Molecule Information

General Information of the Molecule (ID: Mol00747)

• Name: AAC(6')-Ib family aminoglycoside 6'-N-acetyltransferase (AAC6IB) ,Pseudomonas aeruginosa
• Synonyms: aac(3)-Ib/aac(6')-Ib; Aminoglycoside 3-N-acetyltransferase/aminoglycoside 6'-N-acetyltransferase fusion protein
• Molecule Type: Protein
• Gene Name: aac(6')-Ib
• Sequence:
  MTNSNDSVTLRLMTEHDLAMLYEWLNRSHIVEWWGGEEARPTLADVQEQYLPSVLAQESV
  TPYIAMLNGEPIGYAQSYVALGSGDGWWEEETDPGVRGIDQSLANASQLG KGLGTKLVR
  ALVELLFNDPE VTKIQTDPSPSNLRAIRCYEKAGFERQGTVTTPDGPAVYMVQTRQAFE
  RTRSDA
• Uniprot ID: Q7BM49_PSEAI

Kingdom: N.A.
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Pseudomonadales
Family: Pseudomonadaceae
Genus: Pseudomonas
Species: Pseudomonas aeruginosa

Type(s) of Resistant Mechanism of This Molecule

  DISM: Drug Inactivation by Structure Modification

Drug Resistance Data Categorized by Drug

Approved Drug(s) 3 drug(s) in total

Gentamicin C

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Disease Class: Pseudomonas aeruginosa infection [1]

• Resistant Disease: Pseudomonas aeruginosa infection [ICD-11: 1A00-1C4Z]
• Resistant Drug: Gentamicin C
• Molecule Alteration: Expression; Inherence
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli DH10B; 316385
• In Vitro Model: Escherichia coli HB101; 634468
• In Vitro Model: Pseudomonas aeruginosa ATCC 27853; 287
• In Vitro Model: Escherichia coli JM109; 562
• In Vitro Model: Escherichia coli k-12; 83333
• In Vitro Model: Pseudomonas aeruginosa Pa695; 287
• Experiment for Molecule Alteration: PCR experiments assay
• Experiment for Drug Resistance: Disk diffusion method assay
• Mechanism Description: The fusion product was functional, as was the product of each gene cloned separately: AAC(3)-I, despite the deletion of the four last amino acids, and AAC(6"), which carried three amino acid changes compared with the most homologous sequence. The AAC(3)-I protein conferred an expected gentamicin and fortimicin resistance, and the AAC(6"), despite the Leu-119-Ser substitution, yielded resistance to kanamycin, tobramycin, and dibekacin, but slightly affected netilmicin and amikacin, and had no apparent effect on gentamicin. The fusion product conveyed a large profile of resistance, combining the AAC(6") activity with a higher level of gentamicin resistance without accompanying fortimicin resistance.

Kanamycin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Disease Class: Pseudomonas aeruginosa infection [1]

• Resistant Disease: Pseudomonas aeruginosa infection [ICD-11: 1A00-1C4Z]
• Resistant Drug: Kanamycin
• Molecule Alteration: Expression; Inherence
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli DH10B; 316385
• In Vitro Model: Escherichia coli HB101; 634468
• In Vitro Model: Pseudomonas aeruginosa ATCC 27853; 287
• In Vitro Model: Escherichia coli JM109; 562
• In Vitro Model: Escherichia coli k-12; 83333
• In Vitro Model: Pseudomonas aeruginosa Pa695; 287
• Experiment for Molecule Alteration: PCR experiments assay
• Experiment for Drug Resistance: Disk diffusion method assay
• Mechanism Description: The fusion product was functional, as was the product of each gene cloned separately: AAC(3)-I, despite the deletion of the four last amino acids, and AAC(6"), which carried three amino acid changes compared with the most homologous sequence. The AAC(3)-I protein conferred an expected gentamicin and fortimicin resistance, and the AAC(6"), despite the Leu-119-Ser substitution, yielded resistance to kanamycin, tobramycin, and dibekacin, but slightly affected netilmicin and amikacin, and had no apparent effect on gentamicin. The fusion product conveyed a large profile of resistance, combining the AAC(6") activity with a higher level of gentamicin resistance without accompanying fortimicin resistance.

Tobramycin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Disease Class: Pseudomonas aeruginosa infection [1]

• Resistant Disease: Pseudomonas aeruginosa infection [ICD-11: 1A00-1C4Z]
• Resistant Drug: Tobramycin
• Molecule Alteration: Expression; Inherence
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli DH10B; 316385
• In Vitro Model: Escherichia coli HB101; 634468
• In Vitro Model: Pseudomonas aeruginosa ATCC 27853; 287
• In Vitro Model: Escherichia coli JM109; 562
• In Vitro Model: Escherichia coli k-12; 83333
• In Vitro Model: Pseudomonas aeruginosa Pa695; 287
• Experiment for Molecule Alteration: PCR experiments assay
• Experiment for Drug Resistance: Disk diffusion method assay
• Mechanism Description: The fusion product was functional, as was the product of each gene cloned separately: AAC(3)-I, despite the deletion of the four last amino acids, and AAC(6"), which carried three amino acid changes compared with the most homologous sequence. The AAC(3)-I protein conferred an expected gentamicin and fortimicin resistance, and the AAC(6"), despite the Leu-119-Ser substitution, yielded resistance to kanamycin, tobramycin, and dibekacin, but slightly affected netilmicin and amikacin, and had no apparent effect on gentamicin. The fusion product conveyed a large profile of resistance, combining the AAC(6") activity with a higher level of gentamicin resistance without accompanying fortimicin resistance.

References

• Ref 1: Molecular characterization of a novel class 1 integron containing bla(GES-1) and a fused product of aac3-Ib/aac6'-Ib' gene cassettes in Pseudomonas aeruginosa. Antimicrob Agents Chemother. 2002 Mar;46(3):638-45. doi: 10.1128/AAC.46.3.638-645.2002.