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Research status of receptor-interacting protein kinase 1 in regulating cancer progression and immune response.
- Source :
- Journal of Shanghai Jiaotong University (Medical Science); Jun2024, Vol. 44 Issue 6, p788-794, 7p
- Publication Year :
- 2024
-
Abstract
- Receptor-interacting protein kinase 1 (RIPK1) is a multi-domain serine/threonine protein kinase that causes downstream signal transduction and biological effects by phosphorylating specific proteins. In recent years, with the in-depth study of RIPK1, scholars have found that it is of great significance in autoimmune diseases, neurodegenerative diseases, and a variety of solid tumors and hematological tumors. On the one hand, RIPK1 promotes cell survival and inflammatory responses by activating specific pathways such as nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK). On the other hand, RIPK1 promotes apoptosis by interacting with cysteinyl aspartate specific proteinase-8 (caspase-8), or promotes necroptosis by interacting with RIPK3 and mixed lineage kinase domain-like protein (MLKL). As an upstream signal, RIPK1 has different expression levels in patients with different tumors. Its scaffold function and kinase activity can regulate cancer progression, initiate adaptive immunity, inhibit tumor progression, and generate an immunosuppressive tumor microenvironment to promote tumor development. Its dual role has been demonstrated in regulating the occurrence and development of tumors and the body's immune response, and can be used as a new therapeutic target to control cancer progression. This paper starts with the structure of RIPK1 to further explore its function in regulating cancer progression and immune response, and to provide new ideas for the development of cancer-targeted drugs. [ABSTRACT FROM AUTHOR]
Details
- Language :
- Chinese
- ISSN :
- 16748115
- Volume :
- 44
- Issue :
- 6
- Database :
- Complementary Index
- Journal :
- Journal of Shanghai Jiaotong University (Medical Science)
- Publication Type :
- Academic Journal
- Accession number :
- 178324998
- Full Text :
- https://doi.org/10.3969/j.issn.1674-8115.2024.06.015