抗人 MAT2B 抗体对
01AB02434
Methionine adenosyltransferase 2 non-catalytic beta subunit (MAT2B) is a regulatory subunit of the cytosolic S-adenosylmethionine synthetase 2 (MAT2A) complex. While MAT2B lacks independent catalytic activity, it modulates the kinetics of MAT2A by increasing its affinity for L-methionine and influencing feedback sensitivity to S-adenosylmethionine (SAM). Structurally, MAT2B adopts a short-chain dehydrogenase/reductase-like fold and binds NADP(H), which stabilizes the MAT2A protein and links cellular redox status to SAM production and RNA m6A methylation. This regulatory mechanism is vital for maintaining the methyl donor pool required for diverse cellular processes. Clinically, MAT2B is broadly expressed in proliferative tissues and its overexpression has been implicated in supporting the metabolic demands of tumor growth.
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技术参数
- 靶点基因名
- MAT2B
- 基因别名
- TGR
- 蛋白别名
- methionine adenosyltransferase 2 non-catalytic beta subunit; MAT2B
- UniProt
- Q9NZL9
- 物种
- Human
产品详情
- 靶点名称
- MAT2B
- 蛋白名称
- methionine adenosyltransferase 2 non-catalytic beta subunit
- 蛋白别名
- Methionine adenosyltransferase 2 subunit beta; Methionine adenosyltransferase II beta; MAT II beta; Putative dTDP-4-keto-6-deoxy-D-glucose 4-reductase
- 靶点基因名
- MAT2B
- 基因别名
- TGR
- UniProt
- Q9NZL9
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Methionine adenosyltransferase 2 non-catalytic beta subunit (MAT2B) is a regulatory subunit of the cytosolic S-adenosylmethionine synthetase 2 (MAT2A) complex. While MAT2B lacks independent catalytic activity, it modulates the kinetics of MAT2A by increasing its affinity for L-methionine and influencing feedback sensitivity to S-adenosylmethionine (SAM). Structurally, MAT2B adopts a short-chain dehydrogenase/reductase-like fold and binds NADP(H), which stabilizes the MAT2A protein and links cellular redox status to SAM production and RNA m6A methylation. This regulatory mechanism is vital for maintaining the methyl donor pool required for diverse cellular processes. Clinically, MAT2B is broadly expressed in proliferative tissues and its overexpression has been implicated in supporting the metabolic demands of tumor growth.