Evidence map›Paper›PMID 31776210›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020

Loss of HIPK2 Protects Neurons from Mitochondrial Toxins by Regulating Parkin Protein Turnover.

Jiasheng Zhang, Yulei Shang, Sherry Kamiya, Sarah J Kotowski, Ken Nakamura, Eric J Huang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. HIPK2 in the physiology of nervous system and its implications in neurological disorders.Biochimica et biophysica acta. Molecular cell research · 2023
    Review
  3. 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

6 authors at 3 institutions in 1 country.

Jiasheng ZhangDepartment of Pathology, University of California, San Francisco, San Francisco, California 94143.ORCID 0000-0001-6097-1384
Yulei ShangDepartment of Pathology, University of California, San Francisco, San Francisco, California 94143.
Sherry KamiyaDepartment of Pathology, University of California, San Francisco, San Francisco, California 94143.
Sarah J KotowskiDepartment of Neurology, University of California, San Francisco, San Francisco, California 94122, and.
Ken NakamuraDepartment of Neurology, University of California, San Francisco, San Francisco, California 94122, and.ORCID 0000-0002-9192-182X
Eric J HuangDepartment of Pathology, University of California, San Francisco, San Francisco, California 94143, eric.huang2@ucsf.edu.ORCID 0000-0002-5381-3801
Gladstone Institutes · USSan Francisco VA Medical Center · USUniversity of California, San Francisco · US

Funding

Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GERMAN, MICHAEL S · 2003 to 2019
$21.8M
Determining how neural activity impairs bioenergetics in PD pathogenesisR01NS091902 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI NAKAMURA, KEN · 2015 to 2019
$2.1M
Mechanisms of HIPK2 in neurodegenerationR01NS098516 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HUANG, ERIC J · 2016 to 2020
$1.7M
BD FACSAria Fusion Cell SorterS10OD021822 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEE, MICHAEL R. · 2016 to 2016
$573k
Mechanisms of ER Stress and Neurodegeneration in Parkinson's DiseaseI01BX001108 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI Eric J Huang · 2011 to 2026
–
BLRD VA I01 BX001108NIDDK NIH HHS P30 DK063720NIH HHS S10 OD021822NINDS NIH HHS R01 NS091902NINDS NIH HHS R01 NS098516
6 · The paper itself

Abstract

Mitochondria are important sources of energy, but they are also the target of cellular stress, toxin exposure, and aging-related injury. Persistent accumulation of damaged mitochondria has been implicated in many neurodegenerative diseases. One highly conserved mechanism to clear damaged mitochondria involves the E3 ubiquitin ligase Parkin and PTEN-induced kinase 1 (PINK1), which cooperatively initiate the process called mitophagy that identifies and eliminates damaged mitochondria through the autophagosome and lysosome pathways. Parkin is a mostly cytosolic protein, but is rapidly recruited to damaged mitochondria and target them for mitophagy. Moreover, Parkin interactomes also involve signaling pathways and transcriptional machinery critical for survival and cell death. However, the mechanism that regulates Parkin protein level remains poorly understood. Here, we show that the loss of homeodomain interacting protein kinase 2 (HIPK2) in neurons and mouse embryonic fibroblasts (MEFs) has a broad protective effect from cell death induced by mitochondrial toxins. The mechanism by which

Indexed as

NeuronsNeuroprotective AgentsAnimalsDopaminergic NeuronsFemaleFibroblastsGene Expression RegulationMaleMembrane Potential, MitochondrialMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMitochondriaNeurotoxinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaHipk2 protein, mouseNeuroprotective AgentsNeurotoxinsparkin proteinPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseProtein KinasesProtein Serine-Threonine KinasesPTEN-Induced Putative KinaseUbiquitin-Protein LigasesHIPK2mitochondriamitophagyParkinPGC-1proteasome

Identifiers

PMID31776210
PMCPMC6961984
OpenAlexW2989764947

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.