Evidence map›Paper›PMID 25231987›Full record

ArticleThe Journal of biological chemistry2014

Exposure of phosphatidylserine by Xk-related protein family members during apoptosis.

Jun Suzuki, Eiichi Imanishi, Shigekazu Nagata

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

116 citing papers in PubMed, 174 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Brain Sphingolipid and Phospholipid Levels Are Altered in XK Disease.Movement disorders : official journal of the Movement Disorder Society · 2026
    Article
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  12. Review
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  16. A cell-based scrambling assay reveals the phospholipid headgroup preference of TMEM16F on the plasma membrane.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Review
  18. Article
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56 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Jun SuzukiDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Sakyo-ku, Kyoto, Kyoto 606-8501, Japan.
Eiichi ImanishiDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Sakyo-ku, Kyoto, Kyoto 606-8501, Japan.
Shigekazu NagataDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Sakyo-ku, Kyoto, Kyoto 606-8501, Japan. Electronic address: snagata@mfour.med.kyoto-u.ac.jp.
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptotic cells expose phosphatidylserine (PtdSer) on their surface as an "eat me" signal. Mammalian Xk-related (Xkr) protein 8, which is predicted to contain six transmembrane regions, and its Caenorhabditis elegans homolog CED-8 promote apoptotic PtdSer exposure. The mouse and human Xkr families consist of eight and nine members, respectively. Here, we found that mouse Xkr family members, with the exception of Xkr2, are localized to the plasma membrane. When Xkr8-deficient cells, which do not expose PtdSer during apoptosis, were transformed by Xkr family members, the transformants expressing Xkr4, Xkr8, or Xkr9 responded to apoptotic stimuli by exposing cell surface PtdSer and were efficiently engulfed by macrophages. Like Xkr8, Xkr4 and Xkr9 were found to possess a caspase recognition site in the C-terminal region and to require its direct cleavage by caspases for their function. Site-directed mutagenesis of the amino acid residues conserved among CED-8, Xkr4, Xkr8, and Xkr9 identified several essential residues in the second transmembrane and second cytoplasmic regions. Real time PCR analysis indicated that unlike Xkr8, which is ubiquitously expressed, Xkr4 and Xkr9 expression is tissue-specific.

Indexed as

ApoptosisAmino Acid SequenceAnimalsApoptosis Regulatory ProteinsBinding SitesCell MembraneConserved SequenceFemaleHEK293 CellsHumansJurkat CellsMaleMembrane ProteinsMice, KnockoutMolecular Sequence DataOrgan SpecificityApoptosis Regulatory ProteinsMembrane ProteinsPhosphatidylserinesXkr4 protein, mouseXkr8 protein, mouseXkr9 protein, mouseApoptosisCaspaseEngulfmentMacrophagePhosphatidylserineScramblaseSite-directed Mutagenesis

Identifiers

PMID25231987
PMCPMC4215210
OpenAlexW2113256330

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.