Fig. 2 BX795 is nontoxic to HCE cells at therapeutic concentration.

Slides:

Advertisements

Similar presentations

Figure 5. FK866 caused apoptosis in MCF-7 cells while nicotinamide adenine dinucleotide (NAD+) reversed FK866-induced apoptosis. (A) Representative quadrant.

Advertisements

Correlation between endogenous STAT5ab signaling and circulating plasma factors. Correlation between endogenous STAT5ab signaling and circulating plasma.

PVSRIPO-mediated APC activation occurs in immunosuppressive conditions

Fig. 3 BX795 blocks the synthesis of HSV-1 virions.

FIP200 deficiency alters mitochondria activation and ROS production in T cells. FIP200 deficiency alters mitochondria activation and ROS production in.

Self-folding triangular devices at two scales.

Cytotoxicity of MSP samples to normal and cancer cell lines.

Comparison of predicted and measured forces and moments.

Nuclear calcium signaling drives nuclear actin polymerization in T cells. Nuclear calcium signaling drives nuclear actin polymerization in T cells. (A)

Fig. 1 BX795 suppresses HSV-1 infection.

Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. (A)

Memory CD8+ T cells that become terminally differentiated by multiple antigen encounters lose core 2 O-glycan synthesis activity. Memory CD8+ T cells that.

VH usage of cross-reactive B cells induced by H5N1 or H7N9 vaccination

Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell.

Tukey boxplots overlaid on data points from objective and subjective measures, displaying results from study 1. Tukey boxplots overlaid on data points.

Characterization of the light-responsive transdermal MNs.

Fig. 7 Correlation of NHP and human ISGs.

Differentiation of AZD4785 from MAPK pathway inhibitors in vitro

Fig. 6 In utero injection of inflammatory cytokines or adoptive transfer of activated T cells leads to pregnancy loss. In utero injection of inflammatory.

Immune cell recruitment after the NIR-boosted and MN-mediated cancer immunotherapy. Immune cell recruitment after the NIR-boosted and MN-mediated cancer.

Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. (A)

Fig. 1 ZIKV RNA in blood and tissues.

Fig. 4 Labeling of Msmeg with DMN-Tre is fast and specific and depends on Ag85A function. Labeling of Msmeg with DMN-Tre is fast and specific and depends.

Fig. 2 AcPGP induces IL-8 and G-CSF release from human bronchial epithelial cells. AcPGP induces IL-8 and G-CSF release from human bronchial epithelial.

Cell viability tests. Cell viability tests. SEM images of (A) MC3T3-E1 cells and (B) MSCs on days 1, 3, and 5 of culture. (C) Survival rates of MC3T3-E1.

Fig. 1. MSCs undergo in vivo apoptosis after infusion without affecting immunosuppression. MSCs undergo in vivo apoptosis after infusion without affecting.

Fig. 4. PVSRIPO infection of DCs is sublethal, is marginally productive, and induces sustained proinflammatory cytokine production. PVSRIPO infection of.

Fig. 2 Preserved long-term functionality of the TEHVs over 1-year follow-up as assessed by ICE and cardiac MRI flow measurements. Preserved long-term functionality.

Fig. 4 High P-eIF2α expression in human prostate tumors with loss of PTEN function is associated with increased risk of metastasis or death after surgery.

Fig. 5. In vivo characterization of adipogenesis by CT.

Shared phenotype of CD4+CLA+CD103+ T cells from human blood and skin.

Fig. 4 CEBPA-p30 mediated activation of Nt5e expression.

Fig. 3 NK cells are enriched in ICB-sensitive tumors in mouse models and patients and are required for response. NK cells are enriched in ICB-sensitive.

MYC degradation screen identifies a compound that stabilizes MYC protein. MYC degradation screen identifies a compound that stabilizes MYC protein. (A)

Fig. 3. Increased expression of exhaustion markers and apoptosis markers on CAR8 cells in the presence of TCR antigen. Increased expression of exhaustion.

Fig. 3 BMS blocks functional responses in primary immune cells driven by IL-23 and IL-12. BMS blocks functional responses in primary immune.

Fig. 2 In situ vaccination of CpG in combination with anti-OX40 antibody cures established local and distant tumors. In situ vaccination of CpG in combination.

BMS blocks functional responses in primary immune cells driven by IFNα

by Joan B. Mannick, Melody Morris, Hans-Ulrich P

Comparison of predicted and measured forces and moments.

Fig. 6 RUNX/CBFB interaction inhibitor, Ro5-3335, significantly decreases mouse neurofibroma growth in vivo. RUNX/CBFB interaction inhibitor, Ro5-3335,

Fig. 1 Caspase-8 and -9 are both activated during intrinsic and extrinsic apoptosis. Caspase-8 and -9 are both activated during intrinsic and extrinsic.

Fig. 5 Simultaneous absence of caspase-3 and -7 is required for significant decrease of caspase-8 and -9 activation in intrinsic apoptosis. Simultaneous.

AEGIS autonomous targeting process.

Fig. 1 A time-course RNA-seq analysis reveals prominent IRF8 expression in the spinal cord during the recovery phase after SCI. A time-course RNA-seq analysis.

