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Enoyl-acyl carrier protein reductase

From Wikipedia, the free encyclopedia

Enoyl-acyl carrier protein reductase (or ENR) (EC 1.3.1.9), is a key enzyme of the type II fatty acid synthesis (FAS) system.[1] ENR is an attractive target for narrow-spectrum antibacterial drug discovery because of its essential role in metabolism and its sequence conservation across many bacterial species. In addition, the bacterial ENR sequence and structural organization are distinctly different from those of mammalian fatty acid biosynthesis enzymes.[2]

At lower concentrations, Triclosan and Triclocarban provide a bacteriostatic effect by binding to ENR. Atromentin and leucomelone possess antibacterial activity, inhibiting the enzyme in the bacteria Streptococcus pneumoniae.[3]

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Transcription

See also

References

  1. ^ Kapoor M, Gopalakrishnapai J, Surolia N, Surolia A (August 2004). "Mutational analysis of the triclosan-binding region of enoyl-ACP (acyl-carrier protein) reductase from Plasmodium falciparum". The Biochemical Journal. 381 (Pt 3): 735–41. doi:10.1042/BJ20040302. PMC 1133883. PMID 15139852.
  2. ^ Ling LL, Xian J, Ali S, Geng B, Fan J, Mills DM, Arvanites AC, Orgueira H, Ashwell MA, Carmel G, Xiang Y, Moir DT (May 2004). "Identification and characterization of inhibitors of bacterial enoyl-acyl carrier protein reductase". Antimicrobial Agents and Chemotherapy. 48 (5): 1541–7. doi:10.1128/aac.48.5.1541-1547.2004. PMC 400533. PMID 15105103.
  3. ^ Zheng CJ, Sohn MJ, Kim WG (December 2006). "Atromentin and leucomelone, the first inhibitors specific to enoyl-ACP reductase (FabK) of Streptococcus pneumoniae". The Journal of Antibiotics. 59 (12): 808–12. doi:10.1038/ja.2006.108. PMID 17323650.

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This page was last edited on 26 August 2023, at 13:57
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