Pathogenic species of the genus Yersinia suppress and reorient the immune system to infect lymphatic tissues, inner organs and at times also the vasculature. For this purpose yersiniae employ a type III secretion system to translocate effector proteins (Yersinia outer proteins; Yops) into immune cells. Yops often exert unique biochemical activities for modulating the activity of Rho GTP-binding proteins, focal adhesion proteins, inflammatory pathways and cell survival/apoptosis. In this review we will put emphasis on the biochemistry, cell- and infection biology of Yersinia effector Yops.
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Cancer Res Commun
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Candel Therapeutics, Needham, MA, United States.
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January 2025
Department of Cardiology, Renji Hospital, School of Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Shanghai Jiao Tong University, Shanghai, China.
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January 2025
Department of Biological Sciences, Kent State University, P.O. Box 5190, Kent, OH 44242, USA. Electronic address:
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January 2025
Department of Biochemistry and Biomedical Sciences, McMaster University, 1280 Main Street West, Hamilton, Ontario, Canada L8S 4K1; Michael DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario, Canada L8S 4K1. Electronic address:
Type VI secretion systems (T6SS) are dynamic protein nanomachines found in Gram-negative bacteria that deliver toxic effector proteins into target cells in a contact-dependent manner. Prior to secretion, many T6SS effector proteins require chaperones and/or accessory proteins for proper loading onto the structural components of the T6SS apparatus. However, despite their established importance, the precise molecular function of several T6SS accessory protein families remains unclear.
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