Application | Comment | Organism |
---|---|---|
medicine | isoform CPT1C expression is frequently up-regulated in human lung tumors. Tumor cells constitutively expressing CPT1C show increased fatty acid oxidation, ATP production, and resistance to glucose deprivation or hypoxia. Conversely, cancer cells lacking CPT1C produce less ATP and are more sensitive to metabolic stress. CPT1Cdepletion via siRNA suppresses xenograft tumor growth and metformin responsiveness in vivo. CPT1C can be induced by hypoxia or glucose deprivation and is regulated by AMPKalpha | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q8TCG5 | isoform CPT1C | - |
Mus musculus | Q8BGD5 | isoform CPT1C | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
brain | brain-specific enzyme | Homo sapiens | - |
brain | brain-specific enzyme | Mus musculus | - |
Synonyms | Comment | Organism |
---|---|---|
CPT1c | - |
Homo sapiens |
CPT1c | - |
Mus musculus |
Organism | Comment | Expression |
---|---|---|
Mus musculus | isoform CPT1C can be induced by hypoxia or glucose deprivation and is regulated by AMPKalpha | up |
Homo sapiens | isoform CPT1C expression is frequently up-regulated in human lung tumors. CPT1C can be induced by hypoxia or glucose deprivation and is regulated by AMPKalpha | up |
General Information | Comment | Organism |
---|---|---|
physiological function | CPT1C expression correlates inversely with mammalian target of rapamycin pathway activation, and contributes to rapamycin resistance in murine primary tumors. Tumor cells constitutively expressing CPT1C show increased fatty acid oxidation, ATP production, and resistance to glucose deprivation or hypoxia. Cancer cells lacking CPT1C produce less ATP and are more sensitive to metabolic stress. CPT1C depletion via siRNA suppresses xenograft tumor growth and metformin responsiveness in vivo | Mus musculus |
physiological function | isoform CPT1C expression is frequently up-regulated in human lung tumors. Tumor cells constitutively expressing CPT1C show increased fatty acid oxidation, ATP production, and resistance to glucose deprivation or hypoxia. Conversely, cancer cells lacking CPT1C produce less ATP and are more sensitive to metabolic stress. CPT1Cdepletion via siRNA suppresses xenograft tumor growth and metformin responsiveness in vivo. CPT1C can be induced by hypoxia or glucose deprivation and is regulated by AMPKalpha | Homo sapiens |