RACK1 is a ribosome-associated protein which functions as a receptor for activated PKCs. It also acts as a scaffold for many other proteins involved in diverse signaling pathways, e.g. Src, JNK, PDE4D and FAK signaling. With such a broad interactome, RACK1 has been suggested to function as a linker between cell signaling and the translation machinery. Accordingly, RACK1 modulates translation at different levels in several model organisms. For instance, it regulates ribosome stalling and mRNA quality control in yeasts and promotes translation efficiency downstream of specific cellular stimuli in mammals. However, the molecular mechanism by which RACK1 exerts these roles is widely uncharacterized. Moreover, the full list of ribosome-recruited RACK1 interactors still needs characterization. Here we discuss in vivo and in vitro findings to better delineate the roles of RACK1 in regulating ribosome function and translation.
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http://dx.doi.org/10.1080/21690731.2015.1120382 | DOI Listing |
Annu Rev Biomed Eng
January 2025
1Weldon School of Biomedical Engineering, Purdue University, West Lafayette, Indiana, USA; email:
Biochemical signals in native tissue microenvironments instruct cell behavior during many biological processes ranging from developmental morphogenesis and tissue regeneration to tumor metastasis and disease progression. The detection and characterization of these signals using spatial and highly resolved quantitative methods have revealed their existence as matricellular proteins in the matrisome, some of which are bound to the extracellular matrix while others are freely diffusing. Including these biochemical signals in engineered biomaterials can impart enhanced functionality and native-like complexity, ultimately benefiting efforts to understand, model, and treat various diseases.
View Article and Find Full Text PDFMol Pharm
January 2025
State Key Laboratory for Organic Electronics and Information Displays & Jiangsu Key Laboratory for Biosensors, Institute of Advanced Materials (IAM), Nanjing University of Posts & Telecommunications, Nanjing 210023, China.
Natural killer (NK) cell immunotherapy is a significant category in tumor therapy due to its potent tumor-killing and immunomodulatory effects. This research delves into exploring the mechanisms underlying the ability of amoxicillin to boost NK cell cytotoxicity in NK cell immunotherapy. Amoxicillin significantly enhances the cytotoxic activity of NK-92MI cells against MCF-7 cells by triggering the initiation of a cytolytic program in target cell-deficient NK-92MI cells and augmenting the degranulation level of NK-92MI cells in the presence of target cells.
View Article and Find Full Text PDFJ Proteome Res
January 2025
Graduate School of Analytical Science and Technology (GRAST), Chungnam National University, Daejeon 34134, Republic of Korea.
The E3 ubiquitin ligase neural precursor cell-expressed developmentally down-regulated 4 (NEDD4) is involved in various cancer signaling pathways, including PTEN/AKT. However, its role in promoting gastric cancer (GC) progression is unclear. This study was conducted to elucidate the role of NEDD4 in GC progression.
View Article and Find Full Text PDFAnal Chem
January 2025
Department of Bioengineering, University of Washington, SeattleWashington98195, United States.
Cell-to-cell heterogeneity in lipid signaling underlies variations in response and recurrence for many cancers, including leukemias. A highly parallel, miniaturized thin-layer chromatographic platform capable of assaying single cells was developed. Ultrasmall volumes (50 pL) of standard fluorescent lipids were separated with excellent repeatability, reproducibility, and limits of detection.
View Article and Find Full Text PDFPLoS Pathog
January 2025
Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, United States of America.
Retroviruses can be detected by the innate immune sensor cyclic GMP-AMP synthase (cGAS), which recognizes reverse-transcribed DNA and activates an antiviral response. However, the extent to which HIV-1 shields its genome from cGAS recognition remains unclear. To study this process in mechanistic detail, we reconstituted reverse transcription, genome release, and innate immune sensing of HIV-1 in a cell-free system.
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