Evidence map›Paper›PMID 34188179›Full record

ArticleExperimental & molecular medicine2021

Disruption of nucleocytoplasmic trafficking as a cellular senescence driver.

Ji-Hwan Park, Sung Jin Ryu, Byung Ju Kim, Hyun-Ji Cho, Chi Hyun Park, Hyo Jei Claudia Choi, Eun-Jin Jang, Eun Jae Yang, Jeong-A Hwang, Seung-Hwa Woo and 15 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. An Indocyanine Green-Based Nanoprobe for In Vivo Detection of Cellular Senescence.Angewandte Chemie (International ed. in English) · 2024
    Article
  17. Review
  18. Review
  19. Review
  20. 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

25 authors at 7 institutions in 2 countries.

Ji-Hwan Park *Korea Bioinformation Center, Korea Research Institute of Bioscience & Biotechnology, Daejeon, 34141, Republic of Korea.
Sung Jin Ryu *Samsung Advanced Institute of Technology, Samsung Electronics Co., Ltd., Suwon, 16677, Republic of Korea.
Byung Ju Kim *Well Aging Research Center, Division of Biotechnology, DGIST, Daegu, 42988, Republic of Korea.
Hyun-Ji ChoWell Aging Research Center, Division of Biotechnology, DGIST, Daegu, 42988, Republic of Korea.
Chi Hyun ParkDepartment of Computer Science and Engineering, Kangwon National University, Chuncheon, 24341, Republic of Korea.
Hyo Jei Claudia ChoiSamsung Advanced Institute of Technology, Samsung Electronics Co., Ltd., Suwon, 16677, Republic of Korea.
Eun-Jin JangWell Aging Research Center, Division of Biotechnology, DGIST, Daegu, 42988, Republic of Korea.
Eun Jae YangDepartment of New Biology, DGIST, Daegu, 42988, Republic of Korea.
Jeong-A HwangDepartment of New Biology, DGIST, Daegu, 42988, Republic of Korea.
Seung-Hwa WooDepartment of New Biology, DGIST, Daegu, 42988, Republic of Korea.
Jun Hyung LeeDepartment of New Biology, DGIST, Daegu, 42988, Republic of Korea.
Ji Hwan ParkDepartment of New Biology, DGIST, Daegu, 42988, Republic of Korea.
Kyung-Mi ChoiDepartment of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea.
Young-Yon KwonDepartment of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea.
Cheol-Koo LeeDepartment of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea.
Joon Tae ParkDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon, 22012, Republic of Korea.
Sung Chun ChoWell Aging Research Center, Division of Biotechnology, DGIST, Daegu, 42988, Republic of Korea.
Yun-Il LeeWell Aging Research Center, Division of Biotechnology, DGIST, Daegu, 42988, Republic of Korea.
Sung Bae LeeDepartment of Brain & Cognitive Science, DGIST, Daegu, 42988, Republic of Korea.ORCID http://orcid.org/0000-0002-8980-6769
Jeong A HanDepartment of Biochemistry and Molecular Biology, Kangwon National University School of Medicine, Chuncheon, 24341, Republic of Korea.
Kyung A ChoDepartment of Biochemistry, Chonnam National University, Medical School, Gwangju, 61469, Republic of Korea.
Min-Sik KimDepartment of New Biology, DGIST, Daegu, 42988, Republic of Korea. mkim@dgist.ac.kr.ORCID http://orcid.org/0000-0001-7317-5360
Daehee HwangDepartment of Biological Sciences, Seoul National University, Seoul, 08826, Republic of Korea. daehee@snu.ac.kr.
Young-Sam LeeWell Aging Research Center, Division of Biotechnology, DGIST, Daegu, 42988, Republic of Korea. lee.youngsam@dgist.ac.kr.
Sang Chul ParkWell Aging Research Center, Division of Biotechnology, DGIST, Daegu, 42988, Republic of Korea. scpark@snu.ac.kr.
Daegu Gyeongbuk Institute of Science and Technology · KRIncheon National University · KRKorea University · KRChonnam National University · KRKangwon National University · KRSamsung (South Korea) · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Senescent cells exhibit a reduced response to intrinsic and extrinsic stimuli. This diminished reaction may be explained by the disrupted transmission of nuclear signals. However, this hypothesis requires more evidence before it can be accepted as a mechanism of cellular senescence. A proteomic analysis of the cytoplasmic and nuclear fractions obtained from young and senescent cells revealed disruption of nucleocytoplasmic trafficking (NCT) as an essential feature of replicative senescence (RS) at the global level. Blocking NCT either chemically or genetically induced the acquisition of an RS-like senescence phenotype, named nuclear barrier-induced senescence (NBIS). A transcriptome analysis revealed that, among various types of cellular senescence, NBIS exhibited a gene expression pattern most similar to that of RS. Core proteomic and transcriptomic patterns common to both RS and NBIS included upregulation of the endocytosis-lysosome network and downregulation of NCT in senescent cells, patterns also observed in an aging yeast model. These results imply coordinated aging-dependent reduction in the transmission of extrinsic signals to the nucleus and in the nucleus-to-cytoplasm supply of proteins/RNAs. We further showed that the aging-associated decrease in Sp1 transcription factor expression was critical for the downregulation of NCT. Our results suggest that NBIS is a modality of cellular senescence that may represent the nature of physiological aging in eukaryotes.

Indexed as

Cellular SenescenceProteomicsCell NucleusDown-Regulation

Identifiers

PMID34188179
PMCPMC8257587
OpenAlexW3175613702

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.