Pharmacological inhibition of DAO impairs DNA damage– and oncogene-induced senescence. Pharmacological inhibition of DAO impairs DNA damage– and oncogene-induced.

Slides:

Advertisements

Similar presentations

Supplemental Figures A B % Senescent Cells Relative to control *

Advertisements

Volume 109, Issue 2, Pages (April 2002)

by Rafijul Bari, Teresa Bell, Wai-Hang Leung, Queenie P

Volume 35, Issue 3, Pages (August 2009)

NF1 silencing confers resistance of PC9 lung adenocarcinoma cells to erlotinib (erl). NF1 silencing confers resistance of PC9 lung adenocarcinoma cells.

Human osteoarthritic chondrocytes are impaired in matrix metalloproteinase-13 inhibition by IFN-γ due to reduced IFN-γ receptor levels R. Ahmad, M. El.

Fig. 3. BET inhibition reduces homologous recombination.

SUPPLEMENTAL TABLE 1. Cell cycle profiles of HeLa cells treated

Ganglioside GM3 Promotes Carcinoma Cell Proliferation via Urokinase Plasminogen Activator-Induced Extracellular Signal-Regulated Kinase-Independent p70S6.

Expression of SYCE2 activates the DSB repair pathway.

NF1 downregulation activates MAPK pathway signaling.

by Silvia Mele, Stephen Devereux, Andrea G

DAO enhances DNA damage–induced ROS accumulation, cooperating with PRODH. DAO enhances DNA damage–induced ROS accumulation, cooperating with PRODH. (A)

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

The mRNA bearing the IRES element is arranged in cytoplasmic clusters.

Xiaolong Wei, Hai Xu, Donald Kufe Cancer Cell

Volume 47, Issue 3, Pages (August 2012)

Volume 35, Issue 3, Pages (August 2009)

Monica Kong-Beltran, Jennifer Stamos, Dineli Wickramasinghe

Volume 17, Issue 1, Pages (January 2005)

Volume 13, Issue 1, Pages (January 2008)

Volume 66, Issue 4, Pages e5 (May 2017)

Knockdown of DAO inhibits DNA damage–induced senescence.

HDAC5, a Key Component in Temporal Regulation of p53-Mediated Transactivation in Response to Genotoxic Stress Nirmalya Sen, Rajni Kumari, Manika Indrajit.

Phosphorylation on Thr-55 by TAF1 Mediates Degradation of p53

BMDC-EV attract immune cells in lymph nodes similarly as in the skin.

Role of HER2 in mediating acquired resistance to EGFR inhibition.

CDK4/6 knockdown causes upregulation of MYC, GLS1, and P‐mTOR and downregulation of HIF‐1α CDK4/6 knockdown causes upregulation of MYC, GLS1, and P‐mTOR.

DNA Damage Foci at Dysfunctional Telomeres

Volume 25, Issue 5, Pages (March 2007)

Mst1 Is an Interacting Protein that Mediates PHLPPs' Induced Apoptosis

Modification of the βIII-tubulin C-terminal tail does not affect the incorporation of the protein into the microtubule network, the microtubule architecture,

DDR1 kinase is required for tubulogenesis and polarity-dependent MT1-MMP localization at the basal surface. DDR1 kinase is required for tubulogenesis and.

Pharmacologic inhibition of eIF5A hypusination sensitizes KRas-driven tumor cells to MEK and KRas inhibition. Pharmacologic inhibition of eIF5A hypusination.

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

ADAM8 is induced by hypoxia and promotes angiogenesis ASixteen h after plating, cells were cultured under normoxic (−) or hypoxic (+, 1% O2) conditions.

SYCE2 potentiates the steady-state DNA repair activity without affecting the cell cycle checkpoint. SYCE2 potentiates the steady-state DNA repair activity.

Fig. 2. Ex vivo inducible knockout of PDCD2 in ESCs results in loss of S phase entry and increased p53.(A) Growth curve of inducible knockout and WT ESCs.

DDR1 kinase is required for tubulogenesis and polarity-dependent MT1-MMP localization at the basal surface. DDR1 kinase is required for tubulogenesis and.

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

Ectopic expression of wt-DAO, but not the inactive mutant, promotes senescence. Ectopic expression of wt-DAO, but not the inactive mutant, promotes senescence.

Therapy-induced senescence of primary cells.

Mechanism of Akt1 in promoting reprogramming.

