Molecule Information
General Information of the Molecule (ID: Mol00789)
Name |
Aminoglycoside 3'-phosphotransferase (A3AP)
,Stenotrophomonas maltophilia
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Molecule Type |
Protein
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Gene Name |
aph(3')-IIc
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Sequence |
MEASNPFTDGLRLPRAWQEALADAHIERQSIGVSRADVARVHRPGQTDAFLKSEVIDAFS
ELGDEIARLRWLQAQGQSAPTVIATTEEGGRRWLLMSALPGRDLASSPELAPRRVAELLA DALRGLHAVPVANCPFDQQLASRLQAAQARVEAGLVDADDFDDERLGQSPQQVFAELRAT RPAHEDLVVSQGDACLPNLTVTDGRFTGFIDCGRLGVADRYQDLALAARSLVHNFGESRC VAALFQRYGAVPDERRLAFYRLLDEFF Click to Show/Hide
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Uniprot ID | |||||
Click to Show/Hide the Complete Species Lineage | |||||
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
Framycetin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Disease Class: Stenotrophomonas maltophilia infection | [1] | |||
Resistant Disease | Stenotrophomonas maltophilia infection [ICD-11: 1A00-1C4Z] | |||
Resistant Drug | Framycetin | |||
Molecule Alteration | Expression | Inherence |
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Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli | 668369 | ||
Experiment for Molecule Alteration |
PCR amplification assay | |||
Experiment for Drug Resistance |
MIC assay | |||
Mechanism Description | Aph(3')-IIc significantly increases MICs of kanamycin, neomycin, butirosin, and paromomycin when expressed in Escherichia coli. Disruption of aph(3')-IIc results in decreased MICs of these drugs. |
Kanamycin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Disease Class: Stenotrophomonas maltophilia infection | [1] | |||
Resistant Disease | Stenotrophomonas maltophilia infection [ICD-11: 1A00-1C4Z] | |||
Resistant Drug | Kanamycin | |||
Molecule Alteration | Expression | Inherence |
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Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli | 668369 | ||
Experiment for Molecule Alteration |
PCR amplification assay | |||
Experiment for Drug Resistance |
MIC assay | |||
Mechanism Description | Aph(3')-IIc significantly increases MICs of kanamycin, neomycin, butirosin, and paromomycin when expressed in Escherichia coli. Disruption of aph(3')-IIc results in decreased MICs of these drugs. |
Paromomycin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Disease Class: Stenotrophomonas maltophilia infection | [1] | |||
Resistant Disease | Stenotrophomonas maltophilia infection [ICD-11: 1A00-1C4Z] | |||
Resistant Drug | Paromomycin | |||
Molecule Alteration | Expression | Inherence |
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Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli | 668369 | ||
Experiment for Molecule Alteration |
PCR amplification assay | |||
Experiment for Drug Resistance |
MIC assay | |||
Mechanism Description | Aph(3')-IIc significantly increases MICs of kanamycin, neomycin, butirosin, and paromomycin when expressed in Escherichia coli. Disruption of aph(3')-IIc results in decreased MICs of these drugs. |
Investigative Drug(s)
1 drug(s) in total
Butirosina
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Drug Inactivation by Structure Modification (DISM) | ||||
Disease Class: Stenotrophomonas maltophilia infection | [1] | |||
Resistant Disease | Stenotrophomonas maltophilia infection [ICD-11: 1A00-1C4Z] | |||
Resistant Drug | Butirosina | |||
Molecule Alteration | Expression | Inherence |
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Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Escherichia coli | 668369 | ||
Experiment for Molecule Alteration |
PCR amplification assay | |||
Experiment for Drug Resistance |
MIC assay | |||
Mechanism Description | Aph(3')-IIc significantly increases MICs of kanamycin, neomycin, butirosin, and paromomycin when expressed in Escherichia coli. Disruption of aph(3')-IIc results in decreased MICs of these drugs. |
References
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