Fig. 1. PGBD5-expressing cells do not tolerate deficiency of nonhomologous end-joining DNA repair. PGBD5-expressing cells do not tolerate deficiency of.

Slides:



Advertisements
Similar presentations
Fig. 1. TP is highly expressed in myeloma.
Advertisements

Induction of apoptosis by CDIP expression.
Fig. 6. AZD6738 induces DNA damage and apoptosis and exhibits antitumor efficacy in xenograft models of high-risk medulloblastoma and neuroblastoma. AZD6738.
Differentiation of AZD4785 from MAPK pathway inhibitors in vitro
Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.
BET inhibition and depletion repress the expression of BRCA1 and RAD51
Fig. 7. Role of PDE5 up-regulation in lung cancer–associated PH.
Fig. 8. Gene and protein changes in ALK-dependent STING pathways in human sepsis. Gene and protein changes in ALK-dependent STING pathways in human sepsis.
Fig. 5. Wisper is associated with TIA1-related protein and regulates lysyl hydroxylase 2 expression. Wisper is associated with TIA1-related protein and.
Analysis of brain and spinal cord of treated Gaa−/− mice and controls
Synergistic effect of S63845 with lapatinib, trastuzumab, or docetaxel
Fig. 1 Localized treatment of TNBC cancers kills tumor cells and minimizes the metastatic burden. Localized treatment of TNBC cancers kills tumor cells.
Fig. 3. BET inhibition reduces homologous recombination.
Fig. 4 Infection-induced CLV dysfunction is associated with decreased LMC coverage. Infection-induced CLV dysfunction is associated with decreased LMC.
Fig. 2. GPC3 expression in normal and tumor tissues.
Fig. 6. Effects of CD31-NP targeting in perfused human kidneys.
Fig. 4 Expression of cleaved caspase 3, PD-L1, and PD-1 in HGGs after reovirus treatment. Expression of cleaved caspase 3, PD-L1, and PD-1 in HGGs after.
Fig. 4. Specific versus nonspecific NP accumulation.
Fig. 1. CD31 is present throughout the human renal vasculature.
Fig. 1. Aberrant JNK pathway activation in mouse models of ALS and in spinal cord tissue from patients with sporadic ALS. Aberrant JNK pathway activation.
Immunofluorescence staining of virus-infected human placental explants
Fig. 4. MATE1 transcription in RCC.
Fig. 3. Genetically engineered PD-L1
Antiproliferative effects of JQ-EZ-05 on VHL−/− ccRCC are on-target
Fig. 1. mGlu7 expression is reduced in RTT autopsy samples.
Fig. 3. Recovery of AVP-deficient rats from anemia induced by sublethal irradiation. Recovery of AVP-deficient rats from anemia induced by sublethal irradiation.
Fig. 7. NPs accumulate at sites of vascular obstruction.
Fig. 7. ApoMSCs exert immunosuppressive activity in GvHD and elicit IDO in engulfing recipient phagocytes. ApoMSCs exert immunosuppressive activity in.
Fig. 7. Inhibitory mechanisms of C12G6.
Fig. 2 Fas controls IL-1RA–sEV secretion in murine MSCs.
Fig. 5. Nutlin-3 treatment rescues the proliferation and differentiation of NPCs in vitro. Nutlin-3 treatment rescues the proliferation and differentiation.
Fig. 4 TNF-α up-regulates Fas/Fap-1 expression to promote IL-1RA–sEV release in murine MSCs. TNF-α up-regulates Fas/Fap-1 expression to promote IL-1RA–sEV.
Fig. 7 DMN-Tre labeling of Mycobacterium tuberculosis is inhibited by tuberculosis drug cocktail, unlike auramine staining. DMN-Tre labeling of Mycobacterium.
Fig. 1. β-APP overexpression or exposure to inflammatory mediators induces sIBM-like pathology in cultured rat myocytes that is abrogated by arimoclomol.
PAAND is driven by local inflammasome activation and IL-1β production
Fig. 1 CSPG4 is expressed in GBM specimens and GBM-NS and associated with more aggressive disease. CSPG4 is expressed in GBM specimens and GBM-NS and associated.
Fig. 3 CSF1 is expressed in human melanoma.
Fig. 5 BRD0705 induces differentiation in AML cell lines and primary patient samples through GSK3α-selective inhibition. BRD0705 induces differentiation.
Fig. 7. Scale-up of AAV vector–mediated liver gene transfer of secretable GAA to nonhuman primates. Scale-up of AAV vector–mediated liver gene transfer.
Fig. 1 LB100 and LB102 specifically inhibit PP2A phosphatase activity and the growth of BCR-ABL+ cells. LB100 and LB102 specifically inhibit PP2A phosphatase.
Correlation of reovirus RNA/protein with proliferating tumor cells
AKT2, but not AKT1, is required for regulating survival of PTEN-deficient prostate tumor spheroids. AKT2, but not AKT1, is required for regulating survival.
Fig. 6 Combination therapy with LVSOD2 and LVshCTGF preserves flap volume and reduces fibrosis after RT. Combination therapy with LVSOD2 and LVshCTGF preserves.
Fig. 4 ALRN-6924 inhibits cellular proliferation and clonogenic capacity, and induces cell cycle arrest and apoptosis in AML cell lines. ALRN-6924 inhibits.
Fig. 2. BET inhibition enhances PARPi-induced DNA damage.
Fig. 4 Lentiviral transgene expression penetrates tissue and provides durable effects in vivo. Lentiviral transgene expression penetrates tissue and provides.
Fig. 2 Endurance exercise up-regulates TERRA in human muscle.
Fig. 2. Spontaneous inflammasome activation by pyrin S242R.
Fig. 5. Mutant KRAS increases HR capacity and MEKi decreases HR capacity in RAS mutant cells, causing increased DNA damage. Mutant KRAS increases HR capacity.
High-affinity mutants of β3 integrin fail to stimulate RhoA activity and fibronectin fibrillogenesis. High-affinity mutants of β3 integrin fail to stimulate.
S. cerevisiae Bre1p confers resistance to apoptosis induced by H2O2.
Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.
Fig. 1. DEL-1 is expressed by human and mouse osteoclasts.
Fig. 1. Matrix stiffness sensitizes myofibroblasts to apoptosis induced by inhibition of their mechanotransduction pathways. Matrix stiffness sensitizes.
Fig. 8 C9orf72 knockdown results in an increase in autophagic flux.
Fig. 2 ObR is cleaved and has reduced signaling capabilities after incubation with Mmp-2. ObR is cleaved and has reduced signaling capabilities after incubation.
Modeling chemotherapy-induced stress to identify rational combination therapies in the DNA damage response pathway by Ozan Alkan, Birgit Schoeberl, Millie.
Therapeutic targeting of PGBD5-induced DNA repair dependency in pediatric solid tumors by Anton G. Henssen, Casie Reed, Eileen Jiang, Heathcliff Dorado.
Biological effects of BRAF silencing: growth curves of A375 (A) and ARO (B) cell lines in the absence or presence of doxycycline. Biological effects of.
Fig. 1 Prophylactic, neutralization, and therapeutic efficacy of HPAC.
Targeting p53-dependent stem cell loss for intestinal chemoprotection
Fig. 4 IP6K1-mediated polyP production by platelets plays a critical role in LPS-induced NPA formation. IP6K1-mediated polyP production by platelets plays.
Microfluidic platform for cell phenotype and gene function analysis
Γ-H2AX foci formation in ATM−/− and DNA-dependent protein kinase catalytic subunit (DNA-PKcs)−/− mouse embryo fibroblasts (MEFs) but not in ATM−/− MEFs.
Fig. 5 C9orf72 knockdown disrupts autophagy induction.
Wnt5A decreases ROR1 expression through proteasomal degradation.
Fig. 2 Increasing KLF17, CDH1, and LASS2 expression reduced malignant progression and promoted apoptosis of tumor cells. Increasing KLF17, CDH1, and LASS2.
Fig. 6 The C9ORF72/SMCR8 complex regulates ULK1.
Fig. 1 Generation and characterization of MeV-based vaccine candidates for Lassa virus. Generation and characterization of MeV-based vaccine candidates.
Mitochondrial import of CerS1 from smooth ER mediates lethal mitophagy
Presentation transcript:

