m6A-ATP,100mM Sodium Solution

m6A-ATP is an adenosine agonist with an ED50 value of 17.250 µM, and is a modulator of adenylate cyclase[1]. m6A-ATP inhibits hemoglobin accumulation and terminal maturation initiation in a concentration-dependent manner. In MEL cells, m6A-ATP reduces the mRNA of β-globin accumulated in the cytoplasm, affecting the structural integrity of this mRNA[2]. m6A-ATP slows down the growth rate of MEL cells, but basically does not inhibit cellular DNA synthesis and reduce cell viability and clonal potential[2]. Adenine, L-homocysteine, and/or L-methionine are all involved in the activated methylation cycle, enhancing m6A-ATP induced inhibition of initiation[3].

M6A modification is the most prevalent, abundant and conserved internal co-transcriptional modification in eukaryotic RNA, especially in higher eukaryotic cells[4]. M6A modification is considered as one of the post-transcriptional regulatory marks of different types of RNAs, including messenger RNAs (mRNAs), transfer RNAs (tRNAs), ribosomal RNAs (rRNAs), circular RNAs (circRNAs), microRNAs (miRNAs) and long Noncoding RNAs (IncRNAs)[4]. M6A modification preferentially occurs within the consensus sequence RRACH (R = G or A; H = A, C or U) in the 3' UTRs and gene coding regions, and is involved in the processing and stability regulation of mRNA[5].

References:
[1]. Ribeiro JA and Sebastio AM. On the type of receptor involved in the inhibitory action of adenosine at the neuromuscular junction. Br J Pharmacol, 1985, 84(4):911-8.
[2]. Sinn P L and Sigmund CD. Human renin mRNA stability is increased in response to cAMP in Calu-6 cells. Hypertension, 1999, 33(3): 900-905.
[3]. Vizirianakis IS, Wong W and Tsiftsoglou AS. Analysis of the inhibition of commitment of murine erythroleukemia (MEL) cells to terminal maturation by N 6-methyladenosine. Biochemical pharmacology, 1992, 44(5): 927-936.
[4]. Shanshan Wang, et al. Dynamic regulation and functions of mRNA m6A modification. Cancer Cell International volume 22, Article number: 48 (2022)..
[5]. Zhao X, Yang Y, Sun BF, et al. FTO-dependent demethylation of N6-methyladenosine regulates mRNA splicing and is required for adipogenesis. Cell research, 2014, 24(12): 1403-1419.

m6A-ATP是一种腺苷激动剂,ED50值为17.250 µM,是腺苷酸环化酶的调节剂[1]。m6A-ATP以浓度依赖的方式抑制血红蛋白的积累及终端成熟起始反应。在MEL细胞中,m6A-ATP降低细胞质中积累的β球蛋白的mRNA,影响该mRNA的结构完整性[2]。m6A-ATP能够减缓MEL细胞的生长速度,但基本没有抑制细胞DNA合成及降低细胞活力和克隆潜力[2]。腺嘌呤、L-高半胱氨酸和/或L-蛋氨酸都参与了活化的甲基化周期,加强了m6A-ATP诱导的起始抑制[3]。

m6A修饰是真核RNA中最普遍、最丰富 和最保守的内部共转录修饰,尤其是在高等真核细胞中[4]。m6A修饰被认为是不同类型RNA的转录后调节标记之一,包括信使RNA(mRNAs)、转移RNA(tRNAs)、核糖体RNA(rRNAs)、环状RNA(circRNAs)、微RNA(miRNA)和长非编码RNA(IncRNAs) [4]。m6A修饰优先发生在3'UTRs和基因编码区的共有序列RRACH内(R = G或A; H = A、C或U),参与mRNA的加工和稳定性调节[5]。