John M. Lamar, Vandana Iyer, C. Michael DiPersio

Dissociation of HP1α from H3K9me3 is critical to potentiation of steady-state ATM activity. Dissociation of HP1α from H3K9me3 is critical to potentiation.

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

Defective MEK-Erk1/2 kinase activation in RIAM-depleted cells accounts for their impaired FA disassembly. Defective MEK-Erk1/2 kinase activation in RIAM-depleted.

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

Effect of the siRNA-mediated knockdown of endogenous MARCH8 on the expression levels of MARCH8 substrates, TfR and CD98, in HepG2 cells. Effect of the.

Global analysis of RV[S/T]F motif phosphorylation during mitosis.

Association of NM-HA and NM-GFP with SGs is transient.

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.

Volume 11, Issue 6, Pages (May 2015)

Curcumin-generated ROS activates Chk1 and Chk2 kinases.

TSA-mediated changes in cell cycle inhibitor proteins.

Overexpression of Pim kinases contributes to increased protein translation in resistant cells through controlling cap-independent translation. Overexpression.

IAA inhibits PI3K, MKK4, and MKK7 kinase activities by directly binding in an ATP-competitive manner. IAA inhibits PI3K, MKK4, and MKK7 kinase activities.

Effect of GSK3β inhibition on cell survival and proliferation of glioblastoma cells. Effect of GSK3β inhibition on cell survival and proliferation of glioblastoma.

Endogenously produced n-3 PUFAs inhibit endometrial cancer cell growth in vitro and in vivo. Endogenously produced n-3 PUFAs inhibit endometrial cancer.

Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. LNCaP,

RUNX3 depletion induces cellular senescence in an ATM/ATR dependent, but p53-independent manner. RUNX3 depletion induces cellular senescence in an ATM/ATR.

Effect of bevacizumab on the proliferation of A2780 cells.

ER stress mediates postslippage AMPK activation.

Association of TCTP with Pim-3 in human pancreatic cancer cell lines.

Autophagy mediates postslippage cell fate.

Curcumin decreases viability and proliferation of Bcr-Abl-expressing cells. Curcumin decreases viability and proliferation of Bcr-Abl-expressing cells.

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.

TCTP enhances the protein stability of Pim-3 by blocking the ubiquitin–proteasome degradation of Pim-3. TCTP enhances the protein stability of Pim-3 by.

Sp1 complementation assay.

DHA and dietary n-3 PUFAs inhibit endometrial cancer cell growth in vitro and in xenograft models. DHA and dietary n-3 PUFAs inhibit endometrial cancer.

Presentation transcript:

Pharmacological inhibition of DAO impairs DNA damage– and oncogene-induced senescence. Pharmacological inhibition of DAO impairs DNA damage– and oncogene-induced senescence. (A–D) U2OS (A, C) and HepG2 (B, D) cells treated with etoposide in the presence of 50 or 100 μM CBIO were subjected to SA-β-gal staining (A, B) and colony-formation assay (C, D). (E, F) U2OS (E) and HepG2 (F) cells were treated with 2 and 10 μM etoposide, respectively, for 2 d in the presence of 50 μM CBIO, and the expression levels of the indicated proteins were determined by immunoblot analysis. The protein levels relative to the γ-tubulin levels, except for the phosphorylated p53 (p53 pS15), which was normalized to the total p53 levels, were quantified using NIH ImageJ software and are indicated at the bottom of each lane. (G, H) Hs68 cells treated with 0.5 μM etoposide for 7 d in the presence of 50 μM CBIO were subjected to SA-β-gal staining (G) and EdU incorporation assay (H). The percentage of EdU-positive cells (H, left panel) and representative microscopic images (H right panel) are shown. Bars, 50 μm. (I) Hs68 cells treated with 0.5 μM etoposide for 2 d in the presence of 50 μM CBIO were subjected to immunoblot analysis. The protein levels were quantified as in (E, F). (J) WI-38 cells were transfected with pcDNA3-HA containing oncogenic RasG12V, and the protein expression of RasG12V was confirmed by immunoblot analysis. (K, L) WI-38 cells transfected as in (J) were selected with 300 μg/ml G418 and treated with 50 μM CBIO. After incubation for 8 d, the cells were subjected to SA-β-gal staining (K) and EdU incorporation assay (L). Data are mean ± SD (n = 3 independent experiments). Statistical significance is shown using the t test analysis; **P < 0.01. Taiki Nagano et al. LSA 2019;2:e201800045 © 2019 Nagano et al.