Identification of NSC as a FADD-kinase inhibitor.

Slides:



Advertisements
Similar presentations
B A P-AXL P-AXL AXL AXL P-MET P-MET MET MET P-Akt-473 P-Akt-473 AKT
Advertisements

Supplementary Figure 1 Lapatinib nM mM pEGFR MDA-MB231 EGFR pEGFR
by Pascal Gelebart, Mona Anand, Hanan Armanious, Anthea C
TGF-β1 induces ILK activity in renal tubular epithelial cells.
MEL23 and MEL24 inhibit Mdm2 and p53 ubiquitination in cells.
Luminex phosphorylation measurements are reproducible and have broad dynamic range Individual difference in insulin‐induced phosphorylation of ERK measured.
Inhibition of FGFR signaling and tumor growth in SNU-16 xenograft model by administration of E7090. Inhibition of FGFR signaling and tumor growth in SNU-16.
Human T cells undergoing apoptosis and necroptosis release mitochondria, and apoptotic mitochondria recruit neutrophils. Human T cells undergoing apoptosis.
NM-3 induces p21 levels and down-regulation of Cdk2 activity.
p38 MAPK activation is required for phosphorylation of Akt at Ser473.
Leto et al., Supplementary Figure S3
Mechanism of piperlongumine induced Sp downregulation.
ONC201 activates the ATF4 pathway through the eIF2α kinases HRI and PKR. ONC201 activates the ATF4 pathway through the eIF2α kinases HRI and PKR. (A) Western.
Human T cells undergoing apoptosis and necroptosis release mitochondria, and apoptotic mitochondria recruit neutrophils. Human T cells undergoing apoptosis.
Knocking down Wnt3 increases the cells' response to trastuzumab and reduces cells' invasiveness. Knocking down Wnt3 increases the cells' response to trastuzumab.
The p53 pathway is involved in the inhibition of cell proliferation observed in 15-LOX-1-overexpressing cells. The p53 pathway is involved in the inhibition.
Phosphorylation of AMPK-Thr172 before and after metformin treatment in muscle from subjects with type 2 diabetes. Phosphorylation of AMPK-Thr172 before.
LSD1, a histone demethylase, is required for the assembly of the Notch repressor complex. LSD1, a histone demethylase, is required for the assembly of.
The dynamics of Akt activation in cultured human keratinocytes.
The sesquiterpene lactone PN up-regulates MDM2 and p53 proteins.
Quantification of NMT knockdown.
GA blocks HIF activity and reduces HIF target expression.
Variation in dUTPase expression in cell lines.
CDCP1 is required for invadopodia formation and ECM degradation by human breast cancer cells. CDCP1 is required for invadopodia formation and ECM degradation.
Silencing hOGG1 triggers caspase-3 and caspase-7 activation in response to H2O2 in GM00637 cells. Silencing hOGG1 triggers caspase-3 and caspase-7 activation.
The role of p53 in H2O2-mediated cell death of hOGG1-deficient H1299 lung carcinoma p53 null cells. The role of p53 in H2O2-mediated cell death of hOGG1-deficient.
Effect of LY on phosphorylation of various MAP kinase substrates in HeLa cells in vitro. Effect of LY on phosphorylation of various MAP kinase.
Activation of CHOP and DR5 by DIM-C-pPhtBu.
BME treatment increases granzyme B expression in NK 3.3 cells.
Competition between FLYWCH1/β-catenin and TCF4/β-catenin complexes for their interaction to Tcf-DNA-binding sites. Competition between FLYWCH1/β-catenin.
TGF-β1 modulates extracellular matrix–mediated MT1-MMP expression.
Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. A.
Inhibition of stress-associated MAPK signaling attenuates SASP expression in CAFs. A, N-CAFs were treated with 100 nmol/L GEM plus DMSO or the above-listed.
Lamellarin D induces cell death through a Fas-independent pathway.
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.
Effect of G9a on the expression of GSH synthesis enzymes.
Effect of other nucleoside analogues on p38 MAPK phosphorylation levels. Effect of other nucleoside analogues on p38 MAPK phosphorylation levels. A, MM.1S.
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.
Effect of SFN on the protein expression of Nrf2, HO-1, and NQO1 in JB6-shMock and JB6-shNrf2 cells. Effect of SFN on the protein expression of Nrf2, HO-1,
