Autophagy Defends Cells Against Invading Group A Streptococcus

By I. Nakagawa, A. Amano, N. Mizushima, A. Yamamoto, H. Yamaguchi, T. Kamimoto, Atsuki Nara, J. Funao, M. Nakata, Kayoko Tsuda and 2 more. Science, 2004

1,184 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/29cb540b9a137bb868698f3d7e785d2d7625815f

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Citations in the corpus

Novel targets for Huntington’s disease in an mTOR-independent autophagy pathway (2008, background): “Autophagy induction may also be a valuable strategy in the treatment of infectious diseases, including tuberculosis, and may protect against cell death in certain context”
Autophagy in malignant transformation and cancer progression (2015, neutral): “…hence sustaining colorectal carcinogenesis, and gallbladder carcinoma), as well as Chlamydia pneumoniae (an etiological determinant in some forms of lung cancer) (Nakagawa et al , 2004; Travassos et al , 2010; Yasir et al , 2011; Conway et al , 2013; Griffin et al , 2013; Zhang et al , 2014).”
The molecular machinery of autophagy: unanswered questions (2005, background): “The pathway might act as a means of defense against invasion by various bacteria and viruses; however, autophagy might also be subverted by pathogens to establish a replicative niche within the host cell (Dorn et al., 2002; Kirkegaard et al., 2004; Nakagawa et al., 2004).”
Autophagosome formation: core machinery and adaptations (2007, background): “These intracellular bacteria are then targeted by autophag”
PAMPs and DAMPs: Signal 0s that Spur Autophagy and Immunity (2012, background): “A diverse array of pathogens interact with components of the autophagic pathway including Brucellus abortus (80, 81), Coxiella burnetii (82), Porphyromonas gingivalis (83), Salmonella enterica (84), Chlamydia trachomatis (85), Listeria monocytogenes (86), Group A Streptococcus (87, 88), Mycobacteriu”
Eating oneself and uninvited guests: autophagy-related pathways in cellular defense. (2005, background): “…from clasrole in the degradation of both extracellular bacterial sic autophagosomes in that they are significantly larger pathogens that invade the cell (e.g., Group A Streptoand contain primarily GAS rather than cytoplasmic orcoccus) (Nakagawa et al., 2004) and true intracellular ganelles.”
Protein turnover via autophagy: implications for metabolism. (2007, background): “Although information of selectivity for other endogenous cytosolic proteins is very limited, pathogenic bacteria invading host cytosol appear to be enclosed selectively in a process termed xenophagy (81, 84).”
An Overview of the Molecular Mechanism of Autophagy (2009, background): “Finally, some pathogens are selectively targeted by autophagy, such as Mycobacterium tuberculosis and Streptococcus pyogenes (Gutierrez et al. 2004; Nakagawa et al. 2004).”
Eaten alive: a history of macroautophagy (2010, background): “In 2004, Yoshimori's group, and simultaneously the laboratories of Deretic and Colombo, provided landmark studies showing autophagy is an important defence mechanism against certain invading bacterial pathogens, such as Mycobacterium tuberculosis and Streptococcus pyogenes”
Toll-like receptor 4 is a sensor for autophagy associated with innate immunity. (2007, background): “LC3 type II, the indicator of autophagosome formation (Nakagawa et al., 2004), was increased in RAW264.”
Toll‐like receptors control autophagy (2008, methodology): “HeLa cells were maintained in DMEM, 10% FBS. BMMs were derived from C57/BL6 mice or GFP–LC3 mice (Dr N Mizushima, Japan) as described previously (Via et al, 1998).”
Atg8 family LC3/GABARAP proteins are crucial for autophagosome–lysosome fusion but not autophagosome formation during PINK1/Parkin mitophagy and starvation (2016, background): “, 2010) or invading bacteria during xenophagy (Gutierrez et al., 2004; Nakagawa et al., 2004; Ogawa et al., 2005).”
Autophagy: process and function. (2007, background): “Various pathogenic bacteria, such as Streptococcus pyogenes (Nakagawa et al. 2004) and Shigella flexneri (icsB mutant) (Ogawa et al.”