Evidence map›Paper›PMID 38997262›Full record

ArticleCell death discovery2024

PTBP1 protects Y RNA from cleavage leading to its apoptosis-specific degradation.

Takeshi Kamakura, Kazuaki Kameda, Masahiko Manabe, Kan Torii, Yuki Sugiura, Seiko Ito, Shunya Nakayama, Takanobu Shimizu, Etsuko Nagashima, Kosuke Kamiya and 5 more

Abstract read
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

15 authors.

Takeshi Kamakura *Department of Regulation of Infectious Cancer, Research Institute of Microbiological Disease, Osaka University, Suita, Osaka, 565-0871, Japan.ORCID http://orcid.org/0009-0002-4523-8971
Kazuaki Kameda *Department of Innovative Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.ORCID http://orcid.org/0000-0001-8418-5118
Masahiko Manabe *Department of Innovative Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Kan Torii *Department of Regulation of Infectious Cancer, Research Institute of Microbiological Disease, Osaka University, Suita, Osaka, 565-0871, Japan.
Yuki SugiuraMulti-Omics Platform, Center for Cancer Immunotherapy and Immunobiology, Kyoto University, Kyoto, 606-8501, Japan.
Seiko ItoDepartment of Innovative Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Shunya NakayamaDepartment of Innovative Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Takanobu ShimizuDepartment of Innovative Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Etsuko NagashimaDepartment of Innovative Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Kosuke KamiyaDepartment of Innovative Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Masahiro OkaDepartment of Regulation of Infectious Cancer, Research Institute of Microbiological Disease, Osaka University, Suita, Osaka, 565-0871, Japan.
Masafumi TanakaDepartment of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Motoyuki OtsukaDepartment of Gastroenterology and Hepatology, Academic Field of Medicine, Density and Pharmaceutical Sciences, Okayama University, Okayama, 700-8558, Japan.
Masato OhtsukaDepartment of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Ai KotaniDepartment of Regulation of Infectious Cancer, Research Institute of Microbiological Disease, Osaka University, Suita, Osaka, 565-0871, Japan. aikotani@k-lab.jp.ORCID http://orcid.org/0000-0002-0976-8687

Funding

Japan Agency for Medical Research and Development (AMED) 23ama221213h0002Japan Agency for Medical Research and Development (AMED) 23ama221215h0002Japan Agency for Medical Research and Development (AMED) 23fk0210133h0001MEXT | Japan Society for the Promotion of Science (JSPS) JP23H02940MEXT | JST | Core Research for Evolutional Science and Technology (CREST) JPMJCR19H5
6 · The paper itself

Abstract

Some RNAs such as 28S rRNA, U1 small nuclear RNA (snRNA), and Y RNAs are known to be cleaved during apoptosis. The underlying mechanism, functions, and biological significance of RNA degradation in apoptosis remain elusive. Y RNAs are non-coding RNAs widely conserved from bacteria to mammals, and are major components of Ro ribonucleoprotein (RNP) complexes which contain the 60 kDa Ro protein (SS-A) and the 50 kDa La protein (SS-B). The autoantigenic Ro and La proteins were identified by autoantibodies present in the sera from patients with Systemic lupus erythematosus (SLE) and Sjögren's syndrome (SjS). We previously identified novel, functional small RNAs named AGO-taxis small RNAs (ASRs) that are specifically bound to Argonaute protein 1 (AGO1), which are processed from Y RNAs. Cell-free analysis combined with fractionation methods revealed that the apoptosis-specific biogenesis of ASRs or cleavage of Y RNA was induced by truncation of polypyrimidine tract-binding protein 1 (PTBP1), which is an endoribonuclease inhibitor of Y RNAs by caspase 3. Caspase 3-resistant PTBP1 mutant protected cleavage of Y RNAs in apoptosis induced by staurosporine. Furthermore, caspase 3-resistant PTBP1 mutant knock-in mice showed elevated cytokines, dysregulation of the germinal center formation compared to the wild-type mice at LPS stimulation, and high positivity of antinuclear antibody. Those results suggest that cleavage of Y RNAs or biogenesis of ASR during apoptosis has critical biological functions and their deregulation result in immune dysregulation and the formation of autoantibody, possibly leading to the development of autoimmune diseases.

Identifiers

PMID38997262
PMCPMC11245482

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.