Evidence map›Paper›PMID 19404301›Full record

ArticleGenes and immunity2009

Variation in the upstream region of P-Selectin (SELP) is a risk factor for SLE.

D L Morris, R R Graham, L-P Erwig, P M Gaffney, K L Moser, T W Behrens, T J Vyse, D S Cunninghame Graham

Open access · hybridAbstract read
In one paragraph

Article in Genes and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Identification of NETs-related genes as diagnostic biomarkers in ischemic stroke using RNA sequencing and single-cell analysis.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Article
  3. The impact ofSaudi journal of biological sciences · 2023
    Article
  4. TheJournal of inflammation research · 2023
    Article
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  13. The Relationship between P-Selectin Polymorphisms and Thrombosis in Antiphospholipid Syndrome: A Pilot Case-Control Study.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2014
    Article
  14. Article
  15. Article
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

8 authors at 5 institutions in 3 countries.

D L MorrisSection of Molecular Genetics and Rheumatology, Imperial College Faculty of Medicine, Hammersmith Hospital, London W12 ONN, UK.
R R Graham
L-P Erwig
P M Gaffney
K L Moser
T W Behrens
T J Vyse
D S Cunninghame Graham
Hammersmith Hospital · GBOklahoma Medical Research Foundation · USBroad Institute · USInstitute of Medical Sciences · INUniversity of Minnesota Medical Center · US

Funding

Wellcome Trust
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a complex autoimmune disease. Genome-wide linkage studies implicated a region containing the adhesion molecule P-Selectin. This family-based study revealed two regions of association within P-Selectin. The strongest signal, from a 21.4-kb risk haplotype, stretched from the promoter into the first two consensus repeat (CR) regions (P=8 x 10(-4)), with a second association from a 14.6-kb protective haplotype covering CR 2-9 (P=0.0198). The risk haplotype is tagged by the rare C allele of rs3753306, which disrupts the binding site of the trans-activating transcription factor HNF-1. One other variant (rs3917687) on the risk haplotype was significant after permutation (P(10000)<1 x 10(-5)), replicated in independent pseudo case-control analysis and was significant by meta-analysis (P=4.37 x 10(-6)). A third associated variant on the risk haplotype (rs3917657) replicated in 306 US SLE families and was significant in a joint UK-SLE data set after permutation. The protective haplotype is tagged by rs6133 (a non-synonymous variant in CR8 (P=9.00 x 10(-4)), which also shows association in the pseudo case-control analysis (P=1.09 x 10(-3)) and may contribute to another signal in P-Selectin. We propose that polymorphism in the upstream region may reduce expression of P-Selectin, the mechanism by which this promotes autoimmunity is unknown, although it may reduce the production of regulatory T cells.

Indexed as

Genetic Predisposition to DiseasePromoter Regions, GeneticGenome-Wide Association StudyHumansLupus Erythematosus, SystemicMinnesotaP-SelectinUnited KingdomP-Selectin

Identifiers

PMID19404301
PMCPMC2834331
OpenAlexW2084474031

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.