Evidence map›Paper›PMID 33319072›Full record

ArticleBiochemistry and biophysics reports2020

Mint3 is dispensable for pancreatic and kidney functions in mice.

Yoohwa Chung, Yurika Saitoh, Tetsuro Hayashi, Yuya Fukui, Nobuo Terada, Motoharu Seiki, Yoshinori Murakami, Takeharu Sakamoto

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochemistry and biophysics reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 55% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

8 authors at 4 institutions in 1 country.

Yoohwa ChungDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, 108-8639, Japan.
Yurika SaitohCenter for Medical Education, Teikyo University of Science, Adachi-ku, Tokyo, 120-0045, Japan.
Tetsuro HayashiDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, 108-8639, Japan.
Yuya FukuiDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, 108-8639, Japan.
Nobuo TeradaDivision of Health Sciences, Shinshu University Graduate School of Medicine, Matsumoto, Nagano, 390-8621, Japan.
Motoharu SeikiDivision of Cancer Cell Research, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, 108-8639, Japan.
Yoshinori MurakamiDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, 108-8639, Japan.
Takeharu SakamotoDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo, 108-8639, Japan.
The University of Tokyo · JPKanazawa University · JPShinshu University · JPTeikyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Munc-18 interacting protein 3 (Mint3) is an activator of hypoxia-inducible factor-1 in cancer cells, macrophages, and cancer-associated fibroblasts under pathological conditions. However, exactly which cells highly express Mint3 in vivo and whether Mint3 depletion affects their physiological functions remain unclear. Here, we surveyed mouse tissues for specific expression of Mint3 by comparing Mint3 expression in wild-type and Mint3-knockout mice. Interestingly, immunohistochemical analyses revealed that Mint3 was highly expressed in islet cells of the pancreas, distal tubular epithelia of the kidney, choroid plexus ependymal cells of the cerebrum, medullary cells of the adrenal gland, and epithelial cells of the seminal gland. We also studied whether Mint3 depletion affects the physiological functions of the islets and kidneys. Mint3-knockout mice did not show any abnormalities in glucose-tolerance and urine-biochemical tests, indicating that Mint3 depletion was compensated for in these organs. Thus, loss of Mint3 might be compensated in the islets and kidneys under physiological conditions in mice.

Indexed as

ImmunohistochemistryIsletKidneyKnockout mouseMint3

Identifiers

PMID33319072
PMCPMC7725678
OpenAlexW3112087557

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.