Evidence map›Paper›PMID 34286109›Full record

ArticleBiochemistry and biophysics reports2021

A potent endocytosis inhibitor Ikarugamycin up-regulates TNF production.

Ai Minamidate, Michio Onizawa, Chikako Saito, Rie Hikichi, Tomoaki Mochimaru, Mai Murakami, Chiharu Sakuma, Takehito Asakawa, Yuichi Hiraoka, Shigeru Oshima and 5 more

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

Article in Biochemistry and biophysics reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Ai MinamidateDepartment of Gastroenterology and Hepatology, Tokyo Medical and Dental University, Tokyo, Japan.
Michio OnizawaDepartment of Gastroenterology and Hepatology, Tokyo Medical and Dental University, Tokyo, Japan.
Chikako SaitoDepartment of Gastroenterology and Hepatology, Fukushima Medical University, Fukushima, Japan.
Rie HikichiDepartment of Gastroenterology and Hepatology, Fukushima Medical University, Fukushima, Japan.
Tomoaki MochimaruDepartment of Gastroenterology and Hepatology, Fukushima Medical University, Fukushima, Japan.
Mai MurakamiDepartment of Gastroenterology and Hepatology, Fukushima Medical University, Fukushima, Japan.
Chiharu SakumaDepartment of Gastroenterology and Hepatology, Fukushima Medical University, Fukushima, Japan.
Takehito AsakawaDepartment of Gastroenterology and Hepatology, Tokyo Medical and Dental University, Tokyo, Japan.
Yuichi HiraokaLaboratory of Molecular Neuroscience, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Shigeru OshimaDepartment of Gastroenterology and Hepatology, Tokyo Medical and Dental University, Tokyo, Japan.
Takashi NagaishiDepartment of Gastroenterology and Hepatology, Tokyo Medical and Dental University, Tokyo, Japan.
Kiichiro TsuchiyaDepartment of Gastroenterology and Hepatology, Tokyo Medical and Dental University, Tokyo, Japan.
Hiromasa OhiraDepartment of Gastroenterology and Hepatology, Fukushima Medical University, Fukushima, Japan.
Ryuichi OkamotoDepartment of Gastroenterology and Hepatology, Tokyo Medical and Dental University, Tokyo, Japan.
Mamoru WatanabeDepartment of Gastroenterology and Hepatology, Tokyo Medical and Dental University, Tokyo, Japan.
Tokyo Medical and Dental University · JPFukushima Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ikarugamycin (IK) is an antibiotic which has been reported to have a variety of functions, such as inhibition of clathrin-mediated endocytosis (CME), anti-tumor effects and regulation of the immune system. Whether IK influences cytokine production is poorly understood. We have investigated the relationship between IK and production of tumor necrosis factor-α (TNF). TNF plays a pivotal role in pathogenesis of many diseases. Although the dynamics of soluble TNF (sTNF) has been widely explored so far, the functions of the membrane form of TNF (mTNF) have not been fully elucidated. We demonstrated that IK increases the amount of mTNF and prolongs the duration of TNF expression. This effect is unrelated to the shedding activity of disintegrin and metalloproteinase domain-containing protein 17 (ADAM 17). Our results revealed that there is a mechanism to terminate inflammation at the cellular level which IK dysregulates. Furthermore, IK can be a tool to study TNF signaling due to its effect of increasing mTNF expression.

Indexed as

ADAM 17, disintegrin and metalloproteinase domain-containing protein 17CME, clathrin-mediated endocytosisEndocytosisIkarugamycinIK, ikarugamycinInflammationLPS, lipopolysaccharidemTNF, membrane form of TNFsTNF, soluble TNFTAPI-1, TNF alpha processing inhibitor-1TNFTNFR, TNF receptorTNF, tumor necrosis factor-α

Identifiers

PMID34286109
PMCPMC8274290
OpenAlexW3178229928

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.