M1G (pyrimido [1,2-a]purin-10 (3H)-one) is a heterocyclic compound which is a by-product of base excision repair (BER) of a specific type of DNA adduct called M 1 dG. The M 1 dG adduct in turn is formed by a condensation reaction between guanosine nucleotides in DNA and either malondialdehyde (propanedial) [1] or acrolein. [2] .

2016年8月1日 · Here, we show that G-C + (in which + indicates protonation) and A-U Hoogsteen base pairs are strongly disfavored in A-RNA. As a result, N1 -methyladenosine and N1 -methylguanosine, which occur in...

2020年3月27日 · Here, we quantify variation in m1A/G RNA modification levels at functionally important positions in the human mitochondrial genome across 11,552 samples from 39 tissue/cell types and find that...

2023年5月12日 · Our study suggests that Trmt10c, Alkbh3, and Ythdf3 may be m1A-regulating enzymes in neurons during OGD/R induction. The level and pattern of m1A modification change significantly during OGD/R...

Here, we show that G–C + and A–U Hoogsteen base pairs are strongly disfavored in A-RNA. As a result, N1 -methyl adenosine and N1 -methyl guanosine, which occur in DNA as a form of alkylation damage, and in RNA as a posttranscriptional modification, have …

Methylation and N1 position of guanosine, or 1-methylguanosine (m1G), is presented on different tRNAs. Studies have shown that the presence of m1G at those locations are good for stabilizing tRNA tertiary structure, correct folding and preventing translational error.

M1G和6-oxo-M1G在RLC中都是比脱氧核苷M1dG更好的氧化代谢底物（5倍）。 M1dG的替代修复途径或生物加工过程使感兴趣的M1G的命运成为体内氧化损伤的潜在标志。

Here, we show that G-C (+) (in which + indicates protonation) and A-U Hoogsteen base pairs are strongly disfavored in A-RNA. As a result,N (1)-methyladenosine and N (1)-methylgu …

We utilized the aldehyde reactive probe (ARP) to produce a stable ARP-M 1 G-deoxyribose (ARP-M 1 G-dR) conjugate to minimize adduct loss. This conjugate has increased the hydrophobicity that enhances separation of ARP-M 1 G-dR from unmodified DNA nucleosides by using solid phase extraction.

The key mechanisms of m1A and m1G modified tRNA in various diseases involve several important pathways. Overexpression of TRMT6/61A in neoplasm promotes tumour proliferation by up-regulating m1A levels in tRFs in BLCA and stimulating PPARδ translation in HCC.