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Your search keyword '"Torraca, Vincenzo"' showing total 142 results
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142 results on '"Torraca, Vincenzo"'

1. RUNDC1 inhibits autolysosome formation and survival of zebrafish via clasping ATG14-STX17-SNAP29 complex

Author

Zhang, Rui, Yang, Yuyan, He, Chao, Zhang, Xin, Torraca, Vincenzo, Wang, Shen, Liu, Nan, Yang, Jiaren, Liu, Shicheng, Yuan, Jinglei, Gou, Dongzhi, Li, Shi, Dong, Xueying, Xie, Yufei, He, Junling, Bai, Hua, Hu, Mengyu, Liao, Zhiquan, Huang, Yuan, Lyu, Hao, Xiao, Shuai, Guo, Dong, Ali, Declan William, Michalak, Marek, Ma, Cong, Chen, Xing-Zhen, Tang, Jingfeng, and Zhou, Cefan

Published
2023
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8. ILKAP Promotes the Metastasis of Hepatocellular Carcinoma Cells by Inhibiting β‐Catenin Degradation and Enhancing the WNT Signaling Pathway.

Author

Zhang, Rui, Yuan, Jinglei, Liu, Shicheng, Torraca, Vincenzo, Liao, Zhiquan, Wu, Yueyan, Tan, Hongfei, Yao, Xia, Hou, Xueyang, Lyu, Hao, Xiao, Shuai, Guo, Dong, Ali, Declan William, Michalak, Marek, Chen, Xing‐Zhen, Zhou, Cefan, and Tang, Jingfeng

Subjects
HEPATOCELLULAR carcinoma, WNT signal transduction, CELLULAR signal transduction, METASTASIS, WNT genes, WNT proteins
Abstract

The incidence of Hepatocellular carcinoma (HCC) and HCC‐related deaths have remarkably increased over the recent decades. It has been reported that β‐catenin activation can be frequently observed in HCC cases. This study identified the integrin‐linked kinase‐associated phosphatase (ILKAP) as a novel β‐catenin‐interacting protein. ILKAP is localized both in the nucleus and cytoplasm and regulates the WNT pathway in different ways. First, it is demonstrated that ILKAP activates the WNT pathway in HCC cells by increasing the protein level of β‐catenin and other proteins associated with the WNT signaling, such as c‐Myc and CyclinD1. Next, it is shown that ILKAP promotes the metastasis of HCC both in vitro and in vivo in a zebrafish xenograft model. It is also found that ILKAP dephosphorylates the GSK3β and CK1, contributing to the reduced ubiquitination of β‐catenin. Furthermore, it is identified that ILKAP functions by mediating binding between TCF4 and β‐catenin to enhance expression of WNT target genes. Taken together, the study demonstrates a critical function of ILKAP in metastasis of HCC, since ILKAP is crucial for the activation of the WNT pathway via stabilization of β‐catenin and increased binding between TCF4 and β‐catenin. [ABSTRACT FROM AUTHOR]

Published
2024
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25. Editorial: Nucleic Acid-Associated Inflammation

Author

Laguette, Nadine, Langevin, Christelle, Olagnier, David, Torraca, Vincenzo, Vanpouille-Box, Claire, and Verrier, Eloi R.

Subjects
Inflammation, Immunology, Pathogen-Associated Molecular Pattern Molecules, Immunity, DNA, Editorial, Virus Diseases, Nucleic Acids, Receptors, Pattern Recognition, nucleic acid sensing, RNA, type I interferon, Animals, Humans
Published
2021

31. Shigella-Induced Emergency Granulopoiesis Protects Zebrafish Larvae from Secondary Infection

Author

Willis, Alexandra R., Torraca, Vincenzo, Gomes, Margarida C., Shelley, Jennifer, Mazon-Moya, Maria, Filloux, Alain, Lo Celso, Cristina, Mostowy, Serge, Wellcome Trust, Medical Research Council (MRC), Lister Institute of Preventive Medicine, Commission of the European Communities, and Sansonetti, Philippe J

Subjects
emergency granulopoiesis, animal structures, neutrophils, stem cells, fungi, Observation, Shigella, zebrafish, Microbiology, QR1-502, 0605 Microbiology
Abstract

Emergency granulopoiesis is a hematopoietic program of stem cell-driven neutrophil production used to counteract immune cell exhaustion following infection. Shigella flexneri is a Gram-negative enteroinvasive pathogen controlled by neutrophils. In this study, we use a Shigella-zebrafish (Danio rerio) infection model to investigate emergency granulopoiesis in vivo. We show that stem cell-driven neutrophil production occurs in response to Shigella infection and requires macrophage-independent signaling by granulocyte colony-stimulating factor (Gcsf). To test whether emergency granulopoiesis can function beyond homoeostasis to enhance innate immunity, we developed a reinfection assay using zebrafish larvae that have not yet developed an adaptive immune system. Strikingly, larvae primed with a sublethal dose of Shigella are protected against a secondary lethal dose of Shigella in a type III secretion system (T3SS)-dependent manner. Collectively, these results highlight a new role for emergency granulopoiesis in boosting host defense and demonstrate that zebrafish larvae can be a valuable in vivo model to investigate innate immune memory., IMPORTANCE Shigella is an important human pathogen of the gut. Emergency granulopoiesis is the enhanced production of neutrophils by hematopoietic stem and progenitor cells (HSPCs) upon infection and is widely considered a homoeostatic mechanism for replacing exhausted leukocytes. In this study, we developed a Shigella-zebrafish infection model to investigate stem cell-driven emergency granulopoiesis. We discovered that zebrafish initiate granulopoiesis in response to Shigella infection, via macrophage-independent signaling of granulocyte colony-stimulating factor (Gcsf). Strikingly, larvae primed with a sublethal dose of Shigella are protected against a secondary lethal dose of Shigella in a type III secretion system (T3SS)-dependent manner. Taken together, we show that zebrafish infection can be used to capture Shigella-mediated stem cell-driven granulopoiesis and provide a new model system to study stem cell biology in vivo. Our results also highlight the potential of manipulating stem cell-driven granulopoiesis to boost innate immunity and combat infectious disease.

