Evidence map›Paper›PMID 30408063›Full record

ArticlePloS one2018

The common truncation variant in pancreatic lipase related protein 2 (PNLIPRP2) is expressed poorly and does not alter risk for chronic pancreatitis.

Balázs Csaba Németh, Zsófia Gabriella Pesei, Eszter Hegyi, Ákos Szücs, Andrea Szentesi, Péter Hegyi, Mark E Lowe, Miklós Sahin-Tóth

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Trial
  2. Review
  3. Characterization of novel PNLIP variants in congenital pancreatic lipase deficiency.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2023
    Article
  4. Article
  5. Review
  6. Article
  7. 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 2 countries.

Balázs Csaba NémethCenter for Exocrine Disorders, Department of Molecular and Cell Biology, Boston University Henry M. Goldman School of Dental Medicine, Boston, MA, United States of America.
Zsófia Gabriella PeseiCenter for Exocrine Disorders, Department of Molecular and Cell Biology, Boston University Henry M. Goldman School of Dental Medicine, Boston, MA, United States of America.
Eszter HegyiCenter for Exocrine Disorders, Department of Molecular and Cell Biology, Boston University Henry M. Goldman School of Dental Medicine, Boston, MA, United States of America.ORCID 0000-0002-9137-7561
Ákos SzücsFirst Department of Surgery, Semmelweis University, Budapest, Hungary.
Andrea SzentesiFirst Department of Medicine, University of Szeged, Szeged, Hungary.
Péter HegyiInstitute for Translational Medicine, University of Pécs, Pécs, Hungary.
Mark E LoweDepartment of Pediatrics, Washington University School of Medicine, St Louis, MO, United States of America.
Miklós Sahin-TóthCenter for Exocrine Disorders, Department of Molecular and Cell Biology, Boston University Henry M. Goldman School of Dental Medicine, Boston, MA, United States of America.ORCID 0000-0003-4513-9922
Boston University · USSemmelweis University · HUUniversity of Pecs · HUUniversity of Szeged · HUWashington University in St. Louis · US

Funding

Year 9 Administrative Supplement to INSPPIRE 2U01DK108334 · NIDDK · UNIVERSITY OF IOWA · PI MARK E. LOWE, Aliye Uc · 2015 to 2026
$10.5M
Chymotrypsin in pancreatitisR01DK082412 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAHIN-TOTH, MIKLOS · 2009 to 2024
$5.8M
Molecular Pathomechanism of Hereditary PancreatitisR01DK058088 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAHIN-TOTH, MIKLOS · 2001 to 2019
$5.3M
Molecular Mechanisms of Dietary Fat Digestion by Pancreatic LipasesR01DK080820 · NIDDK · WASHINGTON UNIVERSITY · PI LOWE, MARK E. · 2009 to 2017
$2.7M
Proteotoxicity in the Pathophysiology of Chronic PancreatitisR01DK097241 · NIDDK · WASHINGTON UNIVERSITY · PI LOWE, MARK E. · 2014 to 2016
$999k
NIDDK NIH HHS R01 DK058088NIDDK NIH HHS R01 DK080820NIDDK NIH HHS R01 DK082412NIDDK NIH HHS R01 DK097241NIDDK NIH HHS U01 DK108334
6 · The paper itself

Abstract

A nonsense variant (p.W358X) of human pancreatic lipase related protein 2 (PNLIPRP2) is present in different ethnic populations with a high allele frequency. In cell culture experiments, the truncated protein mainly accumulates inside the cells and causes endoplasmic reticulum stress. Here, we tested the hypothesis that variant p.W358X might increase risk for chronic pancreatitis through acinar cell stress. We sequenced exon 11 of PNLIPRP2 in a cohort of 256 subjects with chronic pancreatitis (152 alcoholic and 104 non-alcoholic) and 200 controls of Hungarian origin. We observed no significant difference in the distribution of the truncation variant between patients and controls. We analyzed mRNA expression in human pancreatic cDNA samples and found the variant allele markedly reduced. We conclude that the p.W358X truncation variant of PNLIPRP2 is expressed poorly and has no significant effect on the risk of chronic pancreatitis.

Indexed as

Genetic Predisposition to DiseaseAcinar CellsAdultAgedAllelesEndoplasmic Reticulum StressFemaleGene Expression Regulation, EnzymologicGene FrequencyHumansLipaseMaleMiddle AgedMutant ProteinsMutationPancreasLipaseMutant Proteinspancreatic lipase related protein 2

Identifiers

PMID30408063
PMCPMC6226108
OpenAlexW2900369511

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.