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

Slides:

Advertisements

Similar presentations

Figure S1. qPCR analysis of the EMT markers ZEB2 and SNAI1 in Syndecan-1 and control siRNA transfected MDA-MB-231 and MCF-7 cells reveals no significant.

Advertisements

ABAE positive cells 6h after treatment

p < Figure S1 p55 viral protein level Relative HIV-1

Fig. 4. Effect of Mcl-1 overexpression on H2O2-induced JNK activation and apoptosis. (A) Expression of Mcl-1 protein in several.

A B C D Supplementary Figure 1 CMV p300

miR-133a positively regulated p53/p21 pathway.

Deiminated REF in regulation of ATP synthase expression.

Dual-Luciferase Activation Assay with Potential Targets of ZmbZIP22.

MiR‐199a directly targets ERBB2 and ERBB3, whereas miR‐125b targets ERBB3. miR‐199a directly targets ERBB2 and ERBB3, whereas miR‐125b targets ERBB3. (A)

Distinct but Concerted Roles of ATR, DNA-PK, and Chk1 in Countering Replication Stress during S Phase Rémi Buisson, Jessica L. Boisvert, Cyril H. Benes,

Pnut is phosphorylated during early Drosophila embryogenesis.

Expression of SYCE2 activates the DSB repair pathway.

A20 inhibits caspase-8 cleavage and TRAIL-induced apoptosis.

PCB126 induces apoptosis of chondrocytes via ROS-dependent pathways

Yuming Wang, Jennifer A. Fairley, Stefan G.E. Roberts Current Biology

Volume 47, Issue 3, Pages (August 2012)

Volume 13, Issue 1, Pages (January 2008)

Knockdown of DAO inhibits DNA damage–induced senescence.

Linking the Rb and Polycomb Pathways

HURP is an obstacle for KIF18A on K-fibers in metaphase cells.

Volume 26, Issue 6, Pages (June 2007)

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

Mutant and Wild-Type Tumor Suppressor p53 Induces p300 Autoacetylation

Cellular 5′-3′ mRNA Exonuclease Xrn1 Controls Double-Stranded RNA Accumulation and Anti-Viral Responses Hannah M. Burgess, Ian Mohr Cell Host & Microbe

Volume 25, Issue 5, Pages (March 2007)

Klotho is a target gene of PPAR-γ

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

Mitotic chromosome misalignment is independent of DNA replication.

The effects of KY19382 on chondrocyte proliferation and differentiation. The effects of KY19382 on chondrocyte proliferation and differentiation. (A) ATDC5.

Fig. 5. Prip silencing enhances the co-localization of GABARAP with insulin vesicles and β-tubulin.Co-localization of GABARAP (green) with insulin (red)

Fig. 2. p85β regulates cell adhesion

Abraxas binds to BRCT–PALB2(L21P) and is involved in the recruitment of this fusion protein or of endogenous PALB2 to sites of DNA damage. Abraxas binds.

The Atg3bp1 mutants display enhanced disease resistance and alter classical MTI responses. The Atg3bp1 mutants display enhanced disease resistance and.

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

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.

Sufu is required for the stabilization of Gli2 and Gli3 proteins in vivo. Sufu is required for the stabilization of Gli2 and Gli3 proteins in vivo. (A)

SLK/LOK-phosphorylated and activated ezrin prevents MISP localization at the cell cortex. SLK/LOK-phosphorylated and activated ezrin prevents MISP localization.

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

CREB1 promotes the induction of endogenous ERα target genes.

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.

S. cerevisiae Bre1p confers resistance to apoptosis induced by H2O2.

KIF13A depletion leads to a drop in virus titers, without affecting viral protein expression. KIF13A depletion leadsto a drop in virus titers, without.

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

BEZ235 induces MAPK signaling in a FOXO3A-dependent manner.

Assay of ROS accumulation in cells exposed to high levels of glucose.

Ca2+-mediated differentiation of primary mouse keratinocytes is independent of epiplakin. Ca2+-mediated differentiation of primary mouse keratinocytes.

