A5071108556- Heat shock proteins research
- RNA Research and Splicing
- Ubiquitin and proteasome pathways
- DNA Repair Mechanisms
- Signaling Pathways in Disease
- Chemokine receptors and signaling
- Ion Channels and Receptors
- Hydrogen's biological and therapeutic effects
- Porphyrin Metabolism and Disorders
- HIV-related health complications and treatments
- Cell Adhesion Molecules Research
- Physiological and biochemical adaptations
- Sulfur Compounds in Biology
- Genomic variations and chromosomal abnormalities
- Air Quality and Health Impacts
- Advanced Proteomics Techniques and Applications
- Ion Transport and Channel Regulation
- Carcinogens and Genotoxicity Assessment
- Genomics and Chromatin Dynamics
- Ion channel regulation and function
- Monoclonal and Polyclonal Antibodies Research
- RNA and protein synthesis mechanisms
- Adipokines, Inflammation, and Metabolic Diseases
- Endoplasmic Reticulum Stress and Disease
- Ion-surface interactions and analysis
The University of Tokyo
1995-2023
University of Miyazaki
2014
National Cancer Research Institute
1997
Tokyo University of Science
1995
Abstract Cells are under threat of osmotic perturbation; cell volume maintenance is critical in cerebral edema, inflammation and aging, which prominent changes intracellular or extracellular osmolality emerge. After stress-enforced swelling shrinkage, the cells regulate to recover their volume. However, mechanisms recognizing stress remain obscured. We previously clarified that apoptosis signal-regulating kinase 3 (ASK3) bidirectionally responds regulates recovery. Here, we show...
Biomolecular condensates are membraneless structures formed through phase separation. Recent studies have demonstrated that the material properties of biomolecular crucial for their biological functions and pathogenicity. However, maintenance in cells remains elusive. Here, we show sodium ion (Na+) influx regulates condensate liquidity under hyperosmotic stress. ASK3 higher fluidity at high intracellular Na+ concentration derived from extracellular solution. Moreover, identified TRPM4 as a...
Abstract Cells are under threat of osmotic perturbation; and cell volume maintenance is critical in cerebral edema, inflammation aging, which prominent changes intracellular or extracellular osmolality emerge. After stress-enforced swelling shrinkage, the cells regulate to recover their volume. However, mechanisms recognizing stress remain obscured. We previously clarified that apoptosis signal-regulating kinase 3 (ASK3) bidirectionally responds regulates recovery. Here, we report...
Raw264.7 cells are monocytic that can differentiate to activated macrophages after lipopoly-saccharide (LPS) stimulation. Here, we analyzed the factors secreted by in response LPS. The culture media of LPS-treated was able stimulate growth MEF1F2 and NIH3T3 mouse fibroblast cell lines. We identified five LPS-induced chemokines, CCL2, CCL5, CCL12, CxCL2, CxCL10, microarray analysis tested their stimulatory activity. used commercially available bacterially expressed proteins, found only CxCL2...
Summary Biomolecular condensates are membraneless structures formed through phase separation. Recent studies have demonstrated that the material properties of biomolecular crucial for their biological functions and pathogenicity. However, maintenance in cells remains elusive. Here, we show sodium ion (Na + ) influx regulates condensate liquidity under hyperosmotic stress. The fluidity ASK3 increases at high intracellular Na concentration derived from extracellular solution. Moreover,...
Summary The proteasome has an essential role in proteostasis maintenance and is critical for cell survival under proteotoxic conditions including hyperosmotic stress. However, it unknown how activity linked to survival/death We have previously reported that apoptosis signal-regulating kinase 3 (ASK3) contributes through its inactivation 19S regulatory particle subunits of the were enriched ASK3 inactivator candidates identified our genome-wide small interfering RNA (siRNA) screen. In this...
Abstract Recent studies have shown that adipose tissue is an immunological organ. While inflammation in energy-storing white tissues has been the focus of intense research, regulatory mechanisms heat-producing brown remain largely unknown. We previously identified apoptosis signal-regulating kinase 1 (ASK1) as a critical regulator adipocyte maturation; PKA-ASK1-p38 axis facilitates uncoupling protein (UCP1) induction cell-autonomously. Here, we show ASK1 suppresses innate immune pathway and...