Evidence map›Paper›PMID 24699135›Full record

ArticleExperimental & molecular medicine2014

Tetraspanin CD9 modulates ADAM17-mediated shedding of LR11 in leukocytes.

Shokichi Tsukamoto, Masahiro Takeuchi, Takeharu Kawaguchi, Emi Togasaki, Atsuko Yamazaki, Yasumasa Sugita, Tomoya Muto, Shio Sakai, Yusuke Takeda, Chikako Ohwada and 7 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. LR11/SorLA and its role in cardiovascular disease.International journal of cardiology. Heart & vasculature · 2026
    Review
  2. Article
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  5. Article
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  11. Review
  12. Review
  13. Tetraspanins Function as Regulators of Cellular Signaling.Frontiers in cell and developmental biology · 2017
    Review
  14. Article
  15. Review
  16. 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

17 authors at 3 institutions in 1 country.

Shokichi Tsukamoto1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Masahiro Takeuchi1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Takeharu Kawaguchi1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Emi Togasaki1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Atsuko Yamazaki1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Yasumasa Sugita1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Tomoya Muto1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Shio Sakai1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan [3] Division of Transfusion Medicine and Cell Therapy, Chiba University Hospital, Chiba, Japan.
Yusuke Takeda1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Chikako Ohwada1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Emiko Sakaida1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Naomi Shimizu1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan [3] Division of Transfusion Medicine and Cell Therapy, Chiba University Hospital, Chiba, Japan.
Keigo NishiiDepartment of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Meizi JiangDepartment of Clinical-Laboratory and Experimental-Research Medicine, Toho University Medical Center Sakura Hospital, Sakura, Japan.
Koutaro YokoteDepartment of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Hideaki BujoDepartment of Clinical-Laboratory and Experimental-Research Medicine, Toho University Medical Center Sakura Hospital, Sakura, Japan.
Chiaki Nakaseko1] Department of Hematology, Chiba University Hospital, Chiba, Japan [2] Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Chiba University Hospital · JPChiba University · JPToho University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LR11, also known as SorLA or SORL1, is a type-I membrane protein from which a large extracellular part, soluble LR11 (sLR11), is released by proteolytic shedding on cleavage with a disintegrin and metalloproteinase 17 (ADAM17). A shedding mechanism is presumed to have a key role in the functions of LR11, but the evidence for this has not yet been demonstrated. Tetraspanin CD9 has been recently shown to regulate the ADAM17-mediated shedding of tumor necrosis factor-α and intercellular adhesion molecule-1 on the cell surface. Here, we investigated the role of CD9 on the shedding of LR11 in leukocytes. LR11 was not expressed in THP-1 monocytes, but it was expressed and released in phorbol 12-myristate 13-acetate (PMA)-induced THP-1 macrophages (PMA/THP-1). Confocal microscopy showed colocalization of LR11 and CD9 proteins on the cell surface of PMA/THP-1. Ectopic neo-expression of CD9 in CCRF-SB cells, which are LR11-positive and CD9-negative, reduced the amount of sLR11 released from the cells. In contrast, incubation of LR11-transfected THP-1 cells with neutralizing anti-CD9 monoclonal antibodies increased the amount of sLR11 released from the cells. Likewise, the PMA-stimulated release of sLR11 increased in THP-1 cells transfected with CD9-targeted shRNAs, which was negated by treatment with the metalloproteinase inhibitor GM6001. These results suggest that the tetraspanin CD9 modulates the ADAM17-mediated shedding of LR11 in various leukemia cell lines and that the association between LR11 and CD9 on the cell surface has an important role in the ADAM17-mediated shedding mechanism.

Indexed as

ADAM17 ProteinADAM ProteinsCell Line, TumorHumansLDL-Receptor Related ProteinsLeukocytesMacrophagesMembrane Transport ProteinsProteolysisTetraspanin 29ADAM17 ProteinADAM17 protein, humanADAM ProteinsLDL-Receptor Related ProteinsMembrane Transport ProteinsSORL1 protein, humanTetraspanin 29

Identifiers

PMID24699135
PMCPMC3944444
OpenAlexW2024341936

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.