Wild-type menin is rapidly degraded via the ubiquitin-proteasome pathway in a rat insulinoma cell line.

Zongzhe Jiang, Shengrong Wan, Bowen Xing

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Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

0.2field-weighted citation impact, top 44% of its field

1 · What the graph read from it

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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.

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1 citing paper in PubMed, 4 citations in OpenAlex.

Clinically Defined Mutations inCancer research communications · 2023
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5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Zongzhe JiangExperimental Medicine Center, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.

Shengrong WanEndocrinology Department, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.

Bowen XingDiabetes Research Center, School of Medicine, Shenzhen University, Shenzhen 518060, Guangdong, China.

Affiliated Hospital of Southwest Medical University · CNShenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Menin is encoded by multiple endocrine neoplasia type 1 (MEN1) gene, the germ line mutations of which are the main cause of pancreatic neuroendocrine tumors (PNETs). To date, a large number of frameshift, nonsense and missense mutations of MEN1 have been identified to be responsible for part of MEN1-defficient PNETs patients due to truncation or rapid degradation of menin protein. However, the stability of the wild-type (WT) menin in PNETs is totally unknown. In the present study, we observed ubiquitination of WT menin in 293T cells by transfection of ectopic WT menin and HA-ubiquitin. As expected, either endogenous or ectopic WT menin is stable in 293T cells, whereas in INS-1 cells, a rat insulinoma cell line derived from PNETs, either endogenous or ectopic WT menin is rapidly degraded through ubiquitin-proteasome pathway. Furthermore, the degradation of WT menin is more rapid in the presence of serum. Our findings suggest that in part of PNETs patients with WT MEN1, a ubiquitin-proteasome system targeting menin is untimely activated.

Indexed as

ProteolysisAnimalsInsulinomaNeoplasm ProteinsPancreatic NeoplasmsProteasome Endopeptidase ComplexRatsTranscription FactorsUbiquitinMen1 protein, ratNeoplasm ProteinsProteasome Endopeptidase ComplexTranscription FactorsUbiquitinINS-1 cellInsulinomaMeninUbiquitin-proteasome

Identifiers

PMID31652443

DOI10.1042/BSR20190471

PMCPMC6822493

OpenAlexW2980237337

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LicenceCC BY

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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.