Curcumin-generated ROS activates Chk1 and Chk2 kinases.

PTB-independent ShcA pools require Src to promote mammary tumorigenesis. PTB-independent ShcA pools require Src to promote mammary tumorigenesis. A, Src.

Tousled‐like kinase 2 regulates recovery from a DNA damage‐induced G2 arrest U2OS cells were transfected with four independent siRNAs from the pools used.

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

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

Effect of G9a on the expression of GSH synthesis enzymes.

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

Increased migration and podia formation in NFIB-suppressed human osteosarcoma cells. Increased migration and podia formation in NFIB-suppressed human osteosarcoma.

Combination of miR-520d-3p and EphA2 siRNA treatment shows enhanced EphA2 inhibition and antitumor efficiency in vitro. Combination of miR-520d-3p and.

Pirh2 represses p73-dependent transactivation.

RUNX3 depletion induces cellular senescence and inflammatory cytokine expression in cells undergoing TGFβ-mediated EMT. A, Cells were transfected with.

PVT1 binds to the FOXM1 protein and increases its protein level by enhancing its stability. PVT1 binds to the FOXM1 protein and increases its protein level.

SAHA blocks IR-induced increase of RAD51 protein in MM cells.

The effects of AZD1775 and olaparib on DNA damage response signaling.

Effect of bevacizumab on the proliferation of A2780 cells.

ER stress mediates postslippage AMPK activation.

p53β regulates cellular senescence.

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

Induction of Autophagy Is Dependent on the Delivery of the T3E HopM1.

Autophagy mediates postslippage cell fate.

CREB1 binds at the proximal region of the TGFB2 promoter and induces its transcriptional activation. CREB1 binds at the proximal region of the TGFB2 promoter.

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.

Presentation transcript:

DAO enhances DNA damage–induced ROS accumulation, cooperating with PRODH. DAO enhances DNA damage–induced ROS accumulation, cooperating with PRODH. (A) U2OS cells transfected with siRNAs for DAO (DAO-1 and DAO-2) were treated with 2 μM etoposide for 2 d, and the ROS level was measured. (B, C) U2OS (B) and HepG2 (C) cells treated with 2 and 10 μM etoposide, respectively, for 2 d in the presence of 50 μM CBIO were subjected to ROS assay. (D) U2OS cells transfected with pcDNA3-HA-DAO and treated with 2 μM etoposide were subjected to ROS assay. (E, F) U2OS cells overexpressing DAO were treated with etoposide in the presence of 1 mM NAC for 7 d and subjected to SA-β-gal staining (E) and EdU incorporation assay (F). (G) U2OS cells treated as in (E, F) but for 2 d instead of 7 d were subjected to immunoblot analysis. The protein levels relative to the γ-tubulin levels were quantified using NIH ImageJ software and are indicated at the bottom of each lane. (H, I) U2OS cells treated with etoposide in combination with 50 μM CBIO and 1 mM NAC as indicated for 7 d were subjected to SA-β-gal staining (H) and EdU incorporation assay (I). (J) U2OS cells treated as in (H, I) but for 2 d instead of 7 d were subjected to immunoblot analysis. The protein levels were quantified as in (G). (K, L) U2OS cells treated as in (H, I) but 5 mM THFA instead of NAC were subjected to SA-β-gal staining (K) and EdU incorporation assay (L). (M) U2OS cells treated as in (K, L) but for 2 d instead of 7 d were subjected to immunoblot analysis. The protein levels were quantified as in (G). (N, O) Hs68 cells treated as in (K, L) were subjected to SA-β-gal staining (N) and EdU incorporation assay (O). (P) Hs68 cells treated as in (N, O) but for 2 d instead of 7 d were subjected to immunoblot analysis. The protein levels were quantified as in (G). Data are mean ± SD (n = 3 independent experiments). Statistical significance is shown using the t test analysis; *P < 0.05, **P < 0.01, and n.s. = not significant (P > 0.05). Taiki Nagano et al. LSA 2019;2:e201800045 © 2019 Nagano et al.