Figure 2
(A) Host cells sense damaged membranes through the action of galectin proteins, such as the case with galectin-8 in Salmonella-induced vesicle rupture (depicted). This brings the NDP52–TBK1 (TANK binding kinase 1) complex as first responders prior to the bacteria being coated in ubiquitin by E3-ligases (such as LRSM1 and LUBAC complex). (B) The ubiquitin coat acts as a ‘magnet’ to attract other autophagy receptor proteins such as OPTN, p62/SQSTM1 and TAX1BP1. The autophagy receptors interact with LC3 proteins through their LIR sequences and the ubiquitin coat via their respective ubiquitin binding domains (UBA, UBZ and UBAN). This allows the sequestration of cytosolic bacteria into autophagosomes and restriction of their proliferation.
Methods for host targeting intracellular pathogens

(A) Host cells sense damaged membranes through the action of galectin proteins, such as the case with galectin-8 in Salmonella-induced vesicle rupture (depicted). This brings the NDP52–TBK1 (TANK binding kinase 1) complex as first responders prior to the bacteria being coated in ubiquitin by E3-ligases (such as LRSM1 and LUBAC complex). (B) The ubiquitin coat acts as a ‘magnet’ to attract other autophagy receptor proteins such as OPTN, p62/SQSTM1 and TAX1BP1. The autophagy receptors interact with LC3 proteins through their LIR sequences and the ubiquitin coat via their respective ubiquitin binding domains (UBA, UBZ and UBAN). This allows the sequestration of cytosolic bacteria into autophagosomes and restriction of their proliferation.

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