Molecule Information
General Information of the Molecule (ID: Mol04052)
| Name |
NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 10 (NDUFA10)
,Homo sapiens
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| Synonyms |
Complex I-42kD; NADH-ubiquinone oxidoreductase 42 kDa subunit
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| Molecule Type |
Protein
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| Gene Name |
NDUFA10
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| Gene ID | |||||
| Location |
chr2:239892450-240025743[-]
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| Sequence |
MALRLLKLAATSASARVVAAGAQRVRGIHSSVQCKLRYGMWHFLLGDKASKRLTERSRVI
TVDGNICTGKGKLAKEIAEKLGFKHFPEAGIHYPDSTTGDGKPLATDYNGNCSLEKFYDD PRSNDGNSYRLQSWLYSSRLLQYSDALEHLLTTGQGVVLERSIFSDFVFLEAMYNQGFIR KQCVDHYNEVKSVTICDYLPPHLVIYIDVPVPEVQRRIQKKGDPHEMKITSAYLQDIENA YKKTFLPEMSEKCEVLQYSAREAQDSKKVVEDIEYLKFDKGPWLKQDNRTLYHLRLLVQD KFEVLNYTSIPIFLPEVTIGAHQTDRVLHQFRELPGRKYSPGYNTEVGDKWIWLK Click to Show/Hide
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| 3D-structure |
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| Function |
Accessory subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I), that is believed not to be involved in catalysis. Complex I functions in the transfer of electrons from NADH to the respiratory chain. The immediate electron acceptor for the enzyme is believed to be ubiquinone. .
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Type(s) of Resistant Mechanism of This Molecule
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Breast adenocarcinoma [ICD-11: 2C60.1] | [1] | |||
| Metabolic Type | Glucose metabolism | |||
| Resistant Disease | Breast adenocarcinoma [ICD-11: 2C60.1] | |||
| Resistant Drug | Trastuzumab | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Identified from the Human Clinical Data | |||
| In Vivo Model | Breast Cancer patients | Homo Sapiens | ||
| Experiment for Molecule Alteration |
Western blot analysis | |||
| Mechanism Description | The analysis of differentially expressed proteins exhibited the deregulation of energetic metabolism and mitochondrial pathways. A down-regulation of carbohydrate metabolism and up-regulation of mitochondria organization proteins, the tricarboxylic acid cycle, and oxidative phosphorylation, were observed in nRSs. Of note, Complex I-related proteins were increased in this condition and the inhibition by metformin highlighted that their activity is necessary for nRS survival. Furthermore, a correlation analysis showed that overexpression of Complex I proteins NDUFA10 and NDUFS2 was associated with high clinical risk and worse survival for HER2+ BC patients | |||
References
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