Evidence map›Paper›PMID 28174748›Full record

ArticleCellular and molecular gastroenterology and hepatology2016

Requirement of Gα

Noboru Watanabe, Hirosato Mashima, Kouichi Miura, Takashi Goto, Makoto Yoshida, Akiteru Goto, Hirohide Ohnishi

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. The role of GαBiochemistry and biophysics reports · 2018
    Article
  12. Article
  13. Transcriptional Regulation by ATOH1 and its Target SPDEF in the Intestine.Cellular and molecular gastroenterology and hepatology · 2017
    Article
  14. Intestinal GPCRs Control Paneth Cell Maturation and Susceptibility to Experimental Colitis.Cellular and molecular gastroenterology and hepatology · 2016
    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

7 authors at 2 institutions in 1 country.

Noboru WatanabeDepartment of Gastroenterology and Hepato-Biliary-Pancreatology, Akita University Graduate School of Medicine, Akita, Japan.
Hirosato MashimaDepartment of Gastroenterology and Hepato-Biliary-Pancreatology, Akita University Graduate School of Medicine, Akita, Japan; Department of Gastroenterology, Saitama Medical Center, Jichi Medical University, Saitama, Japan.
Kouichi MiuraDepartment of Gastroenterology and Hepato-Biliary-Pancreatology, Akita University Graduate School of Medicine, Akita, Japan.
Takashi GotoDepartment of Gastroenterology and Hepato-Biliary-Pancreatology, Akita University Graduate School of Medicine, Akita, Japan.
Makoto YoshidaDepartment of Pathology, Akita University Graduate School of Medicine, Akita, Japan.
Akiteru GotoDepartment of Pathology, Akita University Graduate School of Medicine, Akita, Japan.
Hirohide OhnishiDepartment of Gastroenterology and Hepato-Biliary-Pancreatology, Akita University Graduate School of Medicine, Akita, Japan.
Akita University · JPJichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsProliferation, differentiation, and morphogenesis of the intestinal epithelium are tightly regulated by a number of molecular pathways. Coordinated action of intestine is achieved by gastrointestinal hormones, most of which exert these actions through G-protein-coupled receptors. We herein investigated the role of Gα

methodsIntestinal tissues from control (

resultsPaneth cells were enlarged, increased in number, and mislocalized in Int-Gq/G11 DKO small intestine. Paneth cells also reacted with PAS and Muc2 antibody, indicating an intermediate character of Paneth and goblet cells. The nuclear β-catenin, T-cell factor 1, and Sox9 expression were reduced severely in the crypt base of Int-Gq/G11 DKO intestine. Proliferation was activated in the crypt base and apoptosis was enhanced along the crypt. Int-Gq/G11 DKO mice were susceptible to DSS colitis. Proliferation was inhibited in the crypt of unaffected and regenerative areas. Cystic crypts, periodic acid-Schiff-positive cells, and Muc2-positive cells were unusually observed in the ulcerative region.

conclusionsThe Gα

Indexed as

Atoh1, atonal homolog 1BrdU, bromodeoxyuridineDefa1, defensin α1Dll1, delta-like 1DSS, dextran sodium sulfateFGF, fibroblast growth factorFzd, frizzledGna11GnaqHes, hairy/enhancer of splitIEC, intestinal epithelial cellIhh, Indian hedgehogIntermediate CellmRNA, messenger RNANICD, Notch intracellular cytoplasmic domainPaneth CellPAS, periodic acid–SchiffPCR, polymerase chain reactionPKC, protein kinase CqPCR, quantitative real-time polymerase chain reactionTcf, T-cell factorTEM, transmission electron micrographTUNEL, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelingWnt

Identifiers

PMID28174748
PMCPMC5247319
OpenAlexW2515787642

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.