| Project/Area Number |
23K14541
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 49070:Immunology-related
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| Research Institution | Osaka University |
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Principal Investigator |
Guenther Carla 大阪大学, 免疫学フロンティア研究センター, 特任研究員(常勤) (00967135)
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| Project Period (FY) |
2023-04-01 – 2028-03-31
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| Project Status |
Granted (Fiscal Year 2023)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2027: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2026: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2025: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2024: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2023: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
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| Keywords | Mechanotransduction / Innate Immune regulation / Oncoimmunology / Aging / Cell Signaling / Mechanoimmunology / CLR / Immunology |
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| Outline of Research at the Start |
Identifying central regulatory pathways that control innate immune cell gene expression and resulting phenotypes in response to mechanical stimuli on resting cells and stimulated cells.
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| Outline of Annual Research Achievements |
The research project has progressed into three subprojects: 1) Innate immune cell type was found to depend on substrate stiffness (hard or soft) regardless of stimulation. This mechanism also works in the presence of cancer cells but is twisted to support cancer growth (manuscript was submitted). 2) The mechanism with which cells sense stiffness seems to be disturbed in aged immune cells. This might be due to decline of protein quality in age and might result in immune system dysregulation arising with advanced age. The manuscript is in preparation.
3) An important regulatory protein, that merges stiffness signals with bacterial signals inside of immune cells was identified. Other proteins interacting with this regulator will be identified to clarify the mechanism.
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| Current Status of Research Progress |
Current Status of Research Progress
1: Research has progressed more than it was originally planned.
Reason
The research project has yielded many results to the extend, that three subprojects have developed. The main project has progressed into a manuscript that is currently submitted and has been deposited into bioRxiv. A smaller manuscript on disturbed mechanosignaling in aged cells is in preparation and planned to be submitted by the end of the year.
A third project on key intracellular signaling regulators has emerged due to interesting findings but these findings are just initial results and much more work over next few years is required to yield another manuscript. Nevertheless these findings are novel and challenge the current view on intracellular signaling.
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| Strategy for Future Research Activity |
The main focus this year is on fully publishing the first manuscript and doing the required revisions. In the meantime work on the second manuscript is done. The age related manuscript has become a bit complicated and so a collaboration with an expert in protein translation is discussed and has already resulted in new ideas for experiments and a strategy for further progress. The same collaborator is also helping with establishing a key assay for the third project.
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