人 NDUFB8 抗体对
01AB01256
NADH:ubiquinone oxidoreductase subunit B8 (NDUFB8) is an accessory subunit of mitochondrial Complex I, the first enzyme in the electron transport chain, which is crucial for cellular energy production. NDUFB8 is not directly involved in the catalytic transfer of electrons but plays an essential role in maintaining the structural integrity and proper assembly of Complex I, thereby ensuring efficient electron transfer from NADH to ubiquinone and supporting ATP synthesis in mitochondria. The protein consists of 186 amino acids and is embedded in the mitochondrial inner membrane, contributing to the stability of the respiratory chain complex. Dysfunction or deficiency of NDUFB8 can disrupt mitochondrial electron transport, leading to impaired energy metabolism and has been associated with mitochondrial diseases, including some forms of mitochondrial complex I deficiency, which can manifest as neuromuscular and metabolic disorders.
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技术参数
- 靶点基因名
- NDUFB8
- 蛋白别名
- NADH:ubiquinone oxidoreductase subunit B8; NDUFB8
- UniProt
- O95169
- 物种
- Human
产品详情
- 靶点名称
- NDUFB8
- 蛋白名称
- NADH:ubiquinone oxidoreductase subunit B8
- 蛋白别名
- NADH dehydrogenase [ubiquinone] 1 beta subcomplex subunit 8; mitochondrial; Complex I-ASHI; CI-ASHI; NADH-ubiquinone oxidoreductase ASHI subunit
- 靶点基因名
- NDUFB8
- UniProt
- O95169
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
NADH:ubiquinone oxidoreductase subunit B8 (NDUFB8) is an accessory subunit of mitochondrial Complex I, the first enzyme in the electron transport chain, which is crucial for cellular energy production. NDUFB8 is not directly involved in the catalytic transfer of electrons but plays an essential role in maintaining the structural integrity and proper assembly of Complex I, thereby ensuring efficient electron transfer from NADH to ubiquinone and supporting ATP synthesis in mitochondria. The protein consists of 186 amino acids and is embedded in the mitochondrial inner membrane, contributing to the stability of the respiratory chain complex. Dysfunction or deficiency of NDUFB8 can disrupt mitochondrial electron transport, leading to impaired energy metabolism and has been associated with mitochondrial diseases, including some forms of mitochondrial complex I deficiency, which can manifest as neuromuscular and metabolic disorders.