Knockdown of DAO inhibits DNA damage–induced senescence.

Slides:



Advertisements
Similar presentations
Supplemental Figures A B % Senescent Cells Relative to control *
Advertisements

Smita Srivastava, Patricia S. Grace, Joel D. Ernst  Cell Host & Microbe 
p < Figure S1 p55 viral protein level Relative HIV-1
E2F7/8 and HIF1 are required for hypoxic VEGFA expression.
An siRNA screen identifies LIMT as an ERK‐dependent negative regulator of mammary cell migration An siRNA screen identifies LIMT as an ERK‐dependent negative.
NoRC regulates telomeric heterochromatin.
Cell Physiol Biochem 2016;39: DOI: /
ADAM8 maintains the aggressive phenotype of TNBC cells in 3D‐culture A–DCells were transfected with siRNAs as in Fig 2D and E for 24 h, and tested for.
* * * A B D C E CP110 Tubulin WB: CP110 WB: HA CP110 KRAS Tubulin
Expression of SYCE2 activates the DSB repair pathway.
MiR-34a contributes to megakaryocytic differentiation of K562 cells independently of p53 by Francisco Navarro, David Gutman, Eti Meire, Mario Cáceres,
SEMA3C silencing inhibits CRPC cell growth and induces apoptosis
Ras Induces Mediator Complex Exchange on C/EBPβ
LATS2 promotes death of lumB cells.
DAO enhances DNA damage–induced ROS accumulation, cooperating with PRODH. DAO enhances DNA damage–induced ROS accumulation, cooperating with PRODH. (A)
Selective Inhibition of p300 HAT Blocks Cell Cycle Progression, Induces Cellular Senescence, and Inhibits the DNA Damage Response in Melanoma Cells  Gai.
The mRNA bearing the IRES element is arranged in cytoplasmic clusters.
Smita Srivastava, Patricia S. Grace, Joel D. Ernst  Cell Host & Microbe 
Human Mitochondrial NAD(P)+–Dependent Malic Enzyme Participates in Cutaneous Melanoma Progression and Invasion  Yung-Lung Chang, Hong-Wei Gao, Chien-Ping.
Volume 47, Issue 3, Pages (August 2012)
Workflow of the integrated proteomics approach to identify the abnormal network in NF1-KD PC12 cells. Workflow of the integrated proteomics approach to.
Plk1 inhibition or depletion causes robust cortical NuMA localization in mitosis. Plk1 inhibition or depletion causes robust cortical NuMA localization.
HDAC5, a Key Component in Temporal Regulation of p53-Mediated Transactivation in Response to Genotoxic Stress  Nirmalya Sen, Rajni Kumari, Manika Indrajit.
BDNF expression in the cerebellum and brain stem region.
Volume 21, Issue 9, Pages (November 2017)
BMDC-EV attract immune cells in lymph nodes similarly as in the skin.
Pharmacological inhibition of DAO impairs DNA damage– and oncogene-induced senescence. Pharmacological inhibition of DAO impairs DNA damage– and oncogene-induced.
Role of HER2 in mediating acquired resistance to EGFR inhibition.
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)
SiRNA knockdown of dynein IC2-C recovered the inhibition of neurite outgrowth in NF1-KD PC12 cells. siRNA knockdown of dynein IC2-C recovered the inhibition.
Cortical NuMA enrichment upon Plk1 inhibition is dynein independent.
Fig. 5. Prip silencing enhances the co-localization of GABARAP with insulin vesicles and β-tubulin.Co-localization of GABARAP (green) with insulin (red)
SYCE2 potentiates the steady-state DNA repair activity without affecting the cell cycle checkpoint. SYCE2 potentiates the steady-state DNA repair activity.
Fig. 1. Loss of PC following INT depletion
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.
Effects of SYCE2 expression on DSB repair.
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.
Fig. 4. Perinuclear dynein regulators are not required for primary ciliogenesis.RPE cells were transfected with siRNA and either nocodazole-treated, fixed,
Fig. 1. Loss of PC following INT depletion
SYCE2 potentiates the steady-state ATM activity.
IL-6 inhibits insulin-induced formation of p85/IRS-1 complexes.
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.
KIF13A depletion leads to a drop in virus titers, without affecting viral protein expression. KIF13A depletion leadsto a drop in virus titers, without.
Association of NM-HA and NM-GFP with SGs is transient.
SiRNA directed at Ngn1 inhibited differentiation of inner ear stem cells to β-III tubulin-positive cells. a, Inner ear stem cells treated with siRNA to.
Volume 11, Issue 6, Pages (May 2015)
Effect of siRNA-mediated depletion of selected OST subunits on stability. Effect of siRNA-mediated depletion of selected OST subunits on stability. (A)
Volume 26, Issue 12, Pages e4 (March 2019)
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.
Effect of sustained suppression of HDAC2 in MKN-1 cells on in vitro tumorigenicity. Effect of sustained suppression of HDAC2 in MKN-1 cells on in vitro.
CDCP1 is required for invadopodia formation and ECM degradation by human breast cancer cells. CDCP1 is required for invadopodia formation and ECM degradation.
TSA-mediated changes in cell cycle inhibitor proteins.
Effect of GSK3β inhibition on cell survival and proliferation of glioblastoma cells. Effect of GSK3β inhibition on cell survival and proliferation of glioblastoma.
ARID1A promotes DSB end resection.
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,
Autophagy Activation Is Mediated by the Secretion of T3Es.
RUNX3 depletion induces cellular senescence and inflammatory cytokine expression in cells undergoing TGFβ-mediated EMT. A, Cells were transfected with.
FBXL19-AS1 knockdown inhibits proliferation, migration and invasion, and reduces the expression levels of angiogenesis related proteins in lung cancer.
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.
p53β regulates cellular senescence.
Autophagy mediates postslippage cell fate.
Coculture with U937 cells enhances DNMT1 expression in gastric cancer cells. Coculture with U937 cells enhances DNMT1 expression in gastric cancer cells.
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:

Knockdown of DAO inhibits DNA damage–induced senescence. Knockdown of DAO inhibits DNA damage–induced senescence. (A) U2OS cells transfected with siRNAs for DAO (DAO-1 and DAO-2) were treated with 2 μM etoposide for 7 d, and the expression levels of DAO were determined by qPCR. (B) HepG2 cells transfected with siRNAs for DAO (DAO-1 and DAO-2) were treated with 10 μM etoposide for 48 h, and the expression levels of DAO were determined by immunoblot analysis. (C, D) U2OS (C) and HepG2 (D) cells depleted of DAO were treated with 2 and 10 μM etoposide for 7 d and 48 h, respectively, and subjected to SA-β-gal staining. The percentage of SA-β-gal–positive cells (C left panel, D) and representative microscopic images (C right panel) are shown. Bars, 50 μm. (E) U2OS cells depleted of DAO were treated with 2 μM etoposide for 7 d and subjected to colony-formation assay. Relative proliferation rate (upper panel) and representative images (lower panel) are shown. (F) U2OS cells treated as in (E) 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. Data are mean ± SD (n = 3 except in (A) where n = 2 independent experiments). Statistical significance is shown using the t test analysis; *P < 0.05, **P < 0.01. Taiki Nagano et al. LSA 2019;2:e201800045 © 2019 Nagano et al.