IndraLab
Statements
ELK1 is active.
9
29
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1
"However, both of these stimuli strongly activate two other mapks, jnk1 and jnk2, and stimulate elk-1 transcriptional activity and phosphorylation jnk phosphorylation sites include ser383 and ser389, the major residues whose phosphorylation is responsible for enhancement of elk-1 trascriptional activity."
"Subsequent studies with dominant negative elk-1, wild type, and variant gal4-elk-1 fusion proteins confirmed that phosphorylation of elk-1 at serines 383 and 389 in the c-terminal region of elk-1 is an important downstream target associated with activation of an sre by e2. Both e2 (er?-Dependent) and growth factors (er?-Independent) activated the sre in breast cancer cells via the ras/mapk pathway"
"However, both of these stimuli strongly activate two other mapks, jnk1 and jnk2, and stimulate elk-1 transcriptional activity and phosphorylation jnk phosphorylation sites include ser383 and ser389, the major residues whose phosphorylation is responsible for enhancement of elk-1 trascriptional activity."
"However, both of these stimuli strongly activate two other mapks, jnk1 and jnk2, and stimulate elk-1 transcriptional activity and phosphorylation jnk phosphorylation sites include ser383 and ser389, the major residues whose phosphorylation is responsible for enhancement of elk-1 trascriptional activity."
ELK1 is transcriptionally active.
5
9
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"MSK1 induction requires simultaneous activation of both ERK and p38 MAPK. Other downstream targets of p38 MAPK include transcription factors such as Elk1 and myocyte-enhancing factor (MEF) 2, whereby p38 MAPK directly phosphorylates nuclear substrates and augments their activity (Chen et al. 2001)."
ELK1 is transcriptionally inactive.
2
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