IndraLab
Statements
reach
"Moreover, ablating alpha6beta4 integrin function in the T4-2s by expressing the dominant negative beta4Deltacyto, reduced both basal (XREF_FIG) and EGF stimulated (XREF_FIG D) RAC activity, and overexpression of beta4WT in the S-1 cells led to an increase in both basal (XREF_FIG) and EGF stimulated RAC activity (XREF_FIG C)."
reach
"Binding of ligands (epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha)) to their receptors initiates several signal transduction cascades, specifically the mitogen activated protein kinase (MAPK), protein kinase B (Akt), and c-Jun N-terminal kinase (JNK) pathways, resulting in DNA synthesis and cell proliferation [XREF_BIBR]."
sparser
"Interestingly, direct analysis of primary SOS1/2 KO primary MEFs has shown that single ablation of either SOS1 or SOS2 did not impair the overall level of EGF-dependent RAC activation, whereas combined SOS1/2 depletion significantly reduced the levels of RAC activation [ xref ], suggesting functionally redundant contributions of SOS1 and SOS2 with regards to RAC activation after EGF stimulation [ xref ]."
sparser
"Our conclusion is supported by the following lines of evidence: (1) FBXW2 binds to β-catenin under physiological conditions, and FBXW2-β-catenin binding is dependent on an evolutionarily conserved FBXW2 consensus binding motif (TSMGGT) on β-catenin (Fig. xref ); (2) FBXW2 ectopic expression or siRNA knockdown decreases or increases the levels of total and phosphorylated β-catenin (β-catenin pS552 ), and β-catenin transcriptional activity, respectively (Fig. xref ); (3) FBXW2 ectopic expression or siRNA knockdown shortens or extends the protein half-lives of both β-catenin and β-catenin pS552 , respectively, and FBXW2 promotes β-catenin polyubiquitylation via K48 linkage for degradation (Fig. xref ); (4) EGF-activated AKT1 is responsible for β-catenin phosphorylation on Ser552, which facilitates its FBXW2 binding for degradation."