Presentation is loading. Please wait.

Presentation is loading. Please wait.

NEDD9 binding to AURKA decreases the efficacy of AURKA inhibitors in vitro. NEDD9 binding to AURKA decreases the efficacy of AURKA inhibitors in vitro.

Published byKristin Engebretsen Modified over 5 years ago

Similar presentations

Presentation on theme: "NEDD9 binding to AURKA decreases the efficacy of AURKA inhibitors in vitro. NEDD9 binding to AURKA decreases the efficacy of AURKA inhibitors in vitro."— Presentation transcript:

1 NEDD9 binding to AURKA decreases the efficacy of AURKA inhibitors in vitro.
NEDD9 binding to AURKA decreases the efficacy of AURKA inhibitors in vitro. A, Western blot analysis of AURKA, phT288-AURKA, NEDD9 in shCon or shNEDD9-MDA-MB-231LN cells treated with PHA B, quantification of phT288-AURKA expression as in A, n = 3, normalized to total AURKA and plotted as relative intensity units (RIU) ± SEM. Two-way ANOVA: P < , (shCon/shN1 or shN2), P = (shN1/shN2). Quantification of phS10-Histone H3 (IF), n = 3, 1000 cells/treatment, P = 0.006, P = (shCon/shN1 or shN2), no significant difference (shN1/shN2; C). Western blot analysis of total AURKA, phT288-AURKA, NEDD9 expression in cells treated with increasing concentrations of MLN8054. D, quantification as in B for the Western blots shown in C. P < , (shCon/shN1 or shN2), P = (shN1/shN2). Quantification of immunofluorescence shown in Supplementary Fig. S2E, n = 3, 1,000 cells/treatment, P = , P = (shCon/shN1 or shN2), no significant difference (shN1/shN2). Ryan J. Ice et al. Cancer Res 2013;73: ©2013 by American Association for Cancer Research

Download ppt "NEDD9 binding to AURKA decreases the efficacy of AURKA inhibitors in vitro. NEDD9 binding to AURKA decreases the efficacy of AURKA inhibitors in vitro."

Similar presentations

A B C MDA-MB-231 OHT: h FOXM1 PLK CDC25b ERα Tubulin

A B C MDA-MB-231 OHT: h FOXM1 PLK CDC25b ERα Tubulin
Dihydromyricetin decreases the sphere formation through downregulation of Sox2 in human osteosarcoma. Dihydromyricetin decreases the sphere formation through.

Dihydromyricetin decreases the sphere formation through downregulation of Sox2 in human osteosarcoma. Dihydromyricetin decreases the sphere formation through.
MEKi reduces sheddase activity via increased TIMP1 association, and TIMP1 neutralization enhances MAPKi efficacy. MEKi reduces sheddase activity via increased.

MEKi reduces sheddase activity via increased TIMP1 association, and TIMP1 neutralization enhances MAPKi efficacy. MEKi reduces sheddase activity via increased.
TANs mediate obesity-induced tumor progression and aggravated desmoplasia. TANs mediate obesity-induced tumor progression and aggravated desmoplasia. A,

TANs mediate obesity-induced tumor progression and aggravated desmoplasia. TANs mediate obesity-induced tumor progression and aggravated desmoplasia. A,
A and B, CO-1686–resistant NCI-H1975 cell clones, COR1-1 and COR10-1 display a reduced dependence on EGFR signaling for survival. A and B, CO-1686–resistant.

A and B, CO-1686–resistant NCI-H1975 cell clones, COR1-1 and COR10-1 display a reduced dependence on EGFR signaling for survival. A and B, CO-1686–resistant.
Pharmacologic inhibition of eIF5A hypusination sensitizes KRas-driven tumor cells to MEK and KRas inhibition. Pharmacologic inhibition of eIF5A hypusination.

Pharmacologic inhibition of eIF5A hypusination sensitizes KRas-driven tumor cells to MEK and KRas inhibition. Pharmacologic inhibition of eIF5A hypusination.
HIPK2 decreases the stability of Notch1-IC through proteasome-dependent degradation. HIPK2 decreases the stability of Notch1-IC through proteasome-dependent.

HIPK2 decreases the stability of Notch1-IC through proteasome-dependent degradation. HIPK2 decreases the stability of Notch1-IC through proteasome-dependent.
Effect of 14 hit compounds on SMN protein expression in type I SMA patient fibroblast cells (GM03813). Effect of 14 hit compounds on SMN protein expression.

Effect of 14 hit compounds on SMN protein expression in type I SMA patient fibroblast cells (GM03813). Effect of 14 hit compounds on SMN protein expression.
PTK6 downregulation suppresses SNAIL and increases E-cadherin expression. PTK6 downregulation suppresses SNAIL and increases E-cadherin expression. A,

PTK6 downregulation suppresses SNAIL and increases E-cadherin expression. PTK6 downregulation suppresses SNAIL and increases E-cadherin expression. A,
Arginine-to-lysine mutations conferring TRIM22 restriction and lysine-to-arginine mutations causing loss of TRIM22 restriction. Arginine-to-lysine mutations.

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.

IL-6 inhibits insulin-induced formation of p85/IRS-1 complexes.
CK2 phosphorylates mammalian FMRP S499.

CK2 phosphorylates mammalian FMRP S499.
LSD1, a histone demethylase, is required for the assembly of the Notch repressor complex. LSD1, a histone demethylase, is required for the assembly of.

LSD1, a histone demethylase, is required for the assembly of the Notch repressor complex. LSD1, a histone demethylase, is required for the assembly of.
CPI-444 efficacy requires CD8+ T cells and is associated with increased CD73 expression. CPI-444 efficacy requires CD8+ T cells and is associated with.

CPI-444 efficacy requires CD8+ T cells and is associated with increased CD73 expression. CPI-444 efficacy requires CD8+ T cells and is associated with.
Aβ-mediated Ras-MAPK signaling and Cyclin D1 expression in B103 cells are dependent on APP expression and can be reversed with MEK or Ras inhibition. Aβ-mediated.

Aβ-mediated Ras-MAPK signaling and Cyclin D1 expression in B103 cells are dependent on APP expression and can be reversed with MEK or Ras inhibition. Aβ-mediated.
Fig. 6 RUNX/CBFB interaction inhibitor, Ro5-3335, significantly decreases mouse neurofibroma growth in vivo. RUNX/CBFB interaction inhibitor, Ro5-3335,

Fig. 6 RUNX/CBFB interaction inhibitor, Ro5-3335, significantly decreases mouse neurofibroma growth in vivo. RUNX/CBFB interaction inhibitor, Ro5-3335,
FOXO3a phosphorylation and expression.

FOXO3a phosphorylation and expression.
CDCP1 is required for invadopodia formation and ECM degradation by human breast cancer cells. CDCP1 is required for invadopodia formation and ECM degradation.

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.

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.
coTCRcys-transduced T cells control tumor growth in vivo.

coTCRcys-transduced T cells control tumor growth in vivo.

Similar presentations

Ads by Google