Literature summary for 3.4.21.122 extracted from

Sun, C.; Dobi, A.; Mohamed, A.; Li, H.; Thangapazham, R.L.; Furusato, B.; Shaheduzzaman, S.; Tan, S.H.; Vaidyanathan, G.; Whitman, E.; Hawksworth, D.J.; Chen, Y.; Nau, M.; Patel, V.; Vahey, M.; Gutkind, J.S.; Sreenath, T.; Petrovics, G.; Sesterhenn, I.A.; McLeod, D.G.; Srivastava, S.
TMPRSS2-ERG fusion, a common genomic alteration in prostate cancer activates C-MYC and abrogates prostate epithelial differentiation (2008), Oncogene, 27, 5348-5353 .

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	O15393	-	-

General Information	Comment	Organism
physiological function	prostate cancer cells show a high prevalence of TMPRSS2-ERG rearrangements which leads to androgenic induction of the ETS-related gene (ERG) expression. ERG knockdown in TMPRSS2-ERG expressing CaP cells induces striking morphological changes and inhibits cell growth. ERG mediates activation of C-MYC oncogene and the repression of prostate epithelial differentiation genes PSA and SLC45A3/prostein	Homo sapiens

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Release 2023.1 (January 2023)