Evidence map›Paper›PMID 24989671›Full record

ArticleGenes and immunity2014

Characterization of a weakly expressed KIR2DL1 variant reveals a novel upstream promoter that controls KIR expression.

P W Wright, H Li, A Huehn, G M O'Connor, S Cooley, J S Miller, S K Anderson

Open access · greenAbstract read
In one paragraph

Article in Genes and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

13 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  6. Ascorbic Acid PromotesJournal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  7. Single Nucleotide Polymorphism inFrontiers in immunology · 2020
    Article
  8. Review
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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 3 institutions in 1 country.

P W WrightBasic Science Program, Leidos Biomedical Research Inc., Lab of Experimental Immunology, Frederick National Lab, Frederick, MD, USA.
H LiBasic Science Program, Leidos Biomedical Research Inc., Lab of Experimental Immunology, Frederick National Lab, Frederick, MD, USA.
A HuehnCancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD, USA.
G M O'ConnorCancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD, USA.
S CooleyDivision of Hematology, Oncology and Transplantation, University of Minnesota, Minneapolis, MN, USA.
J S MillerDivision of Hematology, Oncology and Transplantation, University of Minnesota, Minneapolis, MN, USA.
S K Anderson1] Basic Science Program, Leidos Biomedical Research Inc., Lab of Experimental Immunology, Frederick National Lab, Frederick, MD, USA [2] Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD, USA.
National Cancer Institute · USLeidos Biomedical Research Inc. (United States)University of Minnesota · US

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Douglas Yee · 1998 to 2026
$100.4M
Molecular Studies of Cellular CytotoxicityZIABC010013 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI ANDERSON, STEPHEN K · 2009 to 2025
$17.2M
CCR NIH HHS HHSN261200800001CIntramural NIH HHS ZIA BC010013NCI NIH HHS HHSN261200800001ENCI NIH HHS P30 CA077598PHS HHS P01111412
6 · The paper itself

Abstract

Members of the human KIR (killer cell immunoglobulin-like receptor) class I major histocompatibility complex receptor gene family contain multiple promoters that determine the variegated expression of KIR on natural killer cells. In order to identify novel genetic alterations associated with decreased KIR expression, a group of donors was characterized for KIR gene content, transcripts and protein expression. An individual with a single copy of the KIR2DL1 gene but a very low level of gene expression was identified. The low expression phenotype was associated with a single-nucleotide polymorphism (SNP) that created a binding site for the inhibitory ZEB1 (Zinc finger E-box-binding homeobox 1) transcription factor adjacent to a c-Myc binding site previously implicated in distal promoter activity. Individuals possessing this SNP had a substantial decrease in distal KIR2DL1 transcripts initiating from a novel intermediate promoter located 230 bp upstream of the proximal promoter start site. Surprisingly, there was no decrease in transcription from the KIR2DL1 proximal promoter. Reduced intermediate promoter activity revealed the existence of alternatively spliced KIR2DL1 transcripts containing premature termination codons that initiated from the proximal KIR2DL1 promoter. Altogether, these results indicate that distal transcripts are necessary for KIR2DL1 protein expression and are required for proper processing of sense transcripts from the bidirectional proximal promoter.

Indexed as

Polymorphism, Single NucleotidePromoter Regions, GeneticBase SequenceBinding SitesCell Line, TumorCells, CulturedHEK293 CellsHomeodomain ProteinsHumansMolecular Sequence DataReceptors, KIR2DL1RNA, MessengerTranscription FactorsZinc Finger E-box-Binding Homeobox 1Homeodomain ProteinsKIR2DL1 protein, humanReceptors, KIR2DL1RNA, MessengerTranscription FactorsZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID24989671
PMCPMC4208966
OpenAlexW1997158144

What OpenQuestion holds

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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.