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anthracis are almost identical to DHFR in E.

coli, DHFR functions as a

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coli, the hydrophobic pABG binding pocket of DHFR from B.

As a competitive inhibitor, MTX binds to the active site of DHFR with higher affinity, and prevents the conversion of DHF into THF, which is required for the synthesis of the nucleoside thymidine.

Dihydrofolate reductase, or DHFR, ..

We examined the role that blockage of cells in the cell cycle may play in the stimulation of gene amplification and enhancement of drug resistance. We found that several different inhibitors of DNA synthesis, which were each able to block cells at the G1-S-phase boundary, induced an enhanced cycloheximide-sensitive synthesis of an early S-phase cell cycle-regulated enzyme, dihydrofolate reductase, and of other proteins as well. This response was specific, in that blockage at the G2 phase did not result in overproduction of the enzyme. When the cells were released from drug inhibition, DNA synthesis resumed, resulting in a cycloheximide-sensitive elevation in DNA content per cell. We speculate that the excess DNA synthesis (which could contribute to events detectable later as gene amplification) is a consequence of the accumulation of S-phase-specific proteins in the affected cells, which may then secondarily influence the pattern of DNA replication.

Dihydrofolate reductase inhibitor - Wikipedia

Compared to the DHFR from E.

Johnson EF, Hinz W, Atreya CE, et al. (2002) Mechanistic characterization of Toxoplasma gondii thymidylate synthase (TS‐DHFR)‐dihydrofolate reductase. Journal of Biological Chemistry 277: 43126–43136.

DHF cannot hydrogen bond to the carbonyl oxygen atoms of Leu-5(O) and Ile-94(O), but MTX can, and this partly contributes to the higher binding affinity of MTX to DHFR (8).

Inhibitors of dihydrofolate reductase ..

The ligand referenced in the PDB ID of this DHFR is meant to be a competitive inhibitor, similar to MTX, but specific to anthrax, and not humans.

Thymidylate is a component of DNA (deoxyribonucleic acid), and is synthesised from the or nucleotide salvage pathways. Many cell types rely on the salvage pathway, but often this is insufficient. Thymidylate is synthesised from deoxyuridylate and methylenetetrahydrofolate by thymidylate synthase (TYMS), with the enzymes dihydrofolate reductase (DHFR) and serine hydroxymethyltransferase (SHMT) or methylenetetrahydrofolate dehydrogenase 1 (MTHFD1) which are required to regenerate methylenetetrahydrofolate. The synthesis pathway forms a nuclear complex at the nuclear lamina at sites of DNA replication. DNA polymerases do not distinguish between deoxyuridylate and thymidylate, and when thymidylate synthesis is insufficient, uracil is misincorporated into DNA. This can lead to futile cycles of DNA repair and subsequent DNA single‐ and double‐strand breaks. Impaired thymidylate synthesis can result in neural tube defects, megaloblastic anaemia and severe combined immunodeficiency (SCID). Inhibitors of TYMS and DHFR impair cell replication and have been used in the treatment of cancer.

Inhibition of DHFR can slow the rate of cell proliferation, and DHFR is a drug target in cancerous cells, where cell proliferation is rapid and unregulated.

anthracis exhibits 62% sequence matching in the active site region and 39% sequence matching overall when compared with DHFR from E.
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  • Inhibits Dihydrofolate Reductase ..

    coli DHFR includes

  • DHFR | SelfDecode | Genome Analysis

    DHFR from B.

  • Dihydrofolate reductase inhibitor - Revolvy

    anthracis DHFR susceptible to folate analog inhibitors that are not specific for DHFR from other species.

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