Effect of IL24 on phosphorylation of eIF2α and proliferation in cancer cells. Effect of IL24 on phosphorylation of eIF2α and proliferation in cancer cells.
Src expression in a panel of human TCC cell lines.
KPT-9274 shows specificity for attenuation of PAK4 targets preferentially in RCC cells. KPT-9274 shows specificity for attenuation of PAK4 targets preferentially.
Inhibition of EGFR kinase activity and autophosphorylation by Iressa.
Ki-67 expression in M31- and H3-treated tumors (A) and respective Ki-67 labeling indices in the two groups of tumors (B). Ki-67 expression in M31- and.
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.
PTPH1 depends on its catalytic activity to increase ER nuclear accumulation and to enhance breast cancer sensitivity to TAM. A, effects of PTPH1 and PTPH1/DA.
Changes in signal transduction pathway induced by gefitinib.
by Dana S. Levy, Jason A. Kahana, and Rakesh Kumar
The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. Serum-starved.
Effects of UVB on AKT in SKH-1 mouse epidermis.
SAHA blocks IR-induced increase of RAD51 protein in MM cells.
BCR/ABL expression, tyrosine phosphorylation, and signaling in dasatinib- and imatinib-resistant cell lines and the ubiquitin inhibitor lactacystin modifies.
Increased expression of angiogenic factors and inflammatory cytokines in mice exposed to hypoxia. Increased expression of angiogenic factors and inflammatory.
AKT activation in HCC2429 is SRC- but not Notch-dependent.
Effect of bevacizumab on the proliferation of A2780 cells.
Expression and induction of HER2 and HPSE in 231BMBC cells.
Increased growth factor receptor expression in lungs and tumors of hypoxic mice. Increased growth factor receptor expression in lungs and tumors of hypoxic.
Posttranslational phosphorylation of p53 by platinum drugs in ovarian tumor cells. Posttranslational phosphorylation of p53 by platinum drugs in ovarian.
RA-9 induces G2–M cell-cycle arrest and caspase-mediated apoptosis in ovarian cancer cells. RA-9 induces G2–M cell-cycle arrest and caspase-mediated apoptosis.
Effect of dexamethasone on PCDGF/GP88 mRNA and protein expressions and effect of PCDGF/GP88 on dexamethasone-induced cell death. Effect of dexamethasone.
MTOR kinase inhibition–induced reactivation of AKT substrates is HER2 and PI3K dependent. mTOR kinase inhibition–induced reactivation of AKT substrates.
Elevated STAT3 phosphorylation and RANTES levels in tamoxifen-treated breast cancer cells. Elevated STAT3 phosphorylation and RANTES levels in tamoxifen-treated.
Ceritinib is a potent ALK inhibitor in crizotinib-naïve models.
FGFR2 amplification in primary human gastric tumors predicts for response to NVP-BGJ398. FGFR2 amplification in primary human gastric tumors predicts for.
Depletion of murine Dnmt proteins after 5-Aza-CdR treatment.
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.
Effects of NMT siRNAs on MARCKS and c-Src.
I3C reduces the level of Cdc25A protein in breast cancer cells.
Effect of 6-SHO on mouse prostate cancer HMVP2 cells.
Presentation transcript:

Identification of NSC 47147 as a FADD-kinase inhibitor. Identification of NSC 47147 as a FADD-kinase inhibitor. A, A549-FKR cells were treated with NSC 47147 and SP600125 for 6 hours and CKI-7 for 1 hour at the indicated concentrations followed by bioluminescent measurement. NSC 47147 blocks phosphorylation of FADD with greater potency than the FADD-kinase inhibitors SP600125 and CKI-7. B, A549-FKR cells were treated as described for FKR assay and lysates were analyzed with specific antibodies by Western blotting. Treatment with the FADD-kinase inhibitors CKI-7 and SP600125 shows dose-dependent decrease in p-FADD protein that correlates with FKR activity. Total and p-β-catenin and p-c-jun, respective targets of CKI-7 and SP600125, have been shown for comparison. C, A549 and Jurkat cells were treated for 6 hours with NSC 47147. Western blot analysis reveals that NSC 47147 leads to a decrease in p-FADD and p-β-catenin levels. Katrina A. Schinske et al. Mol Cancer Ther 2011;10:1807-1817 ©2011 by American Association for Cancer Research