Evidence map›Paper›PMID 33693786›Full record

ArticleHuman molecular genetics2021

An Asian-specific MPL genetic variant alters JAK-STAT signaling and influences platelet count in the population.

Pengfei Sun, Wei Zhou, Yi Fu, Chloe Y Y Cheung, Yujun Dong, Min-Lee Yang, He Zhang, Jia Jia, Yong Huo, Cristen J Willer and 10 more

Open access · greenAbstract read
In one paragraph

Article in Human molecular genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Structural basis of MPL activation by thrombopoietin.Blood vessels, thrombosis & hemostasis · 2024
    Article
  2. Review
  3. 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

20 authors at 4 institutions in 3 countries.

Pengfei SunDepartment of Cardiology, Peking University First Hospital, Beijing 100034, China.
Wei ZhouDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Yi FuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China.
Chloe Y Y CheungDepartment of Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong 999077, China.
Yujun DongDepartment of Hematology, Peking University First Hospital, Beijing 100034, China.
Min-Lee YangDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
He ZhangDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Jia JiaDepartment of Cardiology, Peking University First Hospital, Beijing 100034, China.
Yong HuoDepartment of Cardiology, Peking University First Hospital, Beijing 100034, China.
Cristen J WillerDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Y Eugene ChenDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Clara S TangDepartment of Surgery, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong 999077, China.
Hung-Fat TseDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China.
Karen S L LamDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China.
Wei GaoDepartment of Cardiology, Peking University Third Hospital, Beijing 100083, China.
Ming XuDepartment of Cardiology, Peking University Third Hospital, Beijing 100083, China.
Haiyi YuDepartment of Cardiology, Peking University Third Hospital, Beijing 100083, China.
Pak Chung ShamDepartment of Psychiatry and Centre for PanorOmic Sciences, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong 999077, China.
Yan ZhangDepartment of Cardiology, Peking University First Hospital, Beijing 100034, China.ORCID 0000-0002-7508-4160
Santhi K GaneshDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Peking University · CNUniversity of Michigan · USUniversity of Hong Kong · HKMinistry of Education of the People's Republic of China · CN

Funding

Genetic Studies of The Impact of Hematologic Traits On Cardiovascular DiseaseR01HL122684 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GANESH, SANTHI K · 2015 to 2019
$3.4M
NHLBI NIH HHS R01 HL122684
6 · The paper itself

Abstract

Genomic discovery efforts for hematological traits have been successfully conducted through genome-wide association study on samples of predominantly European ancestry. We sought to conduct unbiased genetic discovery for coding variants that influence hematological traits in a Han Chinese population. A total of 5257 Han Chinese subjects from Beijing, China were included in the discovery cohort and analyzed by an Illumina ExomeChip array. Replication analyses were conducted in 3827 independent Chinese subjects. We analyzed 12 hematological traits and identified 22 exome-wide significant single-nucleotide polymorphisms (SNP)-trait associations with 15 independent SNPs. Our study provides replication for two associations previously reported but not replicated. Further, one association was identified and replicated in the current study, of a coding variant in the myeloproliferative leukemia (MPL) gene, c.793C > T, p.Leu265Phe (L265F) with increased platelet count (β = 20.6 109 cells/l, Pmeta-analysis = 2.6 × 10-13). This variant is observed at ~2% population frequency in East Asians, whereas it has not been reported in gnomAD European or African populations. Functional analysis demonstrated that expression of MPL L265F in Ba/F3 cells resulted in enhanced phosphorylation of Stat3 and ERK1/2 as compared with the reference MPL allele, supporting altered activation of the JAK-STAT signal transduction pathway as the mechanism underlying the novel association between MPL L265F and platelet count.

Indexed as

Genome-Wide Association StudyAsian PeopleHumansPlatelet CountPolymorphism, Single NucleotideReceptors, ThrombopoietinSignal TransductionMPL protein, humanReceptors, Thrombopoietin

Identifiers

PMID33693786
PMCPMC8161516
OpenAlexW3135638859

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.