Evidence map›Paper›PMID 21740188›Full record

ArticleDNA and cell biology2011

The bladder tumor suppressor protein TERE1 (UBIAD1) modulates cell cholesterol: implications for tumor progression.

William J Fredericks, Terry McGarvey, Huiyi Wang, Priti Lal, Raghunath Puthiyaveettil, John Tomaszewski, Jorge Sepulveda, Ed Labelle, Jayne S Weiss, Michael L Nickerson and 4 more

Open access · hybridAbstract read
In one paragraph

Article in DNA and cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.5field-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

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Functional study of SCCD pathogenic geneMolecular medicine reports · 2021
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  7. Clinical diversity in patients with Schnyder corneal dystrophy-a novel and known UBIAD1 pathogenic variants.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2018
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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

14 authors at 9 institutions in 2 countries.

William J FredericksDivision of Urology, Department of Surgery, University of Pennsylvania, VAMC Philadelphia, Philadelphia, PA 19104, USA. william.fredericks@uphs.upenn.edu
Terry McGarvey
Huiyi Wang
Priti Lal
Raghunath Puthiyaveettil
John Tomaszewski
Jorge Sepulveda
Ed Labelle
Jayne S Weiss
Michael L Nickerson
Howard S Kruth
Wolfgang Brandt
Ludger A Wessjohann
S Bruce Malkowicz
University of Pennsylvania · USCalifornia University of Pennsylvania · USLeibniz Institute of Plant Biochemistry · DEVeterans Health Administration · USA.T. Still University · USLouisiana State University · USNational Cancer Institute · USNational Institutes of Health · USRowan College at Gloucester County · US

Funding

Mechanism Of Cholesterol Accumulation In Human AtherosclerosisZIAHL002832 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI KRUTH, HOWARD S · 2009 to 2019
$12.3M
CANCER AND INFLAMMATION GENETICSZIABC011300 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DEAN, MICHAEL · 2010 to 2015
$5.8M
6 · The paper itself

Abstract

Convergent evidence implicates the TERE1 protein in human bladder tumor progression and lipid metabolism. Previously, reduced TERE1 expression was found in invasive urologic cancers and inhibited cell growth upon re-expression. A role in lipid metabolism was suggested by TERE1 binding to APOE, a cholesterol carrier, and to TBL2, a candidate protein in triglyceride disorders. Natural TERE1 mutations associate with Schnyder's corneal dystrophy, characterized by lipid accumulation. TERE1 catalyzes menaquinone synthesis, known to affect cholesterol homeostasis. To explore this relationship, we altered TERE1 and TBL2 dosage via ectopic expression and interfering RNA and measured cholesterol by Amplex red. Protein interactions of wild-type and mutant TERE1 with GST-APOE were evaluated by binding assays and molecular modeling. We conducted a bladder tumor microarray TERE1 expression analysis and assayed tumorigenicity of J82 cells ectopically expressing TERE1. TERE1 expression was reduced in a third of invasive specimens. Ectopic TERE1 expression in J82 bladder cancer cells dramatically inhibited nude mouse tumorigenesis. TERE1 and TBL2 proteins inversely modulated cellular cholesterol in HEK293 and bladder cancer cells from 20% to 50%. TERE1 point mutations affected APOE interactions, and resulted in cholesterol levels that differed from wild type. Elevated tumor cell cholesterol is known to affect apoptosis and growth signaling; thus, loss of TERE1 in invasive bladder cancer may represent a defect in menaquinone-mediated cholesterol homeostasis that contributes to progression.

Indexed as

Amino Acid SequenceAnimalsApolipoproteins ECell Line, TumorCholesterolCorneal Dystrophies, HereditaryDimethylallyltranstransferaseDisease ProgressionGene Expression Regulation, NeoplasticGTP-Binding ProteinsHEK293 CellsHumansIntracellular SpaceMiceMice, NudeModels, MolecularApolipoproteins ECholesterolDimethylallyltranstransferaseGTP-Binding ProteinsProteinsTBL2 protein, humanUBIAD1 protein, human

Identifiers

PMID21740188
PMCPMC3206744
OpenAlexW1998520443

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.