Evidence map›Paper›PMID 35987969›Full record

ArticleScientific reports2022

Deubiquitinase USP19 extends the residual enzymatic activity of phenylalanine hydroxylase variants.

Neha Sarodaya, Apoorvi Tyagi, Hyun-Jin Kim, Ju-Seop Kang, Vijai Singh, Seok-Ho Hong, Woo Jin Kim, Kye-Seong Kim, Suresh Ramakrishna

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. [Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024
    Article
  2. 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

9 authors at 4 institutions in 2 countries.

Neha Sarodaya *Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, South Korea.
Apoorvi Tyagi *Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, South Korea.
Hyun-Jin KimDepartment of Pharmacology, College of Medicine, Hanyang University, Seoul, South Korea.
Ju-Seop KangDepartment of Pharmacology, College of Medicine, Hanyang University, Seoul, South Korea.
Vijai SinghDepartment of Biosciences, School of Science, Indrashil University, Rajpur, Mehsana, Gujarat, India.
Seok-Ho HongDepartment of Internal Medicine, School of Medicine, Kangwon National University, Chuncheon, South Korea.
Woo Jin KimDepartment of Internal Medicine and Environmental Health Center, Kangwon National University Hospital, Kangwon National University School of Medicine, Chuncheon, South Korea.
Kye-Seong KimGraduate School of Biomedical Science and Engineering, Hanyang University, Seoul, South Korea. ks66kim@hanyang.ac.kr.
Suresh RamakrishnaGraduate School of Biomedical Science and Engineering, Hanyang University, Seoul, South Korea. suri28@hanyang.ac.kr.
Hanyang University · KRIndrashil University · INKangwon National University · KRKangwon National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phenylalanine hydroxylase (PAH) is a key enzyme in mammals that maintains the phenylalanine (Phe) concentration at an appropriate physiological level. Some genetic mutations in the PAH gene lead to destabilization of the PAH enzyme, leading to phenylketonuria (PKU). Destabilized PAH variants can have a certain amount of residual enzymatic activity that is sufficient for metabolism of Phe. However, accelerated degradation of those variants can lead to insufficient amounts of cellular PAH protein. The optimal protein level of PAH in cells is regulated by a balancing act between E3 ligases and deubiquitinating enzymes (DUBs). In this work, we analyzed the protein expression and stability of two PKU-linked PAH protein variants, R241C and R243Q, prevalent in the Asian population. We found that the tested PAH variants were highly ubiquitinated and thus targeted for rapid protein degradation. We demonstrated that USP19, a DUB that interacts with both PAH variants, plays a regulatory role by extending their half-lives. The deubiquitinating activity of USP19 prevents protein degradation and increases the abundance of both PAH protein variants. Thus, our study reveals a novel mechanism by which deubiquitinating activity of USP19 extends the residual enzymatic activity of PAH variants.

Indexed as

Deubiquitinating EnzymesEndopeptidasesPhenylalanine HydroxylasePhenylketonuriasAnimalsAsian PeopleDisease ProgressionHumansMammalsMutationPhenylalanineDeubiquitinating EnzymesEndopeptidasesPhenylalaninePhenylalanine HydroxylaseUSP19 protein, human

Identifiers

PMID35987969
PMCPMC9392723
OpenAlexW4292450750

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.