Evidence map›Paper›PMID 30361559›Full record

ArticleScientific reports2018

Ptf1a inactivation in adult pancreatic acinar cells causes apoptosis through activation of the endoplasmic reticulum stress pathway.

Morito Sakikubo, Kenichiro Furuyama, Masashi Horiguchi, Shinichi Hosokawa, Yoshiki Aoyama, Kunihiko Tsuboi, Toshihiko Goto, Koji Hirata, Toshihiko Masui, Yuval Dor and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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

14 authors at 3 institutions in 1 country.

Morito SakikuboDepartment of Hepato-Biliary-Pancreatic Surgery and Transplantation, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kenichiro FuruyamaDepartment of Hepato-Biliary-Pancreatic Surgery and Transplantation, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID http://orcid.org/0000-0003-4878-2841
Masashi HoriguchiDepartment of Hepato-Biliary-Pancreatic Surgery and Transplantation, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Shinichi HosokawaDepartment of Hepato-Biliary-Pancreatic Surgery and Transplantation, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yoshiki AoyamaDepartment of Hepato-Biliary-Pancreatic Surgery and Transplantation, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kunihiko TsuboiDepartment of Hepato-Biliary-Pancreatic Surgery and Transplantation, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Toshihiko GotoDepartment of Hepato-Biliary-Pancreatic Surgery and Transplantation, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Koji HirataDepartment of Hepato-Biliary-Pancreatic Surgery and Transplantation, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Toshihiko MasuiDepartment of Hepato-Biliary-Pancreatic Surgery and Transplantation, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yuval DorDepartment of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Tomoyuki FujiyamaDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Mikio HoshinoDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Shinji UemotoDepartment of Hepato-Biliary-Pancreatic Surgery and Transplantation, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yoshiya KawaguchiDepartment of Clinical Application, Center for iPS cell Research and Application, Kyoto, Japan. yoshiyak@cira.kyoto-u.ac.jp.
Kyoto University · JPNational Center of Neurology and Psychiatry · JPUniversity of Tsukuba · JP

Funding

Japan Society for the Promotion of Science (JSPS) LS063
6 · The paper itself

Abstract

Pancreas transcription factor 1 subunit alpha (PTF1A) is one of the key regulators in pancreatogenesis. In adults, it transcribes digestive enzymes, but its other functions remain largely unknown. Recent conditional knockout studies using Ptf1a

Indexed as

ApoptosisEndoplasmic Reticulum StressAcinar CellsActivating Transcription Factor 6AnimalsCell LineageEndoplasmic ReticulumMice, KnockoutPancreas, ExocrineRNA, MessengerRNA SplicingTranscription Factor CHOPTranscription FactorsUp-RegulationX-Box Binding Protein 1Activating Transcription Factor 6Atf6 protein, mouseRNA, MessengerTranscription Factor CHOPtranscription factor PTF1Transcription FactorsX-Box Binding Protein 1Xbp1 protein, mouse

Identifiers

PMID30361559
PMCPMC6202406
OpenAlexW2896724954

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.