Daple is required for activation of Gαi3, Rac1, and AKT signals and in the antagonistic inhibition of β-catenin–dependent Wnt signals downstream of EGF/EGFR.

Slides:

Advertisements

Similar presentations

Nogo-p4 Suppresses TrkA Signaling Induced by Low Concentrations of Nerve Growth Factor Through NgR1 in Differentiated PC12 Cells Neurosignals 2016;24:25-39.

Advertisements

From: IGF-1 Regulates the Extracellular Level of Active MMP-2 and Promotes Müller Glial Cell Motility Invest. Ophthalmol. Vis. Sci ;56(11):

Volume 131, Issue 4, Pages (October 2006)

FAM49B controls T cell activation by regulating cytoskeleton remodeling. FAM49B controls T cell activation by regulating cytoskeleton remodeling. (A) J.FAM49B.

Loss of SMARCA4 expression or activity derepresses miR-27a.

Small-molecule inhibitor QLT-0267 suppresses ILK activity and inhibits its downstream signaling. Small-molecule inhibitor QLT-0267 suppresses ILK activity.

Volume 54, Issue 4, Pages (October 2008)

β-ARs signal cooperatively with mutant EGFR and inactivate LKB1

Volume 131, Issue 4, Pages (October 2006)

Volume 142, Issue 3, Pages e2 (March 2012)

FAS1 domain protein inhibits association of αvβ3 integrin with VEGFR-2 and attenuates VEGF165-induced VEGFR-2 phosphorylation. FAS1 domain protein inhibits.

Nuclear Arp3 mediates formation of TCR-induced nuclear actin filaments

HRTV and SFTSV NSs, but not UUKV NSs, inhibits JAK/STAT IFN signaling.

PKA phosphorylates Thr63 and Ser692 to increase HIF-1α stability.

p38 MAPK activation is required for phosphorylation of Akt at Ser473.

BLNK Required for Coupling Syk to PLCγ2 and Rac1-JNK in B Cells

Volume 128, Issue 7, Pages (June 2005)

Fig. 6 DMF inhibits NF-κB translocation upon infection.

The role of SRC-C3G-RAP1 signaling in transformation induced by CRKL

Regulation of PP6 phosphatase activity by Plk1 in vitro.

TRAF4 is required for EGFR activation in response to EGF stimulation.

mTORC1 signaling is required for STING-mediated type I IFN responses.

Thiocolchicoside inhibits TNF-dependent IκBα phosphorylation, IκBα degradation, p65 phosphorylation, and p65 nuclear translocation. Thiocolchicoside inhibits.

High-affinity binding to the hypervariable region of the β1 I-like domain controls signaling to fibronectin fibrillogenesis. High-affinity binding to the.

AMPK directly increases mTORC2 catalytic activity.

Knocking down Wnt3 increases the cells' response to trastuzumab and reduces cells' invasiveness. Knocking down Wnt3 increases the cells' response to trastuzumab.

Figure 4 DNM1 mutations affect protein levels and self-dimerization (A) HeLa cells were transfected with green fluorescent protein (GFP)-tagged mutant.

High-affinity mutants of β3 integrin fail to stimulate RhoA activity and fibronectin fibrillogenesis. High-affinity mutants of β3 integrin fail to stimulate.

Arginine-to-lysine mutations conferring TRIM22 restriction and lysine-to-arginine mutations causing loss of TRIM22 restriction. Arginine-to-lysine mutations.

IL-6 inhibits insulin-induced formation of p85/IRS-1 complexes.

Synergistic WNT1 and WNT7B signaling is downstream of LRP6 phosphorylation and β-catenin stabilization. Synergistic WNT1 and WNT7B signaling is downstream.

Fig. 3 E2F1 interacts with components of the splicing machinery.

Stimulation of cells with FFAR4 agonist.

Wrch-1 binds to the regulatory p85 subunit of PI3K and is necessary for Akt activation. Wrch-1 binds to the regulatory p85 subunit of PI3K and is necessary.

Downregulation of caveolin-1 by si-RNA in NIH3T3 cells increased survivin expression. Downregulation of caveolin-1 by si-RNA in NIH3T3 cells increased.

Kinetics of BDNF-induced Erk, Akt and PLCγ activation in the presence of 15 mM NaCl or 15 mM KCl. Representative western blots (A) and quantitative plots.

PEDF inhibits Wnt/T-cell factor/β-catenin signaling in resting and wounded skin. PEDF inhibits Wnt/T-cell factor/β-catenin signaling in resting and wounded.

The dynamics of Akt activation in cultured human keratinocytes.

Fig. 1. DEL-1 is expressed by human and mouse osteoclasts.

Fig. 4 Loss of Zic5 derepresses GLUT1/SLC2A1 gene expression.

Fig. 6 RUNX/CBFB interaction inhibitor, Ro5-3335, significantly decreases mouse neurofibroma growth in vivo. RUNX/CBFB interaction inhibitor, Ro5-3335,

by Emilie Clement, Hiroyuki Inuzuka, Naoe T

Variation in dUTPase expression in cell lines.

Fig. 3 Proteomic analysis and Western blot analysis of protein cargos of various EVs. Proteomic analysis and Western blot analysis of protein cargos of.

