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Flaherty et al. demonstrate that the catalytic efficiency of METTL16 regulates expression of MAT2A to determine the intracellular SAM setpoint. Their data indicate that this is required for several SA...

Cell Death & Differentiation - Endothelial USP2a-METTL16 loop potentiates IL-6 signaling via m6A-mediated IL-6R stabilization in pulmonary vascular remodeling

Liu et al. show that diabetes induces immunosuppressive Schwann cells via lactate-METTL16-CTCF signaling in PDAC, promoting PD-1 resistance. Targeting this pathway restores anti-tumor immunity and enh...

Aging | doi:10.18632/aging.206210. Ling Liu, Siying Wang, Xuyu Chen, Qian Luo, Zhaoxia Wang, Juan Li

Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · Gong Z, Dong K, Chen W, Liu Y, Li M, Ma W, Zheng H, Zhang H, Di S, Zhou W, Pan X, Cui X.

Liu et al. show that diabetes induces immunosuppressive Schwann cells via lactate-METTL16-CTCF signaling in PDAC, promoting PD-1 resistance. Targeting this pathway restores anti-tumor immunity and enhances therapy, providing key insights into metabolic-immune interactions and offering a promising strategy to improve immunotherapy outcomes in patients with high risk.

Journal of advanced research · Ren J, Liu W, Zou R, Sun K, Yang M, Zhu X, Yang Z.

Biochimica et biophysica acta. Molecular basis of disease · Shang Z, Zhou M, Yan S, Su S, Zheng R, Wang Y, Xiao Y.

The Biochemical journal · Yang F, Li Y, Zhang Y, Sun W, Wang XJ, Qi J, Sagum C, Bedford MT.

U6 snRNA m6A modification by METTL16 is essential for accurate pre-mRNA splicing. Here, the authors determined the cryo-EM structure of METTL16 bound to U6 snRNA and SAM, revealing how its two domains...

In a groundbreaking study poised to revolutionize our understanding of premature ovarian failure (POF), researchers have unveiled a novel molecular mechanism that protects ovarian granulosa cells from

In a groundbreaking study poised to transform our understanding of renal carcinogenesis, researchers have unveiled a novel molecular mechanism by which CDK13 orchestrates the progression of clear cell

The C-terminal KA-1 domain of human METTL16 (hsMETTL16) reportedly facilitates the m6A43 modification of U6 snRNA in vitro37, and KA-1 domains are conserved among METTL16 homologs in vertebrates and invertebrates38. The KA-1 domain is also present in METTL16 homologs in...

In the relentless battle against non-small-cell lung cancer (NSCLC), a new molecular revelation is shedding light on the troubling phenomenon of resistance to tyrosine kinase inhibitors (TKIs), drugs that have revolutionized treatment but are often undermined by the cancer's adaptive defenses. Recent research published in BMC Cancer uncovers a critical epigenetic modification pathway involving METTL16, a methyltransferase enzyme, that modifies the mRNA of glutathione peroxidase 4 (GPX4) through N6-methyladenosine (m6A), linking the suppression of ferroptosis—a distinctive cell death pathway—to NSCLC’s stubborn resistance to the third-generation TKI, AZD-9291, also known as Osimertinib.