Aliases for NDUFA13 Gene
- NADH Dehydrogenase (Ubiquinone) 1 Alpha Subcomplex, 13 2 3
- Gene Associated With Retinoic And Interferon-Induced Mortality 19 Protein 3 4
- Gene Associated With Retinoic And IFN-Induced Mortality 19 Protein 3 4
- NADH-Ubiquinone Oxidoreductase B16.6 Subunit 3 4
- Cell Death Regulatory Protein GRIM-19 3 4
- Complex I B16.6 Subunit 2 3
- Complex I-B16.6 3 4
- CI-B16.6 3 4
External Ids for NDUFA13 Gene
Previous GeneCards Identifiers for NDUFA13 Gene
This gene encodes a subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I), which functions in the transfer of electrons from NADH to the respiratory chain. The protein is required for complex I assembly and electron transfer activity. The protein binds the signal transducers and activators of transcription 3 (STAT3) transcription factor, and can function as a tumor suppressor. The human protein purified from mitochondria migrates at approximately 16 kDa. Transcripts originating from an upstream promoter and capable of expressing a protein with a longer N-terminus have been found, but their biological validity has not been determined. [provided by RefSeq, Oct 2009]
GeneCards Summary for NDUFA13 Gene
NDUFA13 (NADH Dehydrogenase (Ubiquinone) 1 Alpha Subcomplex, 13) is a Protein Coding gene. Diseases associated with NDUFA13 include thyroid carcinoma, hurthle cell and differentiated thyroid carcinoma. Among its related pathways are Metabolism and EGFR1 Signaling Pathway. GO annotations related to this gene include NADH dehydrogenase (ubiquinone) activity and NADH dehydrogenase activity. An important paralog of this gene is ENSG00000258674.
UniProtKB/Swiss-Prot for NDUFA13 Gene
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. Involved in the interferon/all-trans-retinoic acid (IFN/RA) induced cell death. This apoptotic activity is inhibited by interaction with viral IRF1. Prevents the transactivation of STAT3 target genes. May play a role in CARD15-mediated innate mucosal responses and serve to regulate intestinal epithelial cell responses to microbes.