Evidence map›Paper›PMID 29121083›Full record

ArticlePloS one2017

Structural and biochemical analysis of atypically low dephosphorylating activity of human dual-specificity phosphatase 28.

Bonsu Ku, Won Hong, Chae Won Keum, Myeongbin Kim, Hyunyeol Ryu, Donghwan Jeon, Ho-Chul Shin, Jae Hoon Kim, Seung Jun Kim, Seong Eon Ryu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. 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
0.2field-weighted citation impact, top 43% 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, 5 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

10 authors at 3 institutions in 1 country.

Bonsu KuDisease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Won HongDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul, Republic of Korea.
Chae Won KeumDisease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Myeongbin KimDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul, Republic of Korea.
Hyunyeol RyuDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul, Republic of Korea.
Donghwan JeonDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul, Republic of Korea.
Ho-Chul ShinDisease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Jae Hoon KimDepartment of Biotechnology, College of Applied Life Science, SARI, Jeju National University, Jeju-do, Republic of Korea.
Seung Jun KimDisease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0003-0293-6972
Seong Eon RyuDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul, Republic of Korea.
Hanyang University · KRKorea Research Institute of Bioscience and Biotechnology · KRJeju National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dual-specificity phosphatases (DUSPs) constitute a subfamily of protein tyrosine phosphatases, and are intimately involved in the regulation of diverse parameters of cellular signaling and essential biological processes. DUSP28 is one of the DUSP subfamily members that is known to be implicated in the progression of hepatocellular and pancreatic cancers, and its biological functions and enzymatic characteristics are mostly unknown. Herein, we present the crystal structure of human DUSP28 determined to 2.1 Å resolution. DUSP28 adopts a typical DUSP fold, which is composed of a central β-sheet covered by α-helices on both sides and contains a well-ordered activation loop, as do other enzymatically active DUSP proteins. The catalytic pocket of DUSP28, however, appears hardly accessible to a substrate because of the presence of nonconserved bulky residues in the protein tyrosine phosphatase signature motif. Accordingly, DUSP28 showed an atypically low phosphatase activity in the biochemical assay, which was remarkably improved by mutations of two nonconserved residues in the activation loop. Overall, this work reports the structural and biochemical basis for understanding a putative oncological therapeutic target, DUSP28, and also provides a unique mechanism for the regulation of enzymatic activity in the DUSP subfamily proteins.

Indexed as

Amino Acid MotifsAmino Acid SequenceCrystallography, X-RayDual-Specificity PhosphatasesHumansModels, MolecularPhosphorylationTyrosineDual-Specificity PhosphatasesTyrosine

Identifiers

PMID29121083
PMCPMC5679558
OpenAlexW2767471468

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Registered trials

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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.