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Literature summary for 6.2.1.1 extracted from

  • Yoshii, Y.; Furukawa, T.; Yoshii, H.; Mori, T.; Kiyono, Y.; Waki, A.; Kobayashi, M.; Tsujikawa, T.; Kudo, T.; Okazawa, H.; Yonekura, Y.; Fujibayashi, Y.
    Cytosolic acetyl-CoA synthetase affected tumor cell survival under hypoxia: the possible function in tumor acetyl-CoA/acetate metabolism (2009), Cancer Sci., 100, 821-827.
    View publication on PubMed

Application

Application Comment Organism
medicine cells express higher levels of cytosolic acetyl-CoA synthetase ACSS2 under hypoxia than normoxia. Knockdown of ACSS2 by RNA interference in tumor cells enhances tumor cell death under long-term hypoxia in vitro. The ACSS2 suppression slows tumor growth in vivo. Tumor cells excrete acetate and the quantity increases under hypoxia, the pattern of acetate excretion follows the expression pattern of ACSS2. The ACSS2 knockdown leads to a corresponding reduction in the acetate excretion in tumor cells Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
cytosol
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Mus musculus 5829
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Organism

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
B-16 cell cells express higher levels of cytosolic acetyl-CoA synthetase ACSS2 under hypoxia than normoxia. Knockdown of ACSS2 by RNA interference in tumor cells enhances tumor cell death under long-term hypoxia in vitro. The ACSS2 suppression slows tumor growth in vivo. Tumor cells excrete acetate and the quantity increases under hypoxia, the pattern of acetate excretion follows the expression pattern of ACSS2. The ACSS2 knockdown leads to a corresponding reduction in the acetate excretion in tumor cells Mus musculus
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C127I cell cells express higher levels of cytosolic acetyl-CoA synthetase ACSS2 under hypoxia than normoxia. Knockdown of ACSS2 by RNA interference in tumor cells enhances tumor cell death under long-term hypoxia in vitro. The ACSS2 suppression slows tumor growth in vivo. Tumor cells excrete acetate and the quantity increases under hypoxia, the pattern of acetate excretion follows the expression pattern of ACSS2. The ACSS2 knockdown leads to a corresponding reduction in the acetate excretion in tumor cells Mus musculus
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Colon-26 cell cells express higher levels of cytosolic acetyl-CoA synthetase ACSS2 under hypoxia than normoxia. Knockdown of ACSS2 by RNA interference in tumor cells enhances tumor cell death under long-term hypoxia in vitro. The ACSS2 suppression slows tumor growth in vivo. Tumor cells excrete acetate and the quantity increases under hypoxia, the pattern of acetate excretion follows the expression pattern of ACSS2. The ACSS2 knockdown leads to a corresponding reduction in the acetate excretion in tumor cells Mus musculus
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LL/2 (LLC1) cell cells express higher levels of cytosolic acetyl-CoA synthetase ACSS2 under hypoxia than normoxia. Knockdown of ACSS2 by RNA interference in tumor cells enhances tumor cell death under long-term hypoxia in vitro. The ACSS2 suppression slows tumor growth in vivo. Tumor cells excrete acetate and the quantity increases under hypoxia, the pattern of acetate excretion follows the expression pattern of ACSS2. The ACSS2 knockdown leads to a corresponding reduction in the acetate excretion in tumor cells Mus musculus
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General Information

General Information Comment Organism
physiological function tumor cells express higher levels of cytosolic acetyl-CoA synthetase ACSS2 under hypoxia than normoxia. Knockdown of ACSS2 by RNA interference in tumor cells enhances tumor cell death under long-term hypoxia in vitro. The ACSS2 suppression slows tumor growth in vivo. Tumor cells excrete acetate and the quantity increases under hypoxia, the pattern of acetate excretion follows the expression pattern of ACSS2. The ACSS2 knockdown leads to a corresponding reduction in the acetate excretion in tumor cells Mus musculus