The three canonical members of the family of homeodomain-interacting protein (HIP) kinases fulfill overlapping and distinct roles in cellular stress response pathways. Here we systematically compared all three endogenous HIPKs for their intracellular distribution and mutual interactions. The endogenous HIPKs are contained in high molecular weight complexes of ~700 kDa but do not directly interact physically. Under basal conditions, HIPK1 was mostly cytoplasmic, while HIPK3 was found in the nucleus and HIPK2 occurred in both compartments. Inhibition of nuclear export by leptomycin B resulted in the nuclear accumulation of mainly HIPK1 and HIPK2, indicating constitutive dynamic nucleocytoplasmic shuttling. The carcinogenic chemical stressor sodium arsenite caused the induction of HIPK2-dependent cell death and also resulted in a rapid and complete nuclear translocation of HIPK2, showing that the intracellular distribution of this kinase can undergo dynamic regulation.
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http://dx.doi.org/10.1016/j.bbamcr.2019.04.009 | DOI Listing |
Mar Environ Res
January 2025
Library of Marine Samples, Korea Institute of Ocean Science & Technology, Geoje, 53201, Republic of Korea; Department of Ocean Science, University of Science & Technology, Daejeon, 34113, Republic of Korea. Electronic address:
Nucleocytoplasmic large DNA viruses (NCLDVs) are known to infect phytoplankton and play a significant role in regulating their population dynamics. In this study, we aimed to investigate the co-occurrence patterns between phytoplankton and NCLDVs in the southern coastal ecosystem of South Korea. We collected seawater every month from March 2018 to December 2020 and analyzed the samples using Cytochrome c Oxidase subunit I metabarcoding and metagenomic analyses.
View Article and Find Full Text PDFJ Biol Chem
December 2024
Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Science, Sichuan University, Chengdu, China; State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China. Electronic address:
O-GlcNAcylation, a modification of nucleocytoplasmic proteins in mammals, plays a critical role in various cellular processes. However, the interplay and their underlying mechanisms in chemotherapy-induced tumor regression between O-GlcNAcylation and pyroptosis, a form of programmed cell death associated with innate immunity, remains unclear. Here, we observed that during the etoposide-induced pyroptosis of SH-SY5Y and A549 cells, overall O-GlcNAcylation levels are substantially reduced.
View Article and Find Full Text PDFFront Immunol
December 2024
Liaoning Technology and Engineering Center for Tumor Immunology and Molecular Theranotics, Collaborative Innovation Center for Age-related Disease, Life Science Institute, Jinzhou Medical University, Jinzhou, Liaoning, China.
Front Mol Neurosci
November 2024
Department of Pathology and Laboratory Medicine, University of California, Irvine, Irvine, CA, United States.
Introduction: Spinocerebellar ataxia type 7 (SCA7) is an inherited neurodegenerative disorder characterized by cerebellar and retinal degeneration. SCA7 is caused by a CAG-polyglutamine repeat expansion in the ataxin-7 gene, which encodes a transcription factor protein that is a core component of the STAGA co-activator complex. As ataxin-7 protein regularly shuttles between the nucleus and the cytosol, we sought to test if polyglutamine-expanded ataxin-7 protein results in nuclear membrane abnormalities or defects in nucleocytoplasmic (N/C) transport.
View Article and Find Full Text PDFPLoS Pathog
November 2024
Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, P. R. China.
The hallmark of coronavirus infection lies in its ability to evade host immune defenses, a process intricately linked to the nuclear entry of transcription factors crucial for initiating the expression of antiviral genes. Central to this evasion strategy is the manipulation of the nucleocytoplasmic trafficking system, which serves as an effective target for the virus to modulate the expression of immune response-related genes. In this investigation, we discovered that infection with the infectious bronchitis virus (IBV) dynamically impedes the nuclear translocation of several transcription factors such as IRF3, STAT1, STAT2, NF-κB p65, and the p38 MAPK, leading to compromised transcriptional induction of key antiviral genes such as IFNβ, IFITM3, and IL-8.
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