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Species Resource Title
C.elegans tm1125 Defective apoptotic cell clearance activates innate immune response to protect Caenorhabditis elegans against pathogenic bacteria.
C.elegans tm1094 C. elegans aversive olfactory learning generates diverse intergenerational effects.
C.elegans tm4063 Intergenerational Pathogen-Induced Diapause in Caenorhabditis elegans Is Modulated by mir-243.
C.elegans tm1978 In the Model Host Caenorhabditis elegans, Sphingosine-1-Phosphate-Mediated Signaling Increases Immunity toward Human Opportunistic Bacteria.
C.elegans tm1978 Nucleolar fibrillarin is an evolutionarily conserved regulator of bacterial pathogen resistance.
C.elegans tm1888 Intestinal F-box protein regulates quick avoidance behavior of Caenorhabditis elegans to the pathogenic bacterium Pseudomonas aeruginosa.
C.elegans tm2590 The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans.
C.elegans tm897 , tm2364 Neuron-specific regulation of superoxide dismutase amid pathogen-induced gut dysbiosis.
C.elegans tm2482 The Caenorhabditis elegans Protein FIC-1 Is an AMPylase That Covalently Modifies Heat-Shock 70 Family Proteins, Translation Elongation Factors and Histones.
C.elegans tm1359 , tm2807 , tm4248 , tm5421 A conserved mitochondrial surveillance pathway is required for defense against Pseudomonas aeruginosa.
C.elegans tm2457 , tm2482 An essential role for XBP-1 in host protection against immune activation in C. elegans.
C.elegans tm4067 Stimulation of host immune defenses by a small molecule protects C. elegans from bacterial infection.
C.elegans tm3681 , tm1863 , tm2432 Systematic analysis of tissue-restricted miRISCs reveals a broad role for microRNAs in suppressing basal activity of the C. elegans pathogen response.
C.elegans tm1907 , tm1053 Pseudomonas aeruginosa suppresses host immunity by activating the DAF-2 insulin-like signaling pathway in Caenorhabditis elegans.
Prokaryotes E. coli pUC19 Characterization of a multigene-encoded sodium/hydrogen antiporter (sha) from Pseudomonas aeruginosa: its involvement in pathogenesis.