MTH1酶即MutT同源酶1(MutT homolog 1)，属于Nudix(nucleoside diphosphate linked to x)水解酶超级家族，是由NUDT1基因表达所得的8-羟基鸟嘌呤核苷酸酶，其国际生物化学联合会酶学委员会编号为EC 3.6.1.55。

2023年8月10日 · Human MutT Homolog 1 (MTH1) is a nucleotide pool sanitization enzyme that hydrolyzes oxidized nucleotides to prevent their mis-incorporation into DNA under oxidative...

2-hydroxy-dATP diphosphatase (EC 3.6.1.56, also known as oxidized purine nucleoside triphosphatase, or (2'-deoxy) ribonucleoside 5'-triphosphate pyrophosphohydrolase, or Nudix hydrolase 1 (NUDT1), or MutT homolog 1 (MTH1), or 7,8-dihydro-8-oxoguanine triphosphatase) is an enzyme that in humans is encoded by the NUDT1 gene.

2014年4月2日 · We validate MTH1 as an anticancer target in vivo and describe small molecules TH287 and TH588 as first-in-class nudix hydrolase family inhibitors that potently and selectively engage and inhibit...

2 天之前 · mth1 在细胞内负责清除 ros 损伤的 dntps，防止氧化的 dntps 掺入 dna，维持细胞的正常功能。当细胞增殖或发生炎症时，ros 水平升高，mth1 表达也会上调，这使得高表达 mth1 的细胞对 mth1 抑制更为敏感。

MTH1 functions by hydrolyzing oxidized deoxyribonucleoside triphosphates, thereby preventing the incorporation of oxidized dNTPs into DNA during replication and maintaining normal cell functionality. Additionally, MTH1 is known for removing methylated purine triphosphates, such as O6-methyl-dGTP, from the nucleotide pool.

2023年8月10日 · Human MutT Homolog 1 (MTH1) is a nucleotide pool sanitization enzyme that hydrolyzes oxidized nucleotides to prevent their mis-incorporation into DNA under oxidative stress. Expression and functional roles of MTH1 in platelets are not known. Here, we show MTH1 expression in platelets and its deficie …

mth1 水平在许多癌症中通常升高，因此，抑制 mth1 是抑制肿瘤生长和转移的一种有吸引力的策略。靶向 mth1 抑制可在癌细胞中诱导 dna 损伤，利用它们对氧化应激的脆弱性并选择性地靶向它们进行破坏。

最新的研究表明,MTH1可以清除肿瘤细胞中受损DNA功能结构的氧化构件,使得肿瘤细胞继续分裂与增殖,从而维持肿瘤细胞的生存,而更为重要的是正常细胞不需要MTH1,因此,MTH1有可能只与异常的细胞生长密切相关,这使得MTH1作为治疗靶点成为人们关注的焦点。 该文着重对MTH1与肿瘤关系最新的研究成果进行综述,探讨MTH1维持肿瘤生长的相关机制及其与肿瘤治疗的关系,为靶向MTH1治疗肿瘤提供新的思路,为肿瘤研究工作者提供重要参考。

MTH1 (MutT homolog 1) can effectively sanitize oxidized nucleotides in the nucleotides pool to pro-tect cancer cells from fatal damage caused by high levels of ROS (reactive oxygen species). In con-trast, the normal cells can repair DNA oxidative damage to survive by the alternative pathway when MTH1 is inhibited.