Presentation is loading. Please wait.

Presentation is loading. Please wait.

A, B, apoptosis analysis using Annexin V-FITC/PI was done on 5th, 7th, and 9th day after transfection either with si control or si AEBP1in U87MG and U138MG.

Published byΠρόχορος Δασκαλόπουλος Modified over 5 years ago

Similar presentations

Presentation on theme: "A, B, apoptosis analysis using Annexin V-FITC/PI was done on 5th, 7th, and 9th day after transfection either with si control or si AEBP1in U87MG and U138MG."— Presentation transcript:

1 A, B, apoptosis analysis using Annexin V-FITC/PI was done on 5th, 7th, and 9th day after transfection either with si control or si AEBP1in U87MG and U138MG cell lines. A, B, apoptosis analysis using Annexin V-FITC/PI was done on 5th, 7th, and 9th day after transfection either with si control or si AEBP1in U87MG and U138MG cell lines. C, D, graphical representation of the number of cells in different phases of apoptosis in U87MG and U138MG, respectively. Jayashree Ladha et al. Mol Cancer Res 2012;10: ©2012 by American Association for Cancer Research

Download ppt "A, B, apoptosis analysis using Annexin V-FITC/PI was done on 5th, 7th, and 9th day after transfection either with si control or si AEBP1in U87MG and U138MG."

Similar presentations

PIK3CA gene amplification in glioblastoma and squamous cell carcinoma (SCC) of the lung. PIK3CA gene amplification in glioblastoma and squamous cell carcinoma.

PIK3CA gene amplification in glioblastoma and squamous cell carcinoma (SCC) of the lung. PIK3CA gene amplification in glioblastoma and squamous cell carcinoma.
Targeting the PARP DNA repair pathway enhanced cytotoxicity induced by chemotherapy. Targeting the PARP DNA repair pathway enhanced cytotoxicity induced.

Targeting the PARP DNA repair pathway enhanced cytotoxicity induced by chemotherapy. Targeting the PARP DNA repair pathway enhanced cytotoxicity induced.
IDH1 mutant glioma cells are sensitive to TMZ

IDH1 mutant glioma cells are sensitive to TMZ
miR-133a positively regulated p53/p21 pathway.

miR-133a positively regulated p53/p21 pathway.
A20 inhibits caspase-8 cleavage and TRAIL-induced apoptosis.

A20 inhibits caspase-8 cleavage and TRAIL-induced apoptosis.
Interfering with HMGA2 expression blocks transformation in metastatic lung cancer cells. Interfering with HMGA2 expression blocks transformation in metastatic.

Interfering with HMGA2 expression blocks transformation in metastatic lung cancer cells. Interfering with HMGA2 expression blocks transformation in metastatic.
Knocking down Wnt3 increases the cells' response to trastuzumab and reduces cells' invasiveness. Knocking down Wnt3 increases the cells' response to trastuzumab.

Knocking down Wnt3 increases the cells' response to trastuzumab and reduces cells' invasiveness. Knocking down Wnt3 increases the cells' response to trastuzumab.
Allopurinol up-regulates DR5 expression in PC-3 and DU145 cells.

Allopurinol up-regulates DR5 expression in PC-3 and DU145 cells.
A, IC50 dose–response curves of SYD985, T-DM1, and ADC isotype control in all USC cell lines tested in vitro (i.e., HER2 3+ cell lines, P =

A, IC50 dose–response curves of SYD985, T-DM1, and ADC isotype control in all USC cell lines tested in vitro (i.e., HER2 3+ cell lines, P =
SW fraction induces S phase arrest and apoptosis.

SW fraction induces S phase arrest and apoptosis.
Model for the regulation of HIPK2 activity and p53 phosphorylations by the ATM pathway. Model for the regulation of HIPK2 activity and p53 phosphorylations.

Model for the regulation of HIPK2 activity and p53 phosphorylations by the ATM pathway. Model for the regulation of HIPK2 activity and p53 phosphorylations.
Apoptosis induced by ssHHT in HL60 and its derivative, the HL60/MRP, cells. Apoptosis induced by ssHHT in HL60 and its derivative, the HL60/MRP, cells.

Apoptosis induced by ssHHT in HL60 and its derivative, the HL60/MRP, cells. Apoptosis induced by ssHHT in HL60 and its derivative, the HL60/MRP, cells.
CYP1A1 knockdown increases cell death.

CYP1A1 knockdown increases cell death.
Induction of apoptosis by NMT siRNAs.

Induction of apoptosis by NMT siRNAs.
eNOS regulated IR-induced NO generation and EGFR signal activation.

eNOS regulated IR-induced NO generation and EGFR signal activation.
Frequency and kinetics of killer cell apoptosis are dependent on functional conjugations with multiple NALM-6 tumor cells. Frequency and kinetics of killer.

Frequency and kinetics of killer cell apoptosis are dependent on functional conjugations with multiple NALM-6 tumor cells. Frequency and kinetics of killer.
Increased CCL5 expression, infiltration of Treg cells, and apoptosis of CD8+ T cells in human colorectal tissues. Increased CCL5 expression, infiltration.

Increased CCL5 expression, infiltration of Treg cells, and apoptosis of CD8+ T cells in human colorectal tissues. Increased CCL5 expression, infiltration.
Effects of knockdown of ANRIL on NSCLC cell cycle and apoptosis in vitro. Effects of knockdown of ANRIL on NSCLC cell cycle and apoptosis in vitro. A,

Effects of knockdown of ANRIL on NSCLC cell cycle and apoptosis in vitro. Effects of knockdown of ANRIL on NSCLC cell cycle and apoptosis in vitro. A,
A, chemical structures of PRIMA-1 and PRIMA-1Met.

A, chemical structures of PRIMA-1 and PRIMA-1Met.
In vitro invasion assays were done in the Chemicon invasion chamber containing extracellular matrix. In vitro invasion assays were done in the Chemicon.

In vitro invasion assays were done in the Chemicon invasion chamber containing extracellular matrix. In vitro invasion assays were done in the Chemicon.

Similar presentations

Ads by Google