Evidence map›Paper›PMID 18188647›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2008

The endothelial-specific regulatory mutation, Mvwf1, is a common mouse founder allele.

Jill M Johnsen, Gallia G Levy, Randal J Westrick, Priscilla K Tucker, David Ginsburg

Open access · hybridAbstract read
In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2008. 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
1.5field-weighted citation impact, top 19% 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.

  1. Article
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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

5 authors at 2 institutions in 1 country.

Jill M JohnsenDepartment of Internal Medicine, University of Michigan, Ann Arbor, Michigan, 48109-2216, USA. jjohnsen@med.umich.edu
Gallia G Levy
Randal J Westrick
Priscilla K Tucker
David Ginsburg
University of Michigan–Ann Arbor · USMichigan Medicine · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
UNIVERSITY OF MICHIGAN MULTIPURPOSE ARTHRITIS CENTERP60AR020557 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SOWERS, MARYFRAN R · 1986 to 2001
$2.9M
An endothelial-specific switch in gene expression.F32HL078185 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JOHNSEN, JILL M · 2004 to 2004
$54k
NCI NIH HHS CA46592NCI NIH HHS P30 CA046592NHLBI NIH HHS 1 F32 HL78185-01NHLBI NIH HHS 4 R37-HL036963NHLBI NIH HHS F32 HL078185NIAMS NIH HHS AR20557
6 · The paper itself

Abstract

Mvwf1 is a cis-regulatory mutation previously identified in the RIIIS/J mouse strain that causes a unique tissue-specific switch in the expression of an N-acetylgalactosaminyltransferase, B4GALNT2, from intestinal epithelium to vascular endothelium. Vascular B4galnt2 expression results in aberrant glycosylation of von Willebrand Factor (VWF) and accelerated VWF clearance from plasma. We now report that 13 inbred mouse strains share the Mvwf1 tissue-specific switch and low VWF phenotype, including five wild-derived strains. Genomic sequencing identified a highly conserved 97-kb Mvwf1 haplotype block shared by these strains that encompasses a 30-kb region of high nucleotide sequence divergence from C57BL6/J flanking B4galnt2 exon 1. The analysis of a series of bacterial artificial chromosome (BAC) transgenes containing B4galnt2 derived from the RIIIS/J or C57BL6/J inbred mouse strains demonstrates that the corresponding sequences are sufficient to confer the vessel (RIIIS/J) or intestine (C57BL6/J)-specific expression patterns. Taken together, our data suggest that the region responsible for the Mvwf1 regulatory switch lies within an approximately 30-kb genomic interval upstream of the B4galnt2 gene. The observation that Mvwf1 is present in multiple wild-derived strains suggests that this locus may be retained in wild mouse populations due to positive selection. Similar selective pressures could contribute to the high prevalence of von Willebrand disease in humans.

Indexed as

AllelesAnimalsChromosomes, Artificial, BacterialConserved SequenceEndothelium, VascularGenomeHaplotypesIntestinesLectinsMiceMutationN-AcetylgalactosaminyltransferasesOrgan SpecificityPhenotypePolypeptide N-acetylgalactosaminyltransferaseTransgenesLectinsN-AcetylgalactosaminyltransferasesPolypeptide N-acetylgalactosaminyltransferase

Identifiers

PMID18188647
PMCPMC2226002
OpenAlexW2010604883

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.