ER[alpha] and induces estrogenic effects with approximately 103-104 fold less potency than estradiol (Jefferson 2000, Muthyala 2004).
In order to transactivate
responsive genes leading to cell differentiation, the removal of both of the CoR complexes from the PLZF-RAR[alpha] is required.
The authors suggest that abnormalities of proliferation regulation in endometrial tumors may be connected with accumulation of mutant p53 protein, its disability to transactivate
such target genes as p21, with changes in expression of p16 protein.
Notably, the proinflammatory transcription factor NF-[kappa]B has been shown to transactivate
lipocalin-2 expression through binding with a consensus motif in the promoter region of the lipocalin-2 gene (18), suggesting that this secretory protein might be involved in the inflammatory responses.
ATM targets p53 protein, a transcription factor that can bind to specific DNA sequences and transactivate
certain p53-responsive genes while DNA-PK targets mdm2.
It has been reported that phosphorylation of NF-[kappa]B p65 on Ser 536 is essential for its capacity to transactivate
Chimeric proteins consisting of the DNA binding domain of the yeast transcription factor Gal4 and the ER[alpha] or ER[beta] hormone binding domain, which were transiently transfected in SkBr3 cells, showed a strong transactivation by E2 but not by atrazine (Figure 1E,F), confirming that atrazine did not transactivate
RAF inhibitors transactivate
RAF dimers and ERK signalling in cells with wild-type BRAF.
PPAR-[gamma]2 is known as a master regulator of adipogenesis because of its ability to transactivate
adipogenic target genes such as aP2, GLUT4, fatty acid synthase, LPL, acetyl-CoA carboxylase, and steroyl-CoA desaturase (van Bilsen et al.
Activated PI3K in turn leads to the activation of serine/threonine kinases, termed as Akt or PKB, by phosphorylation at Thr308 and Ser473 which then phosphorylates its downstream target FKHRL1 to be translocated into the nucleus to transactivate
proapoptotic genes such as tumour necrosis factor [alpha], TGF-[beta]1 and Bad.
1; OMIM 191170; PubMed accession number X54156) are common in cancers and are typically missense within exons 4-9, impairing the capacity of p53 to transactivate
genes involved in cell cycle arrest, apoptosis, and DNA repair (1).
Both Epstein-Barr viral nuclear antigen 2 (EBNA-2) and activated Notch1 transactivate
genes by interacting with the cellular protein RBP-J kappa.