Much more than you expected: The non-DHFR-mediated effects of methotrexate
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F17%3A00066062" target="_blank" >RIV/00159816:_____/17:00066062 - isvavai.cz</a>
Výsledek na webu
<a href="http://dx.doi.org/10.1016/j.bbagen.2016.12.014" target="_blank" >http://dx.doi.org/10.1016/j.bbagen.2016.12.014</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.bbagen.2016.12.014" target="_blank" >10.1016/j.bbagen.2016.12.014</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Much more than you expected: The non-DHFR-mediated effects of methotrexate
Popis výsledku v původním jazyce
ACKGROUND: For decades, methotrexate (MTX; amethopterin) has been known as an antifolate inhibitor of dihydrofolate reductase (DHFR), and it is widely used for the treatment of various malignancies and autoimmune diseases. Although the inclusion of MTX in various therapeutic regimens is based on its ability to inhibit DHFR and consequently to suppress the synthesis of pyrimidine and purine precursors, recent studies have shown that MTX is also able to target other intracellular pathways that are independent of folate metabolism. SCOPE OF REVIEW: The main aim of this review is to summarize the most important, up-to-date findings of studies regarding the non-DHFR-mediated mechanisms of MTX action. MAJOR CONCLUSIONS: The effectiveness of MTX is undoubtedly caused by its capability to affect various intracellular pathways at many levels. Although the most important therapeutic mechanism of MTX is strongly based on the inhibition of DHFR, many other effects of this compound have been described and new studies bring new insights into the pharmacology of MTX every year. GENERAL SIGNIFICANCE: Identification of these new targets for MTX is especially important for a better understanding of MTX action in new protocols of combination therapy.
Název v anglickém jazyce
Much more than you expected: The non-DHFR-mediated effects of methotrexate
Popis výsledku anglicky
ACKGROUND: For decades, methotrexate (MTX; amethopterin) has been known as an antifolate inhibitor of dihydrofolate reductase (DHFR), and it is widely used for the treatment of various malignancies and autoimmune diseases. Although the inclusion of MTX in various therapeutic regimens is based on its ability to inhibit DHFR and consequently to suppress the synthesis of pyrimidine and purine precursors, recent studies have shown that MTX is also able to target other intracellular pathways that are independent of folate metabolism. SCOPE OF REVIEW: The main aim of this review is to summarize the most important, up-to-date findings of studies regarding the non-DHFR-mediated mechanisms of MTX action. MAJOR CONCLUSIONS: The effectiveness of MTX is undoubtedly caused by its capability to affect various intracellular pathways at many levels. Although the most important therapeutic mechanism of MTX is strongly based on the inhibition of DHFR, many other effects of this compound have been described and new studies bring new insights into the pharmacology of MTX every year. GENERAL SIGNIFICANCE: Identification of these new targets for MTX is especially important for a better understanding of MTX action in new protocols of combination therapy.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10608 - Biochemistry and molecular biology
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
2017
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Biochimica et Biophysica Acta - General Subjects
ISSN
0304-4165
e-ISSN
—
Svazek periodika
1861
Číslo periodika v rámci svazku
3
Stát vydavatele periodika
NL - Nizozemsko
Počet stran výsledku
5
Strana od-do
499-5035
Kód UT WoS článku
000394076400001
EID výsledku v databázi Scopus
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