Fig. 3 Local Maraba treatment of TNBC tumors provides long-term systemic protection. Local Maraba treatment of TNBC tumors provides long-term systemic.

Fig. 4. Paclitaxel promotes the expression of invasive isoforms of MENA in the primary breast cancer microenvironment. Paclitaxel promotes the expression.

Fig. 1 Concept of study and identification of DRL for cancer cell–based self-targeting therapies. Concept of study and identification of DRL for cancer.

Fig. 3 Prophylactic or therapeutic use of DECON protects from herpes infections in vitro. Prophylactic or therapeutic use of DECON protects from herpes.

Fig. 4 Effects of morphogen priming of engineered mesenchymal condensations on in vitro chondrogenic lineage specification at the time of implantation.

Fig. 1 Prophylactic, neutralization, and therapeutic efficacy of HPAC.

Fig. 2 Effect of CSF sTREM2– and CSF sTREM2–to–p-tau181 ratio on changes in cognition. Effect of CSF sTREM2– and CSF sTREM2–to–p-tau181 ratio on changes.

Fig. 5 Increased myometrial cell contractility in response to fetal T cells from preterm infants. Increased myometrial cell contractility in response to.

In vivo prophylactic and therapeutic efficacy of C12G6 in mice

UNC drives MYC protein loss.

IFN treatment of human midgestation villous explants induces syncytial knot formation. IFN treatment of human midgestation villous explants induces syncytial.

Human basophils are unresponsive to contact-dependent or contact-independent inhibition by Tregs. Human basophils are unresponsive to contact-dependent.

Fig. 7 Heart-specific OMA1 down-regulation protects from hypertrophy induced by TAC. Heart-specific OMA1 down-regulation protects from hypertrophy induced.

Fig. 2 Increasing KLF17, CDH1, and LASS2 expression reduced malignant progression and promoted apoptosis of tumor cells. Increasing KLF17, CDH1, and LASS2.

Fig. 7. JQ1 represses the enhancer-promoter interaction of BRCA1.

Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.

Fig. 7 Differences in the tumor microenvironment between transplant and transgenic BRAFV600E-driven melanoma models may underlie refractoriness of iBIP2.

Fig. 8 DMN-Tre detects Mtb in sputum samples from patients with tuberculosis, similar to the auramine stain. DMN-Tre detects Mtb in sputum samples from.

ATP analogs have little effect on the conformation of the 2CARD domain

Fig. 6 TNF-α neutralization prevents ZIKV-induced seizures in mice.

Fig. 4 Gallium increases P. aeruginosa sensitivity to peroxides.

Fig. 1 ETL kills 4T1 breast carcinoma cells more efficiently than ST under static conditions. ETL kills 4T1 breast carcinoma cells more efficiently than.

Fig. 6 Pharmacologic alterations of β-AR signaling regulate cardiomyocyte abscission and endowment. Pharmacologic alterations of β-AR signaling regulate.

Fig. 2. Cellular response to FolamiRs in vitro.

Neutralizing activity of mAbs isolated from plasmablasts during acute ZIKV infection in DENV-experienced donors. Neutralizing activity of mAbs isolated.

Presentation transcript:

Fig. 2 BX795 is nontoxic to HCE cells at therapeutic concentration. BX795 is nontoxic to HCE cells at therapeutic concentration. (A) Apoptosis analysis [Annexin V–FITC (fluorescein isothiocyanate) versus PI] by flow cytometry. HCE cells were incubated with mock, BX795 (10 μM), or TFT (50 μM) for 24 hours and assayed for apoptosis using the Dead Cell Apoptosis Kit. The numbers shown in each quadrant indicate the percentage of cells. The numbers in bold in the top-right and bottom-right quadrants indicate the percentage of early and late apoptotic cells, respectively. Representative plots from three replicates are shown. (B) Cell viability of infected and treated HCE cells assessed by MTT assay. The cells were infected with MOI 0.1 HSV-1(KOS) and, at 2 hpi, treated with mock or BX795 (10 μM). At 24 hpi, viability was assessed by MTT assay. The data (n = 9) are represented as percentage of nontreated, noninfected cells. Significance between the mock-treated and BX795-treated cells was determined by one-way ANOVA with Tukey’s multiple comparisons test. (C and D) Human MAPK phosphorylation array (C) and a heat map (D) depicting the intensity of the spots on the array from HCE cell lysates. The cells were infected with MOI 5 HSV-1(KOS), and at 2 hpi, fresh culture medium containing mock or BX795 (10 μM) treatments was added. At 4 hpi, the cells were collected and the lysates were assayed using the Human MAPK Phosphorylation Kit. Colored boxes indicate the spots on the array, which significantly differ between the mock-treated and BX795-treated cells. Duplicate spots for each sample are shown on the array. (E) Quantification of the kinases shown in (C) relative to the mock-treated cells. Colored bars indicate the kinases that are significantly different. Representative array from two replicates is shown. One-way ANOVA with Dunnett’s multiple comparisons test was performed to determine the significance. Dinesh Jaishankar et al., Sci Transl Med 2018;10:eaan5861 Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works