Identification of NSC as a FADD-kinase inhibitor.

Fig. 4 PD-L1 expression is found in the spleen and the BM of mice transplanted with JAK2V617F-transduced bone marrow. PD-L1 expression is found in the.

Competition between FLYWCH1/β-catenin and TCF4/β-catenin complexes for their interaction to Tcf-DNA-binding sites. Competition between FLYWCH1/β-catenin.

Effect of expressing an activated mutant (Rac V12) and an inactivated mutant (Rac N17) of Rac on PTHRP gene expression levels and on JNK activation. Effect.

Effects of visfatin on the cell proliferation and phosphorylation of ERK, Akt, and GSK-3β proteins in HCC cells. Effects of visfatin on the cell proliferation.

Fig. 8 C9orf72 knockdown results in an increase in autophagic flux.

Ectopic expression of miR-187 in MCF7 cells results in increased migration, invasion, and anchorage-independent colony formation. Ectopic expression of.

Effect of G9a on the expression of GSH synthesis enzymes.

Western blot analysis of Wnt signaling genes.

Curcumin suppresses the expression of antiapoptotic proteins in multiple myeloma cells. Curcumin suppresses the expression of antiapoptotic proteins in.

Fig. 4 Effects of morphogen priming of engineered mesenchymal condensations on in vitro chondrogenic lineage specification at the time of implantation.

Activation of Wnt signaling pathway in trastuzumab-resistant cell lines. Activation of Wnt signaling pathway in trastuzumab-resistant cell lines. A, bar.

GPC3 promotes hepatocellular carcinoma growth by stimulating the canonical Wnt pathway (A-B) GPC3 induces the stabilization of cytoplasmic β-catenin. GPC3.

PKCζ is tyrosine phosphorylated by EGF and contributes to EGF-induced activation of ERK in Mef cells. PKCζ is tyrosine phosphorylated by EGF and contributes.

Fig. 1 Irradiation with 50 Gy/3 fractions generates LAE characterized by SOD2 depletion and CTGF overexpression. Irradiation with 50 Gy/3 fractions generates.

Changes in signal transduction pathway induced by gefitinib.

by Dana S. Levy, Jason A. Kahana, and Rakesh Kumar

Met is expressed in Her2-overexpressing cell lines and Her2 (+) breast tumors. Met is expressed in Her2-overexpressing cell lines and Her2 (+) breast tumors.

The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. Serum-starved.

Fig. 5 C9orf72 knockdown disrupts autophagy induction.

SAHA blocks IR-induced increase of RAD51 protein in MM cells.

EGCG affects growth factor receptor signaling in H2111, H358, and H460 NSCLC cells. EGCG affects growth factor receptor signaling in H2111, H358, and H460.

Expression and induction of HER2 and HPSE in 231BMBC cells.

FGF19 amplification in liver cancer cell lines is associated with response to NVP-BGJ398. FGF19 amplification in liver cancer cell lines is associated.

Effect of SFN on the total activity and protein expression of HDACs in JB6 P+ cells. Effect of SFN on the total activity and protein expression of HDACs.

Fig. 2 hTERT induces expression of heat shock protein genes through HSF1 and interacts with Hsp70-1. hTERT induces expression of heat shock protein genes.

Presentation transcript:

Daple is required for activation of Gαi3, Rac1, and AKT signals and in the antagonistic inhibition of β-catenin–dependent Wnt signals downstream of EGF/EGFR. Daple is required for activation of Gαi3, Rac1, and AKT signals and in the antagonistic inhibition of β-catenin–dependent Wnt signals downstream of EGF/EGFR. (A) Immunoprecipitation assay assessing Gαi3 activation after EGF stimulation in control (shLuc) and Daple-depleted (shDaple) HeLa cells. Western blot for active Gαi3 (Gαi3-GTP) and total Gαi3. Quantification of blots is shown in fig. S3. (B) Whole-cell lysates of EGF-stimulated HeLa cells in (A) were analyzed for phosphorylated AKT (pSer473), Daple, β-catenin, and actin (loading control). (C) Bar graphs display quantification of phosphorylated/total AKT. Data are means ± SD; n = 3 experiments. (D) Rac1 activity assay in lysates of HeLa cells described in (A) upon EGF stimulation. Data are means ± SD; n = 3. (E and F) Whole-cell lysates of EGF-stimulated HeLa cells expressing Daple-WT or Daple-F1675A (FA) mutant were analyzed for AKT phosphorylation, as described in (B). (G) Bar graphs display quantification as a ratio of phosphorylated to total AKT. Data are means ± SD; n = 3. (H and I) Rac1 activity upon EGF stimulation, assessed in lysates from HeLa cells described in (F). Data are means ± SD; n = 3. (J and K) Quantitative polymerase chain reaction (qPCR) analysis assessing EPCAM (J) and other Wnt target genes (K) induced by EGF in HeLa cells described in (A). Data are means ± SD, fold change in RNA after EGF stimulation; n = 3 experiments. n.s., not significant. Nicolas Aznar et al., Sci. Signal. 2018;11:eaao4220 ©2018 by American Association for the Advancement of Science