Molecule Information

General Information of the Molecule (ID: Mol00744)

Name	Gentamicin 3'-acetyltransferase (AACC1) ,Escherichia coli
Synonyms	RCS36_PI-II0023 Click to Show/Hide
Molecule Type	Protein
Gene Name	aacC1
Sequence	MGIIRTCRLGPDQVKSMRAALDLFGREFGDVATYSQHQPDSDYLGNLLRSKTFIALAAFD QEAVVGALAAYVLPKFEQPRSEIYIYDLAVSGEHRRQGIATALINLLKHEANALGAYVIY VQADYGDDPAVALYTKLGIREEVMHFDIDPSTAT Click to Show/Hide
Uniprot ID	D3VY99_ECOLX
*Click to Show/Hide the Complete Species Lineage*
Kingdom: N.A. Phylum: Proteobacteria Class: Gammaproteobacteria Order: Enterobacterales Family: Enterobacteriaceae Genus: Escherichia Species: Escherichia coli

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

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Gentamicin B

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Drug Resistance Data Categorized by Their Corresponding Mechanisms
Drug Inactivation by Structure Modification (DISM)		Click to Show/Hide
Disease Class: Bacterial infection			[1], [2]
Resistant Disease	Bacterial infection [ICD-11: 1A00-1C4Z]		Disease Info
Resistant Drug	Gentamicin B		Drug Info
Molecule Alteration	Expression	Up-regulation
Experimental Note	Identified from the Human Clinical Data
In Vitro Model	Escherichia coli strain BN		562
	Escherichia coli strain J62		562
	Escherichia coli strain k12 W3110		83333
Experiment for Molecule Alteration	Whole genome sequence assay
Experiment for Drug Resistance	Agar dilution method assay; disk diffusion test assay
Mechanism Description	The most common mechanisms of resistance to aminoglycoside-aminocyclitol (AG) antibiotics in bacteria are exerted by enzymatic modification which results in failure of their binding to ribosomal targets and in prevention of uptake by the cell.

Gentamicin C

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Drug Resistance Data Categorized by Their Corresponding Mechanisms
Drug Inactivation by Structure Modification (DISM)		Click to Show/Hide
Disease Class: Bacterial infection			[1], [2]
Resistant Disease	Bacterial infection [ICD-11: 1A00-1C4Z]		Disease Info
Resistant Drug	Gentamicin C		Drug Info
Molecule Alteration	Expression	Up-regulation
Experimental Note	Identified from the Human Clinical Data
In Vitro Model	Escherichia coli strain BN		562
	Escherichia coli strain J62		562
	Escherichia coli strain k12 W3110		83333
Experiment for Molecule Alteration	Whole genome sequence assay
Experiment for Drug Resistance	Agar dilution method assay; disk diffusion test assay
Mechanism Description	The most common mechanisms of resistance to aminoglycoside-aminocyclitol (AG) antibiotics in bacteria are exerted by enzymatic modification which results in failure of their binding to ribosomal targets and in prevention of uptake by the cell.

Sisomicin

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Drug Resistance Data Categorized by Their Corresponding Mechanisms
Drug Inactivation by Structure Modification (DISM)		Click to Show/Hide
Disease Class: Bacterial infection			[1], [2]
Resistant Disease	Bacterial infection [ICD-11: 1A00-1C4Z]		Disease Info
Resistant Drug	Sisomicin		Drug Info
Molecule Alteration	Expression	Up-regulation
Experimental Note	Identified from the Human Clinical Data
In Vitro Model	Escherichia coli strain BN		562
	Escherichia coli strain J62		562
	Escherichia coli strain k12 W3110		83333
Experiment for Molecule Alteration	Whole genome sequence assay
Experiment for Drug Resistance	Agar dilution method assay; disk diffusion test assay
Mechanism Description	The most common mechanisms of resistance to aminoglycoside-aminocyclitol (AG) antibiotics in bacteria are exerted by enzymatic modification which results in failure of their binding to ribosomal targets and in prevention of uptake by the cell.

References

Ref 1	Characterization of two aminoglycoside-(3)-N-acetyltransferase genes and assay as epidemiological probes. J Antimicrob Chemother. 1991 Sep;28(3):333-46. doi: 10.1093/jac/28.3.333.
Ref 2	On the evolution of Tn21-like multiresistance transposons: sequence analysis of the gene (aacC1) for gentamicin acetyltransferase-3-I(AAC(3)-I), another member of the Tn21-based expression cassette. Mol Gen Genet. 1989 Jun;217(2-3):202-8. doi: 10.1007/BF02464882.