu.
Nanchang University · CNThe University of Texas Health Science Center at San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosome translocation can lead to chimeric proteins that may become oncogenic drivers. A classic example is the fusion of the BCR activator of RhoGEF and GTPase and the ABL proto-oncogene nonreceptor tyrosine kinase, a result of a chromosome abnormality (Philadelphia chromosome) that causes leukemia. To unravel the mechanism underlying BCR-ABL-mediated tumorigenesis, here we compared the stability of ABL and the BCR-ABL fusion. Using protein degradation, cell proliferation, 5-ethynyl-2-deoxyuridine, and apoptosis assays, along with xenograft tumor analysis, we found that the N-terminal segment of ABL, which is lost in the BCR-ABL fusion, confers degradation capacity that is promoted by SMAD-specific E3 ubiquitin protein ligase 1. We further demonstrate that the N-terminal deletion renders ABL more stable and stimulates cell growth and tumorigenesis. The findings of our study suggest that altered protein stability may contribute to chromosome translocation-induced cancer development.

Indexed as

AnimalsApoptosisCarcinogenesisCell ProliferationCell Transformation, NeoplasticFemaleFusion Proteins, bcr-ablHEK293 CellsHumansK562 CellsMice, Inbred BALB CMice, NudeOncogenesPhosphorylationProtein DomainsProtein StabilityFusion Proteins, bcr-ablMAS1 protein, humanProtein-Tyrosine KinasesProto-Oncogene MasProto-Oncogene Proteins c-ablUbiquitin-Protein LigasesABL kinaseABL proto-oncogene non-receptor tyrosine kinaseBCR activator of RhoGEF and GTPasechromosome rearrangementchromosome translocationleukemiaoncogenePhiladelphia chromosomeprotein chimeraprotein degradationproteolysisSMAD-specific E3 ubiquitin protein ligase 1 (Smurf1)ubiquitin

Identifiers

PMID32439806
PMCPMC7335801
OpenAlexW3026963361

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.