Evidence map›Paper›PMID 33168631›Full record

ArticleThe Journal of biological chemistry

LY6D-induced macropinocytosis as a survival mechanism of senescent cells.

Taiki Nagano, Tetsushi Iwasaki, Kengo Onishi, Yuto Awai, Anju Terachi, Shione Kuwaba, Shota Asano, Ryoko Katasho, Kiyoko Nagai, Akio Nakashima and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. An Indocyanine Green-Based Nanoprobe for In Vivo Detection of Cellular Senescence.Angewandte Chemie (International ed. in English) · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

12 authors at 1 institution in 1 country.

Taiki NaganoBiosignal Research Center, Kobe University, Kobe, Japan.
Tetsushi IwasakiBiosignal Research Center, Kobe University, Kobe, Japan; Department of Biology, Graduate School of Science, Kobe University, Kobe, Japan; Department of Biology, Faculty of Science, Kobe University, Kobe, Japan.
Kengo OnishiDepartment of Biology, Graduate School of Science, Kobe University, Kobe, Japan.
Yuto AwaiDepartment of Biology, Faculty of Science, Kobe University, Kobe, Japan.
Anju TerachiDepartment of Biology, Graduate School of Science, Kobe University, Kobe, Japan.
Shione KuwabaDepartment of Biology, Faculty of Science, Kobe University, Kobe, Japan.
Shota AsanoDepartment of Biology, Graduate School of Science, Kobe University, Kobe, Japan.
Ryoko KatashoDepartment of Biology, Graduate School of Science, Kobe University, Kobe, Japan.
Kiyoko NagaiBiosignal Research Center, Kobe University, Kobe, Japan.
Akio NakashimaBiosignal Research Center, Kobe University, Kobe, Japan; Department of Bioresource Science, Graduate School of Agricultural Science, Kobe University, Kobe, Japan.
Ushio KikkawaBiosignal Research Center, Kobe University, Kobe, Japan; Department of Bioresource Science, Graduate School of Agricultural Science, Kobe University, Kobe, Japan.
Shinji KamadaBiosignal Research Center, Kobe University, Kobe, Japan; Department of Biology, Graduate School of Science, Kobe University, Kobe, Japan; Department of Biology, Faculty of Science, Kobe University, Kobe, Japan. Electronic address: skamada@kobe-u.ac.jp.
Kobe University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although senescent cells display various morphological changes including vacuole formation, it is still unclear how these processes are regulated. We have recently identified the gene, lymphocyte antigen 6 complex, locus D (LY6D), to be upregulated specifically in senescent cells. LY6D is a glycosylphosphatidylinositol-anchored cell-surface protein whose function remains unknown. Here, we analyzed the functional relationship between LY6D and the senescence processes. We found that overexpression of LY6D induced vacuole formation and knockdown of LY6D suppressed the senescence-associated vacuole formation. The LY6D-induced vacuoles were derived from macropinocytosis, a distinct form of endocytosis. Furthermore, Src family kinases and Ras were found to be recruited to membrane lipid rafts in an LY6D-dependent manner, and inhibition of their activity impaired the LY6D-induced macropinocytosis. Finally, reduction of senescent-cell survival induced by glutamine deprivation was recovered by albumin supplementation to the culture media in an LY6D-dependent manner. Because macropinocytosis acts as an amino acid supply route, these results suggest that LY6D-mediated macropinocytosis contributes to senescent-cell survival through the incorporation of extracellular nutrients.

Indexed as

Cellular SenescencePinocytosisCell Adhesion MoleculesCell Line, TumorCell SurvivalGPI-Linked ProteinsHumansras Proteinssrc-Family KinasesCell Adhesion MoleculesGPI-Linked ProteinsLY6D protein, humanras Proteinssrc-Family Kinasescellular senescence/endocytosislipid raftLY6DmacropinocytosisRas proteinvacuole

Identifiers

PMID33168631
PMCPMC7948989
OpenAlexW3102542332

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.