Published
2018

33. Shigella sonnei infection of zebrafish reveals that O-antigen mediates neutrophil tolerance and dysentery incidence

Author

Torraca, Vincenzo, primary, Kaforou, Myrsini, additional, Watson, Jayne, additional, Duggan, Gina M., additional, Guerrero-Gutierrez, Hazel, additional, Krokowski, Sina, additional, Hollinshead, Michael, additional, Clarke, Thomas B., additional, Mostowy, Rafal J., additional, Tomlinson, Gillian S., additional, Sancho-Shimizu, Vanessa, additional, Clements, Abigail, additional, and Mostowy, Serge, additional

Published
2019
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39. Shigella sonneiinfection of zebrafish reveals that O-antigen mediates neutrophil tolerance and dysentery incidence

Author

Torraca, Vincenzo, primary, Kaforou, Myrsini, additional, Watson, Jayne, additional, Duggan, Gina M., additional, Guerrero-Gutierrez, Hazel, additional, Krokowski, Sina, additional, Hollinshead, Michael, additional, Clarke, Thomas B., additional, Mostowy, Rafal J., additional, Tomlinson, Gillian S., additional, Sancho-Shimizu, Vanessa, additional, Clements, Abigail, additional, and Mostowy, Serge, additional

Published
2019
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45. Septins and bacterial infection

Author

Torraca, Vincenzo, Mostowy, Serge, Wellcome Trust, Lister Institute of Preventive Medicine, and Commission of the European Communities

Subjects
0301 basic medicine, autophagy, Listeria, Mini Review, Phagocytosis, macromolecular substances, Mitochondrion, Biology, medicine.disease_cause, Septin, Microbiology, Cell and Developmental Biology, 03 medical and health sciences, Listeria monocytogenes, medicine, septins, Cytoskeleton, lcsh:QH301-705.5, Actin, Autophagy, fungi, cytoskeleton, Cell Biology, Cell biology, mitochondria, 030104 developmental biology, lcsh:Biology (General), cell-autonomous immunity, Shigella, biological phenomena, cell phenomena, and immunity, actin, Developmental Biology
Abstract

Septins, a unique cytoskeletal component associated with cellular membranes, are increasingly recognized as having important roles in host defense against bacterial infection. A role for septins during invasion of Listeria monocytogenes into host cells was first proposed in 2002. Since then, work has shown that septins assemble in response to a wide variety of invasive bacterial pathogens, and septin assemblies can have different roles during the bacterial infection process. Here we review the interplay between septins and bacterial pathogens, highlighting septin s as a structural determinant of host defense. We also discuss how investigation of septin assembly in response to bacterial infection can yield insight into basic cellular processes including phagocytosis, autophagy, and mitochondrial dynamics.

Published
2016

49. Frontline Science: Antagonism between regular and atypical Cxcr3 receptors regulates macrophage migration during infection and injury in zebrafish.

Author

Sommer, Frida, Torraca, Vincenzo, Kamel, Sarah M., Lombardi, Amber, and Meijer, Annemarie H.

Subjects
MYCOBACTERIAL diseases, CHEMOKINE receptors, CHROMOSOME duplication, INFECTION
Abstract

The CXCR3‐CXCL11 chemokine‐signaling axis plays an essential role in infection and inflammation by orchestrating leukocyte trafficking in human and animal models, including zebrafish. Atypical chemokine receptors (ACKRs) play a fundamental regulatory function in signaling networks by shaping chemokine gradients through their ligand scavenging function, while being unable to signal in the classic G‐protein‐dependent manner. Two copies of the CXCR3 gene in zebrafish, cxcr3.2 and cxcr3.3, are expressed on macrophages and share a highly conserved ligand‐binding site. However, Cxcr3.3 has structural characteristics of ACKRs indicative of a ligand‐scavenging role. In contrast, we previously showed that Cxcr3.2 is an active CXCR3 receptor because it is required for macrophage motility and recruitment to sites of mycobacterial infection. In this study, we generated a cxcr3.3 CRISPR‐mutant to functionally dissect the antagonistic interplay among the cxcr3 paralogs in the immune response. We observed that cxcr3.3 mutants are more susceptible to mycobacterial infection, whereas cxcr3.2 mutants are more resistant. Furthermore, macrophages in the cxcr3.3 mutant are more motile, show higher activation status, and are recruited more efficiently to sites of infection or injury. Our results suggest that Cxcr3.3 is an ACKR that regulates the activity of Cxcr3.2 by scavenging common ligands and that silencing the scavenging function of Cxcr3.3 results in an exacerbated Cxcr3.2 signaling. In human, splice variants of CXCR3 have antagonistic functions and CXCR3 ligands also interact with ACKRs. Therefore, in zebrafish, an analogous regulatory mechanism appears to have evolved after the cxcr3 gene duplication event, through diversification of conventional and atypical receptor variants. [ABSTRACT FROM AUTHOR]

Published
2020
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