Asset Details
Do you wish to reserve the book?
Subversion of Metabolic Wasting as the Mechanism for folM -Linked Sulfamethoxazole Resistance
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Subversion of Metabolic Wasting as the Mechanism for folM -Linked Sulfamethoxazole Resistance
Do you wish to request the book?
Subversion of Metabolic Wasting as the Mechanism for folM -Linked Sulfamethoxazole Resistance
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Subversion of Metabolic Wasting as the Mechanism for folM -Linked Sulfamethoxazole Resistance
2017
Overview
Loss-of-function mutations in folM are expected to result in increased metabolic flux toward synthesis of the folate precursor dihydropterin pyrophosphate (H2-HMPt-P2). [...]SMX forms dead-end complexes with H2-HMPt-P2 (H2-HMPt-SMX) and depletes the H2-HMPt-P2 pool and thereby inhibits dihydropteroate production through metabolic wasting (3–5). [...]SMX susceptibility is not impacted by the amount of “target” enzyme but is primarily influenced by the intracellular abundance of its cosubstrates PABA and H2-HMPt-P2.
Publisher
American Society for Microbiology
