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E2F1/3 → B-Myb: " Also found in breast tumors with high levels is B-Myb , a transcription factor whose expression is activated by E2F1/3 at the late G1 phase and the level is sustained through the S phase "
B-Myb → EGF: " EGF stimulation and forced expression of EGFR significantly increase B-Myb gene activity and such increase occurs in the G1 phase "
B-Myb → EGFR: " EGF stimulation and forced expression of EGFR significantly increase B-Myb gene activity and such increase occurs in the G1 phase "
B-Myb → EGF: " EGF induced B-Myb expression was not significantly suppressed following inhibition of PI-3K and ERK, two major EGFR downstream pathways "
B-Myb → E2F1: " As EGFR lacks DNA binding domain but contains transactivational activity and E2F1 activates B-Myb expression in the G1/S phase, we further reasoned that nuclear EGFR might cooperate with E2F1 leading to activation of B-Myb "
B-Myb → EGFR: " As EGFR lacks DNA binding domain but contains transactivational activity and E2F1 activates B-Myb expression in the G1/S phase, we further reasoned that nuclear EGFR might cooperate with E2F1 leading to activation of B-Myb "
EGF → EGFR: " Indeed, we found that EGFR co-immunoprecipitated with E2F1 in an EGF dependent manner and that EGF activated in vivo binding of E2F1 to the B-Myb promoter "
B-Myb → E2F1: " Consistently, forced expression of both EGFR and E2F1 in EGFR-null CHO cells greatly enhanced B-Myb promoter activity, compared to the vector control and expression of EGFR or E2F1 alone "
B-Myb → EGFR: " Consistently, forced expression of both EGFR and E2F1 in EGFR-null CHO cells greatly enhanced B-Myb promoter activity, compared to the vector control and expression of EGFR or E2F1 alone "
E2F → EGF: " Promoter mutagenesis studies showed that EGF induced activation of B-Myb promoter required both E2F and EGFR target sites "
E2F → B-Myb: " Promoter mutagenesis studies showed that EGF induced activation of B-Myb promoter required both E2F and EGFR target sites "
B-Myb → EGF: " Promoter mutagenesis studies showed that EGF induced activation of B-Myb promoter required both E2F and EGFR target sites "
EGFR → B-Myb: " In summary, our data suggest that deregulated EGFR signaling pathway facilitate tumor cell proliferation partly via EGFR interaction with E2F1 and subsequent activation of B-Myb gene expression "