Evidence map›Paper›PMID 22665489›Full record

ArticleThe Journal of biological chemistry2012

Transcriptional regulation of the protocadherin β cluster during Her-2 protein-induced mammary tumorigenesis results from altered N-glycan branching.

Huabei Guo, Alison Nairn, Mitche dela Rosa, Tamas Nagy, Shaying Zhao, Kelley Moremen, Michael Pierce

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 26 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

7 authors at 1 institution in 1 country.

Huabei GuoDepartment of Biochemistry and Molecular Biology, University of Georgia, Athens, Georgia 30602, USA.
Alison Nairn
Mitche dela Rosa
Tamas Nagy
Shaying Zhao
Kelley Moremen
Michael Pierce
University of Georgia · US

Funding

TR&D1: Stem Cell and Induced Pluripotent Stem Cell Resources (Pages 116-134)P41GM103490 · NIGMS · UNIVERSITY OF GEORGIA · PI PIERCE, J. MICHAEL · 2012 to 2018
$13.7M
ZINC DEFICIENCY &PROTEIN EXPRESSION IN RAT OLFACTORY BULBSP41RR018502 · NCRR · UNIVERSITY OF GEORGIA (UGA) · PI AZADI, PARASTOO · 2003 to 2011
$13.1M
Tumor Glycomics Laboratory for Discovery of Pancreatic Cancer MarkersU01CA128454 · NCI · UNIVERSITY OF GEORGIA · PI PIERCE, J. MICHAEL · 2007 to 2017
$5.7M
NCI NIH HHS U01 CA128454NCI NIH HHS U01CA128454NCRR NIH HHS P41 RR018502NCRR NIH HHS P41RR018502NIGMS NIH HHS P41 GM103490
6 · The paper itself

Abstract

Changes in the levels of N-acetylglucosaminyltransferase V (GnT-V) can alter the function of several types of cell surface receptors and adhesion molecules by causing altered N-linked glycan branching. Using a her-2 mammary tumor mouse model, her-2 receptor signaling was down-regulated by GnT-V knock-out, resulting in a significant delay in the onset of her-2-induced mammary tumors. To identify the genes that contributed to this GnT-V regulation of early events in tumorigenesis, microarray analysis was performed using her-2 induced mammary tumors from wild-type and GnT-V-null mice. We found that 142 genes were aberrantly expressed (>2.0-fold) with 64 genes up-regulated and 78 genes down-regulated after deletion of GnT-V. Among differentially expressed genes, the expression of a subgroup of the cadherin superfamily, the protocadherin β (Pcdhβ) cluster, was up-regulated in GnT-V-null tumors. Altered expression of the Pcdhβ cluster in GnT-V-null tumors was not due to changes in promoter methylation; instead, impaired her-2-mediated signaling pathways were implicated at least in part resulting from reduced microRNA-21 expression. Overexpression of Pcdhβ genes inhibited tumor cell growth, decreased the proportion of tumor-initiating cells, and decreased tumor formation in vivo, demonstrating that expression of the Pcdhβ gene cluster can serve as an inhibitor of the transformed phenotype. Our results suggest the up-regulation of the Pcdhβ gene cluster as a mechanism for reduced her-2-mediated tumorigenesis resulting from GnT-V deletion.

Indexed as

Gene Expression Regulation, NeoplasticGenes, NeoplasmMultigene FamilyTranscription, GeneticAnimalsBreast NeoplasmsCadherinsCell Transformation, NeoplasticErb-b2 Receptor Tyrosine KinasesFemaleGene DeletionHumansMammary Neoplasms, AnimalMiceMice, KnockoutMicroRNAsalpha-1,6-mannosylglycoprotein beta 1,6-N-acetylglucosaminyltransferaseCadherinsERBB2 protein, humanErbb2 protein, mouseErb-b2 Receptor Tyrosine KinasesMicroRNAsMIRN21 microRNA, humanMIRN21 microRNA, mouseN-AcetylglucosaminyltransferasesRNA, Neoplasm

Identifiers

PMID22665489
PMCPMC3408139
OpenAlexW1999542125

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.