E2F1

E2F1

A gene on chromosome 20q11.2 that encodes a member of the E2F family of DNA-binding transcription factors, which play a key role in regulating the cell cycle and tumour suppressor proteins. E2Fs are targets of transforming proteins of small DNA tumour viruses.
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Transactivation of micrornA-320 by microRNA-383 regulates granulosa cell functions by targeting E2F1 and SF-1 proteins.
miR-223 has been found to affect the cell cycle by regulating E2F1 (35), migration and invasion in cancer cells by targeting EPB41L3 (36), proliferation and tumor growth of cells by targeting IGF1R and downstream Akt/mTOR/p70S6K signaling pathway (37,38).
In this case, for example p21, c-myc, E2F1, SGOL2 (shugoshin 2) and CAD (carbamoyl phosphate synthetase) were involved, whereof the first ones are known cell cycle regulators/transcription factors (Buchmann et al.
sup][5],[23] The inhibition of MAOA will result in lessened apoptosis through elevated expression of the cell cycle enhancers E2F1 and cyclin D1.
Various ligands including E2F1 and SKP2 also bind to the cyclin box fold domain.
As to the mechanisms, levels of inactive or phosphorylated (p) p53, p21, CDK6, CDK4, cyclin Dl, and E2F1 were immunodetected.
2012) also detected PM effects on the expression of some of the miRNA target genes observed in our study, such as the proliferation- and carcinogen-related genes E2F1, EGR1 targeted by hsa-miR-21 and hsa-miR-192, and the inflammation-related gene NFKB1 targeted by miR-146a.
Nevins, "A role for Myc in facilitating transcription activation by E2F1," Oncogene, vol.
Moran, "Cooperative activation of tissue-specific genes by pRB and E2F1," Cancer Research, vol.
Again, there is a clear correlation between mutant P53 GOF that facilitates angiogenesis by increasing the expression of VEGF, via interaction with E2F1 that induces the expression of ID4, which in turn promotes the expression of proangiogenic factors such as IL and GROa, thus eventually leading to increasing angiogenesis in cancerous tissues.
Increased expression of a protein called E2F1, whose overexpression sensitizes cells to apoptosis;
Kao moguci mehanizmi onkogeneze HCC u okviru HCV infekcije navode se: aktivacija celularnih onkogena Ras, c-Myc, E2F1, inaktivacija tumorskih supresorskih gena p21, p53, Rb i narusena regulacija intracelularnih signalnih puteva Wnt/[beta]-catenin, MAPK, JAK/STAT, PI3K/Akt, EGF-[beta], TGF-[beta]) [6-9].