Mouse Mettl3 Stable Cell Line - NIT-1

The Mettl3 gene encodes the catalytic subunit of the N6-methyladenosine (m6A) methyltransferase complex, which is responsible for the most abundant internal modification of eukaryotic mRNA. METTL3 forms a heterodimer with METTL14, acting as a "writing enzyme" to deposit methyl groups at the N6 position of adenosine residues in the conserved RRACH concordant sequence. This epitranscriptome modification is a key regulator of the RNA lifecycle, affecting mRNA stability, alternative splicing, nuclear export, and translation efficiency. In metabolic systems, Mettl3-mediated m6A modification plays a crucial role in maintaining lipid and glucose homeostasis. Studies have shown that the absence of Mettl3 in hepatocytes leads to severe lipid accumulation and progressive liver injury (MASLD), the mechanism of which is through disruption of the mRNA stability of key lipid oxidation genes such as Cpt1a and Cyp7a1. Furthermore, METTL3 is essential for the normal function and survival of pancreatic β-cells, regulating the expression of genes involved in insulin signaling and oxidative stress responses. Dysregulation of the METTL3-m6A axis is a key driver of type 2 diabetes and metabolic syndrome.

The NIT-1-based mouse Mettl3 stable cell line is a specialized endocrine model derived from pancreatic β-cells of transgenic mice. This cell line provides a stable platform for Mettl3 overexpression, enabling researchers to delve into the precise role of RNA methylation in pancreatic endocrine function. This product is particularly suitable for studying how epitranscriptomic changes integrate environmental metabolic signals into cellular insulin output and how these pathways are disrupted during diabetes progression. Researchers use this model to identify specific m6A sites on insulin-related transcripts that regulate β-cell number and secretory capacity under stress. Furthermore, the NIT-1-Mettl3 cell line is a high-fidelity screening tool for screening small molecule activators or inhibitors of the m6A mechanism, which are increasingly becoming novel drugs for treating metabolic disorders.