Evidence map›Paper›PMID 34855082›Full record

ArticleBulletin of experimental biology and medicine2021

Role of JNK in the Regulation of Xenobiotic Metabolizing Function of Hepatocytes.

O S Bryushinina, Yu G Zyuz'kova, E A Yanovskaya, N Y Abdrashitova, G A Frelikh, A P Lakeev, D V Tsuran, V V Udut, G N Zyuz'kov

Abstract read
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In one paragraph

Article in Bulletin of experimental biology and medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 3 institutions in 1 country.

O S BryushininaE. D. Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
Yu G Zyuz'kovaE. D. Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
E A YanovskayaE. D. Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
N Y AbdrashitovaE. D. Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
G A FrelikhE. D. Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
A P LakeevE. D. Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
D V TsuranE. D. Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
V V UdutE. D. Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
G N Zyuz'kovE. D. Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia. zgn@pharmso.ru.
Research Institute of Pharmacology and Regenerative Medicine named ED Goldberg · RUTomsk National Research Medical Center · RURussian Academy of Sciences · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We studied the role of JNK in the regulation of the metabolism of xenobiotic venlafaxine by liver cells under in vitro conditions. The inhibitory role of this protein kinase in the biotransformation of this psychotropic agent by hepatocytes was demonstrated. JNK inhibitor added to the liver homogenate containing antidepressant enhanced and accelerated the formation of the only pharmacologically active venlafaxine metabolite O-desmethylvenlafaxine in the cell suspension. The results show the promise of studying modifiers of activity of intracellular signaling molecules (in particular, mitogen-activated protein kinases) to develop a fundamentally new approach to control the transformation of xenobiotics and to create a new class of pharmaceutical, target regulators of drugs metabolism.

Indexed as

AnimalsBiotransformationDesvenlafaxine SuccinateDose-Response Relationship, DrugHepatocytesJNK Mitogen-Activated Protein KinasesLiverMAP Kinase Signaling SystemMiceMice, Inbred C57BLOximesQuinoxalinesSignal TransductionVenlafaxine HydrochlorideXenobiotics11H-indeno(1,2-b)quinoxalin-11-one oximeDesvenlafaxine SuccinateJNK Mitogen-Activated Protein KinasesOximesQuinoxalinesVenlafaxine HydrochlorideXenobioticsintracellular signal transductionJNKmetabolismP450xenobiotics

Identifiers

PMID34855082
OpenAlexW3215933831

What OpenQuestion holds

Textmetadata
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.