Evidence map›Paper›PMID 31537781›Full record

ArticleNature communications2019

HPD degradation regulated by the TTC36-STK33-PELI1 signaling axis induces tyrosinemia and neurological damage.

Yajun Xie, Xiaoyan Lv, Dongsheng Ni, Jianing Liu, Yanxia Hu, Yamin Liu, Yunhong Liu, Rui Liu, Hui Zhao, Zhimin Lu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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  18. Genetically blockingMolecular therapy. Methods & clinical development · 2021
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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

11 authors at 6 institutions in 1 country.

Yajun XieThe Ministry of Education Key Laboratory of Laboratory Medical Diagnostics, the College of Laboratory Medicine, Chongqing Medical University, 400016, Chongqing, China.
Xiaoyan LvDepartment of Dermatology, West China Hospital, West China School of Medicine, Sichuan University, 610041, Chengdu, China.
Dongsheng NiThe Ministry of Education Key Laboratory of Laboratory Medical Diagnostics, the College of Laboratory Medicine, Chongqing Medical University, 400016, Chongqing, China.
Jianing LiuThe Ministry of Education Key Laboratory of Laboratory Medical Diagnostics, the College of Laboratory Medicine, Chongqing Medical University, 400016, Chongqing, China.
Yanxia HuThe Ministry of Education Key Laboratory of Laboratory Medical Diagnostics, the College of Laboratory Medicine, Chongqing Medical University, 400016, Chongqing, China.
Yamin LiuThe Ministry of Education Key Laboratory of Laboratory Medical Diagnostics, the College of Laboratory Medicine, Chongqing Medical University, 400016, Chongqing, China.
Yunhong LiuClinical Laboratory, The People's Hospital of Longhua, 518109, Shenzhen, China.
Rui LiuState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Chinese Academy of Medical Sciences Research Unit of Oral Carcinogenesis and Management, West China Hospital of Stomatology, Sichuan University, 610041, Chengdu, China.
Hui ZhaoKey Laboratory for Regenerative Medicine, Ministry of Education, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.
Zhimin LuZhejiang Provincial Key Laboratory of Pancreatic Disease, the First Affiliated Hospital, and Institute of Translational Medicine, Zhejiang University School of Medicine, 310029, Hangzhou, China. zhiminlu@zju.edu.cn.
Qin ZhouThe Ministry of Education Key Laboratory of Laboratory Medical Diagnostics, the College of Laboratory Medicine, Chongqing Medical University, 400016, Chongqing, China. zhouqin@cqmu.edu.cn.
Chongqing Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNChinese University of Hong Kong · CNShenZhen People’s Hospital · CNSichuan University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Decreased expression of 4-hydroxyphenylpyruvic acid dioxygenase (HPD), a key enzyme for tyrosine metabolism, is a cause of human tyrosinemia. However, the regulation of HPD expression remains largely unknown. Here, we demonstrate that molecular chaperone TTC36, which is highly expressed in liver, is associated with HPD and reduces the binding of protein kinase STK33 to HPD, thereby inhibiting STK33-mediated HPD T382 phosphorylation. The reduction of HPD T382 phosphorylation results in impaired recruitment of FHA domain-containing PELI1 and PELI1-mediated HPD polyubiquitylation and degradation. Conversely, deficiency or depletion of TTC36 results in enhanced STK33-mediated HPD T382 phosphorylation and binding of PELI1 to HPD and subsequent PELI1-mediated HPD downregulation. Ttc36

Indexed as

AnimalsCell LineHEK293 CellsHippocampusHumansMaleMaze LearningMembrane ProteinsMemoryMiceMice, Inbred C57BLMice, KnockoutMitochondrial ProteinsNuclear ProteinsOxidoreductasesPhosphorylationHpd protein, mouseMembrane ProteinsMitochondrial ProteinsNuclear ProteinsOxidoreductasesPeli1 protein, mouseProtein Serine-Threonine KinasesStk33 protein, mouseTtc36 protein, mouseUbiquitin-Protein Ligases

Identifiers

PMID31537781
PMCPMC6753076
OpenAlexW2973555580

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.