Evidence map›Paper›PMID 24899623›Full record

ArticleBlood2014

A motif in LILRB2 critical for Angptl2 binding and activation.

Mi Deng, Zhigang Lu, Junke Zheng, Xuan Wan, Xiaoli Chen, Kouyuki Hirayasu, Hanzi Sun, Yeeling Lam, Liping Chen, Qihui Wang and 6 more

Abstract read
In one paragraph

Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
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  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. A Switch Protein Adapter for Anti-LILRB4 CAR-T Cells.European journal of immunology · 2025
    Article
  14. Angiopoietin-like protein 2 inhibits thrombus formation.Molecular and cellular biochemistry · 2025
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 7 institutions in 3 countries.

Mi DengDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, TX;
Zhigang LuDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, TX; Laboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Shenzhen Graduate School of Peking University, Shenzhen, China;
Junke ZhengDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, TX; Department of Pathophysiology, Shanghai Universities E-Institute for Chemical Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China;
Xuan WanDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, TX;
Xiaoli ChenDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, TX;
Kouyuki HirayasuDepartment of Immunochemistry, Research Institute for Microbial Diseases and Laboratory of Immunochemistry, World Premier International Immunology Frontier Research Center, Osaka University, and Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Osaka, Japan;
Hanzi SunNational Institute of Biological Sciences, Beijing, China;
Yeeling LamDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, TX;
Liping ChenDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, TX;
Qihui WangChinese Academy of Sciences Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China;
Chun SongShandong University and National New Drug R&D Center in Shandong, Jinan, China; and.
Niu HuangNational Institute of Biological Sciences, Beijing, China;
George F GaoChinese Academy of Sciences Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China;
Youxing JiangDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, TX;
Hisashi AraseDepartment of Immunochemistry, Research Institute for Microbial Diseases and Laboratory of Immunochemistry, World Premier International Immunology Frontier Research Center, Osaka University, and Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Osaka, Japan;
Cheng Cheng ZhangDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, TX; Department of Developmental Biology, University of Texas Southwestern Medical Center, Dallas, TX.
The University of Texas Southwestern Medical Center · USInstitute of Microbiology · CNNational Institute of Biological Sciences, Beijing · CNJapan Science and Technology Agency · JPOsaka University · JPPeking University · CNShandong University · CN

Funding

The role of inhibitory receptors in leukemia developmentR01CA172268 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI ZHANG, CHENGCHENG · 2013 to 2017
$1.6M
NCI NIH HHS 1R01CA172268NCI NIH HHS R01 CA172268
6 · The paper itself

Abstract

A better understanding of the interaction between extrinsic factors and surface receptors on stem cells will greatly benefit stem cell research and applications. Recently, we showed that several angiopoietin-like proteins (Angptls) bind and activate the immune inhibitory receptor human leukocyte immunoglobulin (Ig)-like receptor B2 (LILRB2) to support ex vivo expansion of hematopoietic stem cells (HSCs) and leukemia development. However, the molecular basis for the interaction between Angptls and LILRB2 was unclear. Here, we demonstrate that Angptl2 expressed in mammalian cells forms high-molecular-weight species and that ligand multimerization is required for activation of LILRB2 for downstream signaling. A novel motif in the first and fourth Ig domains of LILRB2 was identified that is necessary for the receptor to be bound and activated by Angptl2. The binding of Angptl2 to LILRB2 is more potent than and not completely overlapped with the binding of another ligand, HLA-G. Immobilized anti-LILRB2 antibodies induce a more potent activation of LILRB2 than Angptl2, and we developed a serum-free culture containing defined cytokines and immobilized anti-LILRB2 that supports a net expansion of repopulating human cord blood HSCs. Our elucidation of the mode of Angptl binding to LILRB2 enabled the development of a new approach for ex vivo expansion of human HSCs.

Indexed as

Angiopoietin-Like Protein 2Angiopoietin-like ProteinsAngiopoietinsAnimalsFetal BloodHematopoietic Stem CellsHematopoietic Stem Cell TransplantationHeterograftsHumansMembrane GlycoproteinsMiceProtein BindingProtein Interaction Domains and MotifsReceptors, ImmunologicRecombinant Fusion ProteinsSignal TransductionAngiopoietin-Like Protein 2Angiopoietin-like ProteinsAngiopoietinsANGPTL2 protein, humanLILRB2 protein, humanMembrane GlycoproteinsReceptors, ImmunologicRecombinant Fusion Proteins

Identifiers

PMID24899623
PMCPMC4126332
OpenAlexW2052318430

What OpenQuestion holds

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Registered trials

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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.