ArticleThe Journal of cell biology2004
Interaction of Brn3a and HIPK2 mediates transcriptional repression of sensory neuron survival.
Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 95 citations in OpenAlex.
- Novel insights into pathomechanisms of retinal neuronal degeneration and reactive gliosis in a murine model of GScientific reports · 2025Article
- Functions of SRPK, CLK and DYRK kinases in stem cells, development, and human developmental disorders.FEBS letters · 2023Review
- HIPK2 in the physiology of nervous system and its implications in neurological disorders.Biochimica et biophysica acta. Molecular cell research · 2023Review
- Novel Variant Identified in the Enhancer Region of Host Transcription Factor, BRN3A, is a Significant Risk Factor for HPV-Induced Uterine Cervix Cancer.International journal of molecular and cellular medicine · 2022Article
- Phenotypic Effects of Homeodomain-Interacting Protein Kinase 2 Deletion in Mice.International journal of molecular sciences · 2021Article
- Therapeutic potential of adenovirus-encoding brain-derived neurotrophic factor for spina bifida aperta by intra-amniotic delivery in a rat model.Gene therapy · 2020Article
- Copy number variants and fixed duplications among 198 rhesus macaques (Macaca mulatta).PLoS genetics · 2020Article
- Loss of HIPK2 Protects Neurons from Mitochondrial Toxins by Regulating Parkin Protein Turnover.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Chromatin Targeting of HIPK2 Leads to Acetylation-Dependent Chromatin Decondensation.Frontiers in cell and developmental biology · 2020Article
- Vertebrate Sensory Ganglia: Common and Divergent Features of the Transcriptional Programs Generating Their Functional Specialization.Frontiers in cell and developmental biology · 2020Review
- Homeodomain-interacting protein kinase (Hipk) plays roles in nervous system and muscle structure and function.PloS one · 2020Article
- Cardiomyocyte Homeodomain-Interacting Protein Kinase 2 Maintains Basal Cardiac Function via Extracellular Signal-Regulated Kinase Signaling.Circulation · 2019Article
- Article
- HIPK2-Mediated Transcriptional Control of NMDA Receptor Subunit Expression Regulates Neuronal Survival and Cell Death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Characterization of retinal ganglion cell, horizontal cell, and amacrine cell types expressing the neurotrophic receptor tyrosine kinase Ret.The Journal of comparative neurology · 2018Article
- HIPK2-T566 autophosphorylation diversely contributes to UV- and doxorubicin-induced HIPK2 activation.Oncotarget · 2017Article
- Homeodomain-Interacting Protein Kinase-2: A Critical Regulator of the DNA Damage Response and the Epigenome.International journal of molecular sciences · 2016Review
- Activation of HIPK2 Promotes ER Stress-Mediated Neurodegeneration in Amyotrophic Lateral Sclerosis.Neuron · 2016Article
- Dopaminergic Neurons and Brain Reward Pathways: From Neurogenesis to Circuit Assembly.The American journal of pathology · 2016Review
- The role of cullin 5-containing ubiquitin ligases.Cell division · 2016Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Pit1-Oct1-Unc86 domain (POU domain) transcription factor Brn3a controls sensory neuron survival by regulating the expression of Trk receptors and members of the Bcl-2 family. Loss of Brn3a leads to a dramatic increase in apoptosis and severe loss of neurons in sensory ganglia. Although recent evidence suggests that Brn3a-mediated transcription can be modified by additional cofactors, the exact mechanisms are not known. Here, we report that homeodomain interacting protein kinase 2 (HIPK2) is a pro-apoptotic transcriptional cofactor that suppresses Brn3a-mediated gene expression. HIPK2 interacts with Brn3a, promotes Brn3a binding to DNA, but suppresses Brn3a-dependent transcription of brn3a, trkA, and bcl-xL. Overexpression of HIPK2 induces apoptosis in cultured sensory neurons. Conversely, targeted deletion of HIPK2 leads to increased expression of Brn3a, TrkA, and Bcl-xL, reduced apoptosis and increases in neuron numbers in the trigeminal ganglion. Together, these data indicate that HIPK2, through regulation of Brn3a-dependent gene expression, is a critical component in the transcriptional machinery that controls sensory neuron survival.
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Registered trials
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.