Fig. 1. PGBD5-expressing cells do not tolerate deficiency of nonhomologous end-joining DNA repair. PGBD5-expressing cells do not tolerate deficiency of nonhomologous end-joining DNA repair. (A) Western blot of PGBD5 protein expression after induction with doxycycline (DOX; 500 ng/ml for 24 hours) of SV40 large T antigen–immortalized MEFs deficient for Atm−/−, AtrS/S, or Ku80−/−. Actin serves as loading control. (B) Induction of apoptosis as measured by ClCas3 staining of MEFs deficient in DNA repair factors upon doxycycline-induced (48 hours) expression of PGBD5 (red) as compared to control phosphate-buffered saline (PBS)–treated cells (blue). *P = 0.010, 0.0080, and 0.0010 for Atm−/−, AtrS/S, and Ku80−/− of doxycycline versus control, respectively. (C) Representative photomicrographs of MEFs upon doxycycline-induced PGBD5 expression for 48 hours (+) as compared to PBS-treated controls (−), stained for 4′,6-diamidino-2-phenylindole (DAPI; blue) and ClCas3 (red). (D to E) Induction of DNA DSBs measured by TUNEL staining (D) and γH2AX staining (E) of MEFs deficient in DNA repair factors upon doxycycline-induced (48 hours) expression of PGBD5 (red) compared to control PBS-treated cells (blue). *P = 0.0010 and 0.0020 for Atm−/− and AtrS/S of doxycycline versus control, respectively (D). *P = 0.0030 and 0.020 for Atm−/− and AtrS/S of doxycycline versus control, respectively (E). Error bars represent SDs of three biological replicates. Anton G. Henssen et al., Sci Transl Med 2017;9:eaam9078 Published by AAAS