ISSN: 3007-6730 (Online)
3007-6722 (Print)
1. Institute of Transfusion Medicine and Immunology, Mannheim Institute of Innate Immunosciences (MI3), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany
2. Laboratory for Translational Cellular and Molecular Biomedicine, Tomsk State University, Tomsk, Russia
The deubiquitinating enzyme cylindromatosis (CYLD) plays a fundamental role in regulating T cell development and activation. Previous studies have shown that CYLD is associated with autophagy, while AMP activated protein kinase (AMPK) pathway regulates the development of autophagy and affects cell metabolism. However, the mechanism by which CYLD affects autophagy and whether it affects the downstream metabolism of AMPKα remains unclear. In this study, we used the CYLD gene knockout model in Jurkat cells to investigate the mechanism of CYLD and autophagy and its relationship with cellular metabolism. The results show that CYLD deletion promotes autophagy through AMPKα/mTOR/ULK1 signaling pathway, promotes mitochondrial autophagy to improve mitochondrial function and attenuates cell lipid metabolism in Jurkat cells.
In Drosophila melanogaster, the siRNA-directed RNAi pathway provides crucial antiviral defenses. Cell-autonomously, Dicer-2 (Dcr-2) recognizes and cleaves viral dsRNA into siRNAs, which are incorporated into the RNA-induced silencing complex (RISC). Argonaute 2 (Ago2) then targets and cleaves viral RNA, preventing replication. Non-cell-autonomously, infected hemocytes secrete exosomes containing viral siRNAs, spreading antiviral signals to other cells. Additionally, tunneling nanotubes can transfer RNAi components between neighboring cells, further enhancing systemic immunity. These findings highlight the sophisticated antiviral strategies in Drosophila, offering insights for broader antiviral research.
In Drosophila melanogaster, the siRNA-directed RNAi pathway provides crucial antiviral defenses. Cell-autonomously, Dicer-2 (Dcr-2) recognizes and cleaves viral dsRNA into siRNAs, which are incorporated into the RNA-induced silencing complex (RISC). Argonaute 2 (Ago2) then targets and cleaves viral RNA, preventing replication. Non-cell-autonomously, infected hemocytes secrete exosomes containing viral siRNAs, spreading antiviral signals to other cells. Additionally, tunneling nanotubes can transfer RNAi components between neighboring cells, further enhancing systemic immunity. These findings highlight the sophisticated antiviral strategies in Drosophila, offering insights for broader antiviral research.
The deubiquitinating enzyme cylindromatosis (CYLD) plays a fundamental role in regulating T cell development and activation. Previous studies have shown that CYLD is associated with autophagy, while AMP activated protein kinase (AMPK) pathway regulates the development of autophagy and affects cell metabolism. However, the mechanism by which CYLD affects autophagy and whether it affects the downstream metabolism of AMPKα remains unclear. In this study, we used the CYLD gene knockout model in Jurkat cells to investigate the mechanism of CYLD and autophagy and its relationship with cellular metabolism. The results show that CYLD deletion promotes autophagy through AMPKα/mTOR/ULK1 signaling pathway, promotes mitochondrial autophagy to improve mitochondrial function and attenuates cell lipid metabolism in Jurkat cells.
In Drosophila melanogaster, the siRNA-directed RNAi pathway provides crucial antiviral defenses. Cell-autonomously, Dicer-2 (Dcr-2) recognizes and cleaves viral dsRNA into siRNAs, which are incorporated into the RNA-induced silencing complex (RISC). Argonaute 2 (Ago2) then targets and cleaves viral RNA, preventing replication. Non-cell-autonomously, infected hemocytes secrete exosomes containing viral siRNAs, spreading antiviral signals to other cells. Additionally, tunneling nanotubes can transfer RNAi components between neighboring cells, further enhancing systemic immunity. These findings highlight the sophisticated antiviral strategies in Drosophila, offering insights for broader antiviral research.utf-8
The deubiquitinating enzyme cylindromatosis (CYLD) plays a fundamental role in regulating T cell development and activation. Previous studies have shown that CYLD is associated with autophagy, while AMP activated protein kinase (AMPK) pathway regulates the development of autophagy and affects cell metabolism. However, the mechanism by which CYLD affects autophagy and whether it affects the downstream metabolism of AMPKα remains unclear. In this study, we used the CYLD gene knockout model in Jurkat cells to investigate the mechanism of CYLD and autophagy and its relationship with cellular metabolism. The results show that CYLD deletion promotes autophagy through AMPKα/mTOR/ULK1 signaling pathway, promotes mitochondrial autophagy to improve mitochondrial function and attenuates cell lipid metabolism in Jurkat cells.utf-8