Presentation is loading. Please wait.

Presentation is loading. Please wait.

A B C E F D IC50 = 567 nM IC50 = 83 nM HAP1 WT HAP1 TOPK

Published byErlin Hadiman Modified over 5 years ago

Similar presentations

Presentation on theme: "A B C E F D IC50 = 567 nM IC50 = 83 nM HAP1 WT HAP1 TOPK"— Presentation transcript:

1 A B C E F D IC50 = 567 nM IC50 = 83 nM HAP1 WT HAP1 TOPK
siTOPK siTOPK siTOPK siTOPK siNT siNT siNT siNT TOPK► TOPK► TOPK► TOPK► β-Actin► β-Actin► β-Actin► β-Actin► B C E Loading control Ponceau TOPK► PC3 T24 HeLa SQ20B H1299 DU145 HFL-I MRC5 HCT116 TOPK Vinculin► TOPK► siNT + E.V. siNT + TOPK F HAP1 WT IC50 = 83 nM HAP1 TOPK IC50 = 567 nM D β-Actin► TOPK► siNT siTOPK_2 siTOPK_3 Fig. S1. TOPK is a novel tumour specific modulator of radiosensitivity. (A) Post-irradiation survival in irradiated cancer-derived cell lines. Transfection with TOPK siRNA (siTOPK) was compared to non-targeting siRNA (siNT) as a control, and knockdown efficiency was confirmed by immunoblotting. (B) Oncomine 3.0 Database summary for TOPK expression. Threshold (p-value) is set at 1x10-4, fold change threshold at 2, with gene rank of top 10%. Red indicates relative overexpression and blue indicates relative underexpression. The number in each square represents the number of studies analysed. (C) Immunoblot of TOPK expression in cancer-derived and normal tissue cell lysates. Ponceau staining is shown as a protein loading control. (D) Deconvolution CFA to test radiosensitisation with two different siRNAs (siTOPK_2 and siTOPK_3) targeting different regions of the TOPK gene. (E) Overexpression of TOPK in HCT116 cells. Empty vector (E.V.) was used as a control. Overexpression was confirmed by immunoblot (inset). (F) Dose-response analysis of the effect of OTS964 on cell viability in HAP1 WT (wild type) and HAP1 TOPK (TOPK knock-out).

Download ppt "A B C E F D IC50 = 567 nM IC50 = 83 nM HAP1 WT HAP1 TOPK"

Similar presentations

Supplementary Figure 1. Caspase 8 expression and activation and Fas expression in NSCLC and normal lung cell lines. A Western blot analysis of DR4 and.

Supplementary Figure 1. Caspase 8 expression and activation and Fas expression in NSCLC and normal lung cell lines. A Western blot analysis of DR4 and.
Exogenous B56γ3 WT F395C WT F395C IgG Vinc Endogenous B56γ2,3 HA-IPInput Figure S1 HA-B56γ3 is unable to interact with endogenous B56γ. Lysates of U2OS.

Exogenous B56γ3 WT F395C WT F395C IgG Vinc Endogenous B56γ2,3 HA-IPInput Figure S1 HA-B56γ3 is unable to interact with endogenous B56γ. Lysates of U2OS.
(+++) Normal breast ATM (++) IDC ATM Lymph node metastasis negative positive P-value - + ++ +++ 35 32 27 16 36 73 50 27 0.085 A B X200 C Vector ATM - WT.

(+++) Normal breast ATM (++) IDC ATM Lymph node metastasis negative positive P-value A B X200 C Vector ATM - WT.
Kinome siRNA survival screen results Acknowledgements Discovery and investigation of novel radiosensitising genes Gaganpreet Tiwana 1, Remko Prevo 1, Balam.

Kinome siRNA survival screen results Acknowledgements Discovery and investigation of novel radiosensitising genes Gaganpreet Tiwana 1, Remko Prevo 1, Balam.
Recurrent SETBP1 mutations in atypical chronic myeloid leukemia Nature Genetics.

Recurrent SETBP1 mutations in atypical chronic myeloid leukemia Nature Genetics.
Fig. 1 (A) (B) (C) * * * * Mock siRNA siRNA Day 3 Day 8 1 2 3 4 DNA-PKcs Beta actin.

Fig. 1 (A) (B) (C) * * * * Mock siRNA siRNA Day 3 Day DNA-PKcs Beta actin.
Figure S1 Figure S1. (A) Screen of USPs for regulating c-Myc stability. Scores of c-Myc protein abundence was derived from two independent experiments.

Figure S1 Figure S1. (A) Screen of USPs for regulating c-Myc stability. Scores of c-Myc protein abundence was derived from two independent experiments.
B Supplementary Fig S1. (A) ZR75- and MCF7-PELP1 knockdown cells were generated as described in methods section. Pooled colonies were analyzed for PELP1.

B Supplementary Fig S1. (A) ZR75- and MCF7-PELP1 knockdown cells were generated as described in methods section. Pooled colonies were analyzed for PELP1.
Figure S1 A B Figure S1. SPATA2 is required for TNFα or zVAD.fmk induced necroptosis in L929 cells. (A) L929 cells were transfected with a pool of four.

Figure S1 A B Figure S1. SPATA2 is required for TNFα or zVAD.fmk induced necroptosis in L929 cells. (A) L929 cells were transfected with a pool of four.
Cell Physiol Biochem 2013;32: DOI: /

Cell Physiol Biochem 2013;32: DOI: /
G1 synchronous cells released at T = 0

G1 synchronous cells released at T = 0
Supplemental Digital Content 4

Supplemental Digital Content 4
Ke Xu, Ph.D. Putuo Hospital and Cancer Institute,

Ke Xu, Ph.D. Putuo Hospital and Cancer Institute,
Constitutive NF-κB activation by the t(11;18)(q21;q21) product in MALT lymphoma is linked to deregulated ubiquitin ligase activity  Honglin Zhou, Ming-Qing.

Constitutive NF-κB activation by the t(11;18)(q21;q21) product in MALT lymphoma is linked to deregulated ubiquitin ligase activity  Honglin Zhou, Ming-Qing.
The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR) Cell.

The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR) Cell.
European Urology Focus

European Urology Focus
Network protein vulnerability in EGFR TKI‐resistant cells and specific for EGFR‐mutated cells. Network protein vulnerability in EGFR TKI‐resistant cells.

Network protein vulnerability in EGFR TKI‐resistant cells and specific for EGFR‐mutated cells. Network protein vulnerability in EGFR TKI‐resistant cells.
In cancer cell lines inhibition of SCF/c-Kit pathway leads to radiosensitization only when SCF is strongly over-expressed  Fabian Eberle, Florian H. Leinberger,

In cancer cell lines inhibition of SCF/c-Kit pathway leads to radiosensitization only when SCF is strongly over-expressed  Fabian Eberle, Florian H. Leinberger,
Genetic alterations in the PI3K–PTEN–AKT pathway detected during disease progression and their functional impacts. Genetic alterations in the PI3K–PTEN–AKT.

Genetic alterations in the PI3K–PTEN–AKT pathway detected during disease progression and their functional impacts. Genetic alterations in the PI3K–PTEN–AKT.
MicroRNA-489 Plays an Anti-Metastatic Role in Human Hepatocellular Carcinoma by Targeting Matrix Metalloproteinase-7  Yixiong Lin, Jianjun Liu, Yuqi Huang,

MicroRNA-489 Plays an Anti-Metastatic Role in Human Hepatocellular Carcinoma by Targeting Matrix Metalloproteinase-7  Yixiong Lin, Jianjun Liu, Yuqi Huang,

Similar presentations

Ads by Google