Results 201 to 210 of about 15,062 (245)

Integrative Multi-Analysis Identifies METTL3-Regulated FGF19 and H6PD as Candidate Targets in Diabetic Cognitive Impairment. [PDF]

Biomolecules
Fu J, Wang H, Yan J, Chen W, Wang R, Gao H, Li C.   +6 more
europepmc   +1 more source

METTL3-driven m⁶A modification of NLRC5 promotes renal fibrosis in chronic kidney disease through Keap1/Nrf2/ARE signaling pathway. [PDF]

Front Immunol
Xu M, Chen R, Zeng X, Pan M, Wang C, Qi Y, An N, Bai Y.   +7 more
europepmc   +1 more source

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Discovery of a PROTAC degrader for METTL3-METTL14 complex

Cell Chemical Biology
N6-methyladenosine (m6A) methylation is the most abundant type of RNA modification that is mainly catalyzed by the METTL3-METTL14 methyltransferase complex. This complex has been linked to multiple cancers and is considered a promising therapeutic target for acute myeloid leukemia (AML).
Qiongyu Shi
exaly   +3 more sources

UVB promotes melanogenesis by regulating METTL3

Journal of Cellular Physiology, 2023
AbstractUltraviolet (UV) radiation is the primary exogenous inducer of skin pigmentation, although the mechanism has not been fully elucidated. N6‐methyladenosine (m6A) modification is one of the key epigenetic form of gene regulation that affects multiple biological processes.
Haoran Guo, Hongliang Zeng, Yibo Hu, Ling Jiang, Li Lei, Jinhua Hung, Chuhan Fu, Hui Li, Yan Long, Jing Chen, Qinghai Zeng   +10 more
openaire   +2 more sources

The Role of METTL3 in the Progression of Cardiac Fibrosis

Current Topics in Medicinal Chemistry, 2023
Abstract: Cardiac fibrosis is known as the expansion of the cardiac interstitium through excessive deposition of extracellular matrix proteins; this process is performed by a multifunctional cell known as the cardiac fibroblast. After the myocardial injury, these cells are activated as a repair program, increase, and switch to a contractile phenotype,
Samir Bolívar, Marian Pérez-Cantillo, Jassiris Monterroza-Torres, César Vásquez-Trincado, Jairo Castellar-Lopez, Evelyn Mendoza-Torres   +5 more
openaire   +2 more sources

RNA secondary structure dependence in METTL3–METTL14 mRNA methylation is modulated by the N-terminal domain of METTL3

Biological Chemistry, 2020
Abstract N 6-methyladenosine (m6A) is the most abundant modification in mRNA. The core of the human N 6-methyltransferase complex (MTC) is formed by a heterodimer consisting of METTL3 and METTL14, which specifically catalyzes m6A formation within an RRACH sequence context.
Nathalie Meiser, Nicole Mench, Martin Hengesbach   +2 more
openaire   +2 more sources

METTL3: a multifunctional regulator in diseases

Molecular and Cellular Biochemistry
N6-methyladenosine (m6A) methylation is the most prevalent and abundant internal modification of mRNAs and is catalyzed by the methyltransferase complex. Methyltransferase-like 3 (METTL3), the best-known m6A methyltransferase, has been confirmed to function as a multifunctional regulator in the reversible epitranscriptome modulation of m6A modification
Na, Li, Xiang, Wei, Jian, Dai, Jinfeng, Yang, Sizheng, Xiong   +4 more
openaire   +2 more sources

METTL3 is required for maintaining β-cell function

Metabolism, 2021
N6-methyladenosine (m6A) mRNA methylation has been shown to regulate obesity and type 2 diabetes. However, whether METTL3, the key methyltransferase for m6A mRNA methylation, regulates β-cell failure in diabetes has not been fully explored. Here, we show that METTL3 is downregulated under the inflammatory and oxidative stress conditions, and islet β ...
Xinzhi, Li, Yuze, Jiang, Xu, Sun, Yongsen, Wu, Zheng, Chen   +4 more
openaire   +2 more sources

Inhibition of Mettl3 by STM2457 and Loss of Macrophage Mettl3 Alleviate Pulmonary Hypertension and Right Heart Remodeling

Lung
m6A RNA methylation is a critical epigenetic modification involved in the pathogenesis of pulmonary arterial hypertension (PAH). While macrophage-mediated inflammation plays a central role in PAH, the specific contributions of m6A regulators within macrophages are not yet fully understood.
Chunfeng, He, Yingqun, Ji, Yan, Zhang, Jinbo, Ou, Di, Wu, Huan, Qin, Jing, Hua, Qiang, Li, Hao, Zheng   +8 more
openaire   +2 more sources