Evidence map›Paper›PMID 42024179›Full record

ArticleScience China. Life sciences2026

The KXD1-TSPAN14 axis controls megakaryopoiesis and platelet production via Notch signaling.

Yefeng Yuan, Jiayi Ai, Hanyu Chen, Peng Zhang, Fei Leng, Kai Guo, Zhuang Qi, Kaifang Liu, Yingzi Zhang, Ting Li and 5 more

Abstract read
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In one paragraph

Article in Science China. Life sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

15 authors.

Yefeng YuanLaboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, National Center for Children's Health; Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China. yyfeng6886@sina.cn.
Jiayi AiLaboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, National Center for Children's Health; Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Hanyu ChenLaboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, National Center for Children's Health; Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Peng ZhangLaboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, National Center for Children's Health; Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Fei LengLaboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, National Center for Children's Health; Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Kai GuoLaboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, National Center for Children's Health; Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Zhuang QiLaboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, National Center for Children's Health; Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Kaifang LiuLaboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, National Center for Children's Health; Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Yingzi ZhangDepartment of Dermatology, Beijing Tongren Hospital, Capital Medical University, Beijing, 100005, China.
Ting LiInstitute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, 100101, China.
Lin YangInstitute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, 100101, China.
Fangyuan NieInstitute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, 100101, China.
Aihua WeiDepartment of Dermatology, Beijing Tongren Hospital, Capital Medical University, Beijing, 100005, China.
Chanjuan HaoLaboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, National Center for Children's Health; Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China.
Wei LiLaboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, National Center for Children's Health; Beijing Children's Hospital, Capital Medical University, Beijing, 100045, China. liwei@bch.com.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platelets, derived from megakaryocytes (MKs), are crucial for blood clotting. Identifying genes that regulate MK development and platelet production could advance treatments for blood disorders. We found that KxDL motif-containing 1 (Kxd1) knockout (KO) mice exhibited doubled platelet counts without impairment of individual platelet function. Kxd1-KO mice showed enhanced MK progenitor differentiation and rapid polyploid MK formation in vivo and in vitro. Mechanistically, KXD1 deficiency increased TSPAN14 levels by disrupting its endolysosomal trafficking, thus activating the ADAM10-Notch axis to drive MK polyploidization. In platelet/MK-specific Tspan14-KO mice, TSPAN14 deficiency impaired MK polyploidization and maturation. Our findings reveal that KXD1 is a key negative regulator of Notch signaling, controlling megakaryopoiesis mediated by TSPAN14. The KXD1-TSPAN14 axis is a promising therapeutic target for platelet disorders, including thrombocytopenia and myeloproliferative neoplasms, and as an interventional pathway for platelet production in transfusion medicine.

Indexed as

Blood PlateletsMegakaryocytesReceptors, NotchTetraspaninsThrombopoiesisAnimalsCell DifferentiationMembrane ProteinsMiceMice, KnockoutSignal TransductionMembrane ProteinsReceptors, NotchTetraspaninsKXD1megakaryocyteNotchplateletTSPAN14

Identifiers

PMID42024179

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.