Evidence map›Paper›PMID 38338729›Full record

ReviewInternational journal of molecular sciences2024

Emerging Roles of YES1 in Cancer: The Putative Target in Drug Resistance.

Eunjin Kook, Kyung-Soo Chun, Do-Hee Kim

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

10 citing papers in PubMed, 14 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.

Eunjin KookDepartment of Chemistry, Kyonggi University, Suwon 16227, Republic of Korea.ORCID 0009-0005-9929-6159
Kyung-Soo ChunCollege of Pharmacy, Keimyung University, Daegu 42691, Republic of Korea.ORCID 0000-0001-9933-2897
Do-Hee KimDepartment of Chemistry, Kyonggi University, Suwon 16227, Republic of Korea.
Kyonggi University · KRKeimyung University · KR

Funding

Kyonggi University Kyonggi University's Graduate Research Assistantship 2023National Research Foundation No. 2020R1A2C1103139
6 · The paper itself

Abstract

Src family kinases (SFKs) are non-receptor tyrosine kinases that are recognized as proto-oncogenic products. Among SFKs, YES1 is frequently amplified and overexpressed in a variety of human tumors, including lung, breast, ovarian, and skin cancers. YES1 plays a pivotal role in promoting cell proliferation, survival, and invasiveness during tumor development. Recent findings indicate that YES1 expression and activation are associated with resistance to chemotherapeutic drugs and tyrosine kinase inhibitors in human malignancies. YES1 undergoes post-translational modifications, such as lipidation and nitrosylation, which can modulate its catalytic activity, subcellular localization, and binding affinity for substrate proteins. Therefore, we investigated the diverse mechanisms governing YES1 activation and its impact on critical intracellular signal transduction pathways. We emphasized the function of YES1 as a potential mechanism contributing to the anticancer drug resistance emergence.

Indexed as

Neoplasmssrc-Family KinasesCell Line, TumorDrug Resistance, NeoplasmHumansProto-Oncogene Proteins c-yesSignal TransductionProto-Oncogene Proteins c-yessrc-Family KinasesYES1 protein, humancancer progressiondrug-resistanceSrc family kinaseYES1

Identifiers

PMID38338729
PMCPMC10855972
OpenAlexW4391229081

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.