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Literature summary for 7.1.2.2 extracted from

  • Willers, I.M.; Cuezva, J.M.
    Post-transcriptional regulation of the mitochondrial H+-ATP synthase: a key regulator of the metabolic phenotype in cancer (2011), Biochim. Biophys. Acta, 1807, 543-551.
    View publication on PubMed
Search for more literature for 7.1.2.2

Inhibitors

Inhibitors Comment Organism Structure
ATPase inhibitor factor 1 i.e. IF1, intrinsic peptide inhibitor, up-regulated in human breast, colon and lung carcinomas. The binding of IF1 to beta-F1-ATPase is regulated by the energetic state of mitochondria. siRNA-mediated silencing of IF1 in cells expressing high levels of IF1 triggers the down-regulation of aerobic glycolysis and an increase in the activity of the H+-ATP synthase Homo sapiens
ATPase inhibitor factor 1 i.e. IF1 Rattus norvegicus
ATPase inhibitor factor 1 i.e. IF1 Saccharomyces cerevisiae
oligomycin
-
 Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrial membrane
-
 Homo sapiens 31966
-
mitochondrial membrane
-
 Rattus norvegicus 31966
-
mitochondrial membrane
-
 Saccharomyces cerevisiae 31966
-

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-
Rattus norvegicus
-
-
-
Saccharomyces cerevisiae
-
 gene ATP2 beta-F1-ATPase
-

Source Tissue

Source Tissue Comment Organism Textmining
carcinoma cell downregulation of beta-F1-ATPase is a hallmark of most human carcinomas. Translational silencing is usually mediated by 3'UTR-mediated sequestration of the mRNA into RNPs Homo sapiens
-
HCT-116 cell HCT-116-derived carcinoma cell lines expressing different levels of beta-F1-ATPase Homo sapiens
-
hepatocyte
-
 Rattus norvegicus
-
liver
-
 Rattus norvegicus
-

Subunits

Subunits Comment Organism
More beta-F1-ATPase is the catalytic subunit of the mitochondrial H+-ATP synthase Homo sapiens
More beta-F1-ATPase is the catalytic subunit of the mitochondrial H+-ATP synthase Rattus norvegicus
More beta-F1-ATPase is the catalytic subunit of the mitochondrial H+-ATP synthase Saccharomyces cerevisiae

Synonyms

Synonyms Comment Organism
mitochondrial H+-ATP synthase
-
 Homo sapiens
mitochondrial H+-ATP synthase
-
 Rattus norvegicus
mitochondrial H+-ATP synthase
-
 Saccharomyces cerevisiae

Expression

Organism Comment Expression
Homo sapiens repression of beta-F1-ATPase expression in development and in cancer, translational silencing is usually mediated by 3'UTR-mediated sequestration of the mRNA into RNPs. Role of ATPase inhibitor factor 1 and of Ras-GAP SH3 binding protein 1, G3BP1, controlling the activity of the H+-ATP synthase and the translation of beta-F1-ATPase mRNA respectively in cancer cells. A trans-acting factor that regulate beta-F1-ATPase mRNA translation, is G3BP1, Ras-GAP SH3 binding protein 1, that interacts with the 3'UTR of beta-mRNA, the interaction specifically represses mRNA translation by preventing its recruitment into active polysomes down
Homo sapiens expression of the catalytic subunit beta-F1-ATPase is tightly regulated at post-transcriptional levels during mammalian development and in the cell cycle additional information
Rattus norvegicus expression of the catalytic subunit beta-F1-ATPase is tightly regulated at post-transcriptional levels during mammalian development and in the cell cycle additional information
Saccharomyces cerevisiae expression of the catalytic subunit beta-F1-ATPase is tightly regulated at post-transcriptional levels during mammalian development and in the cell cycle additional information

General Information

General Information Comment Organism
malfunction deletion of the 3'-UTR in the ATP2 gene leads to deficient protein import and reduced ATP synthesis, mtDNA depletion and respiratory dysfunction Saccharomyces cerevisiae
malfunction down-regulation of beta-F1-ATPase expression in chronic myeloid leukemia leads to adriamycin resistance. Deletion of IEX-1, a stress-inducible gene that apparently targets IF1 for degradation, results in the inhibition of the ATP synthase activity in vivo. Relevance of mitochondrial dysfunction as a central player of tumorigenesis, mechanisms participating in controlling the content and activity of the H+-ATP synthase, which is a bottleneck component of oxidative phosphorylation, overview Homo sapiens
metabolism repression of the bioenergetic function of mitochondria is one of the strategies of the cancer cell in order to ensure its proliferation by diminishing the potential to execute ROS-mediated cell death Homo sapiens
additional information ATP2 mRNA is no Puf3p target and belongs to the class of Puf3-independent mitochondria-localized mRNAs Saccharomyces cerevisiae
additional information expression of the catalytic subunit beta-F1-ATPase is tightly regulated at post-transcriptional levels during mammalian development and in the cell cycle. Downregulation of beta-F1-ATPase is a hallmark of most human carcinomas. Role of the ATPase inhibitor factor 1 and of Ras-GAP SH3 binding protein 1, G3BP1, controlling the activity of the H+-ATP synthase and the translation of beta-F1-ATPase mRNA respectively in cancer cells Rattus norvegicus
additional information expression of the catalytic subunit beta-F1-ATPase is tightly regulated at post-transcriptional levels during mammalian development and in the cell cycle. Downregulation of beta-F1-ATPase is a hallmark of most human carcinomas. Role of the ATPase inhibitor factor 1 and of Ras-GAP SH3 binding protein 1, G3BP1, controlling the activity of the H+-ATP synthase and the translation of beta-F1-ATPase mRNA respectively in cancer cells. A trans-acting factor that regulate beta-F1-ATPasemRNA translation, is G3BP1, Ras-GAP SH3 binding protein 1, that interacts with the 3'UTR of beta-mRNA, the interaction specifically represses mRNA translation by preventing its recruitment into active polysomes Homo sapiens