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Literature summary for 2.3.1.21 extracted from

  • Zaugg, K.; Yao, Y.; Reilly, P.T.; Kannan, K.; Kiarash, R.; Mason, J.; Huang, P.; Sawyer, S.K.; Fuerth, B.; Faubert, B.; Kalliomaeki, T.; Elia, A.; Luo, X.; Nadeem, V.; Bungard, D.; Yalavarthi, S.; Growney, J.D.; Wakeham, A.; Moolani, Y.; Silvester, J.; Ten, A.Y.; Bakker, W.; Tsuchihara, K.; Berger, S.L.; H, H.i.
    Carnitine palmitoyltransferase 1C promotes cell survival and tumor growth under conditions of metabolic stress (2011), Genes Dev., 25, 1041-1051.
    View publication on PubMedView publication on EuropePMC

Application

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

Organism UniProt Comment Textmining
Homo sapiens Q8TCG5 isoform CPT1C
-
Mus musculus Q8BGD5 isoform CPT1C
-

Source Tissue

Source Tissue Comment Organism Textmining
brain brain-specific enzyme Homo sapiens
-
brain brain-specific enzyme Mus musculus
-

Synonyms

Synonyms Comment Organism
CPT1c
-
Homo sapiens
CPT1c
-
Mus musculus

Expression

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

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