Evidence map›Paper›PMID 29555469›Full record

ArticleBiochemical pharmacology2018

p23 protects the human aryl hydrocarbon receptor from degradation via a heat shock protein 90-independent mechanism.

Beverly Pappas, Yujie Yang, Yu Wang, Kyung Kim, Hee Jae Chung, Michael Cheung, Katie Ngo, Annie Shinn, William K Chan

Abstract read
In one paragraph

Article in Biochemical pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.5field-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

33 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  10. Metabolic reprogramming in efferocytosis.Frontiers in cell and developmental biology · 2025
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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

9 authors at 1 institution in 1 country.

Beverly PappasDepartment of Pharmaceutics & Medicinal Chemistry, Thomas J. Long School of Pharmacy & Health Sciences, University of the Pacific, Stockton, CA 95211, United States.
Yujie YangDepartment of Pharmaceutics & Medicinal Chemistry, Thomas J. Long School of Pharmacy & Health Sciences, University of the Pacific, Stockton, CA 95211, United States.
Yu WangDepartment of Pharmaceutics & Medicinal Chemistry, Thomas J. Long School of Pharmacy & Health Sciences, University of the Pacific, Stockton, CA 95211, United States.
Kyung KimDepartment of Pharmaceutics & Medicinal Chemistry, Thomas J. Long School of Pharmacy & Health Sciences, University of the Pacific, Stockton, CA 95211, United States.
Hee Jae ChungDepartment of Pharmaceutics & Medicinal Chemistry, Thomas J. Long School of Pharmacy & Health Sciences, University of the Pacific, Stockton, CA 95211, United States.
Michael CheungDepartment of Pharmaceutics & Medicinal Chemistry, Thomas J. Long School of Pharmacy & Health Sciences, University of the Pacific, Stockton, CA 95211, United States.
Katie NgoDepartment of Pharmaceutics & Medicinal Chemistry, Thomas J. Long School of Pharmacy & Health Sciences, University of the Pacific, Stockton, CA 95211, United States.
Annie ShinnDepartment of Pharmaceutics & Medicinal Chemistry, Thomas J. Long School of Pharmacy & Health Sciences, University of the Pacific, Stockton, CA 95211, United States.
William K ChanDepartment of Pharmaceutics & Medicinal Chemistry, Thomas J. Long School of Pharmacy & Health Sciences, University of the Pacific, Stockton, CA 95211, United States. Electronic address: wchan@pacific.edu.
University of the Pacific · US

Funding

Investigating the molecular mechanisms in controlling the aryl hydrocarbon receptor protein levelsR15ES023104 · NIEHS · UNIVERSITY OF THE PACIFIC-STOCKTON · PI CHAN, WILLIAM K · 2014 to 2019
$750k
NIEHS NIH HHS R15 ES023104
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AHR) is a ligand-activated signaling molecule which is involved in diverse biological functions ranging from cancer metastasis to immune regulation. This receptor forms a cytoplasmic complex with Hsp90, p23, and XAP2. We have previously reported that down-regulation of p23 triggers degradation of the AHR protein, uncovering a potentially dynamic event which controls the cellular AHR levels without ligand treatment. Here we investigate the underlying mechanisms for this p23 effect using wild-type HeLa and the p23 knockdown HeLa cells. Reduction of the Hsp90 and XAP2 contents, however, did not affect the AHR protein levels, implying that this p23 effect on AHR is more than just alteration of the cytoplasmic complex dynamics. Association of p23 with Hsp90 is not important for the modulation of the AHR levels since exogenous expression of p23 mutants with modest Hsp90-binding affinity effectively restored the AHR message and protein levels. The protein folding property of p23 which resides at the terminal 50-amino acid region is not involved for this p23 effect. Results from our interaction study using the affinity purified thioredoxin fusion proteins and GST fusion proteins showed that p23 directly interacts with AHR and the interaction surface lies within AHR amino acid 1-216 and p23 amino acid 1-110. Down-regulation of the p23 protein content promotes the ubiquitination of AHR, indicating that p23 protects AHR from the ubiquitin-meditated protein degradation.

Indexed as

Basic Helix-Loop-Helix ProteinsDNA-Binding ProteinsGene Expression RegulationGene Knockdown TechniquesHeLa CellsHSP90 Heat-Shock ProteinsHumansProtein BindingReceptors, Aryl HydrocarbonRecombinant ProteinsAHR protein, humanBasic Helix-Loop-Helix ProteinsDNA-Binding ProteinsHSP90 Heat-Shock Proteinsprotein p23Receptors, Aryl HydrocarbonRecombinant ProteinsAHRARNTAryl hydrocarbon receptorHsp90p23Protein degradation

Identifiers

PMID29555469
PMCPMC5960609
OpenAlexW2791081108

What OpenQuestion holds

Textmetadata
LicenceTDM
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.