Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Ribozyme-mediated compensatory induction of menin-oncosuppressor function in primary fibroblasts from MEN1 patients.

Cancer gene therapy - 1 Nov 2010

Luzi E, Marini F, Tognarini I, Carbonell Sala S, Galli G, Falchetti A, Brandi M L

Abstract excerpt

Multiple endocrine neoplasia type 1 (MEN1) syndrome is characterized by the occurrence of tumors of parathyroids, neuroendocrine cells of the gastro-enteropancreatic tract and anterior pituitary. MEN1 gene encodes menin-oncosuppressor protein. Loss of heterozygosity at 11q13 is typical of MEN1 tumors. We have analyzed the MEN1 mRNA and menin expression in fibroblasts from normal skin biopsies and from MEN1...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Caspase 8
Share to Fibroblasts
Share to Loss of Heterozygosity

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Multiple Endocrine Neoplasia Type 1

Share to RNA, Catalytic

Share to RNA Interference

Share to RNA, Small Interfering

Share to Up-Regulation

Source

Identifiers

PMID: 20706287
DOI: 10.1038/cgt.2010.39

Genes

MEN1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Ribozyme-mediated compensatory induction of menin-oncosuppressor function in primary fibroblasts from MEN1 patients.PMID 20706287Read ↗

Inactivation of menin, a Smad3-interacting protein, blocks transforming growth factor type β signalingSemantic proximity Read ↗

Menin Missense Mutants Encoded by the MEN1 Gene that Are Targeted to the Proteasome: Restoration of Expression and Activity by CHIP siRNASemantic proximity Read ↗

The Negative Feedback-Loop between the Oncomir Mir-24-1 and Menin Modulates the Men1 Tumorigenesis by Mimicking the “Knudson’s Second Hit”Semantic proximity Read ↗

Menin regulates endocrine diseases by controlling histone modification and gene transcription.Semantic proximity Read ↗

Menin Molecular Interactions: Insights into Normal Functions and TumorigenesisSemantic proximity Read ↗

Expression analysis of endogenous menin, the product of the multiple endocrine neoplasia type 1 gene, in cell lines and human tissues.Semantic proximity Read ↗

Tumor Suppressor Menin Regulates Expression of Insulin-Like Growth Factor Binding Protein 2Semantic proximity Read ↗

Twenty years of menin: emerging opportunities for restoration of transcriptional regulation in MEN1Semantic proximity Read ↗

Transfection of the Multiple Endocrine Neoplasia Type 1 Gene to a Human Endocrine Pancreatic Tumor Cell Line Inhibits Cell Growth and Affects Expression of JunD, δ-Like Protein 1/Preadipocyte Factor-1, Proliferating Cell Nuclear Antigen, and QM/Jif-1Semantic proximity Read ↗

Genetic ablation of the tumor suppressor menin causes lethality at mid-gestation with defects in multiple organs.Semantic proximity Read ↗

A novel splicing mutation (894-9 G --> A) of the MEN1 gene responsible for multiple endocrine neoplasia type 1.Semantic proximity Read ↗

The multiple endocrine neoplasia type 1 gene product, menin, inhibits the human prolactin promoter activitySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.