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- W2800151574 endingPage "HEP05" @default.
- W2800151574 startingPage "HEP05" @default.
- W2800151574 abstract "Rap proteins regulate liver physiopathology. For example, Rap2B promotes hepatocarcinoma (HCC) growth, while Rap1 might play a dual role. The RapGEF, Epac1, activates Rap upon cAMP binding, regulating metabolism, survival, and liver regeneration. A liver specific Epac2 isoform lacking cAMP-binding domain also activates Rap1, promoting fibrosis in alcoholic liver disease. C3G (RapGEF1) is also present in the liver, but mainly as shorter isoforms. Its function in the liver remains unknown. Information from different public genetic databases revealed that C3G mRNA levels increase in HCC, although they decrease in metastatic stages. In addition, several mutations in RapGEF1 gene are present, associated with a reduced patient survival. Based on this, C3G might represent a new HCC diagnostic and prognostic marker, and a therapeutic target." @default.
- W2800151574 created "2018-05-17" @default.
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- W2800151574 creator A5030325378 @default.
- W2800151574 creator A5033639948 @default.
- W2800151574 creator A5056391710 @default.
- W2800151574 date "2018-01-01" @default.
- W2800151574 modified "2023-10-16" @default.
- W2800151574 title "How Rap and its GEFs control liver physiology and cancer development. C3G alterations in human hepatocarcinoma" @default.
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- W2800151574 doi "https://doi.org/10.2217/hep-2017-0026" @default.
- W2800151574 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6168044" @default.
- W2800151574 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30302196" @default.
- W2800151574 hasPublicationYear "2018" @default.
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