Effects of fAS stimulation on cathepsin-B activity, mitochondrial quality and microglial cell survival after autophagy inhibition. Effects of fAS stimulation.

Slides:



Advertisements
Similar presentations
Incomplete Treatment Complete Treatment Control Flow Cytometric Cell Cycple Analysis of Propidium Iodide-Stained HPAC Cells ControlComplete TreatmentIncomplete.
Advertisements

Cell Physiol Biochem 2014;33: DOI: /
Sec1p requires Boi1/2p for proper localization.
C. Pina-Vaz, F. Sansonetty, A. G. Rodrigues, S. Costa-Oliveira, C
Curcumin (diferuloylmethane) down-regulates the constitutive activation of nuclear factor–κB and IκBα kinase in human multiple myeloma cells, leading to.
A novel TNFR1-triggered apoptosis pathway mediated by class IA PI3Ks in neutrophils by Barbara Geering, Ursina Gurzeler, Elena Federzoni, Thomas Kaufmann,
Differential effects of tumor necrosis factor-α and interleukin-1β on cell death in human articular chondrocytes  B. Caramés, Ph.D., M.J. López-Armada,
by Kumudha Balakrishnan, William G. Wierda, Michael J
Histone Deacetylase Inhibitors Sensitize Human Non-small Cell Lung Cancer Cells to Ionizing Radiation Through Acetyl p53-Mediated c-myc Down-Regulation 
Volume 70, Issue 6, Pages (September 2006)
A FOXO3a-BIM cascade mediates sensitivity to PARP and MEK inhibition
Hepatoprotective properties of kombucha tea against TBHP-induced oxidative stress via suppression of mitochondria dependent apoptosis  Semantee Bhattacharya,
Supplemental Figure 1 Li Fraumeni (087) 5C tankyrase1 actin Mock
Synergistic effect of S63845 with lapatinib, trastuzumab, or docetaxel
Valentina Manfé, Edyta Biskup, Peter Johansen, Maria R
SUPPLEMENTAL TABLE 1. Cell cycle profiles of HeLa cells treated
Both CREB1 and ERα suppress the STS-induced loss of mitochondrial membrane potential. Both CREB1 and ERα suppress the STS-induced loss of mitochondrial.
Volume 22, Issue 3, Pages (March 2015)
FcɛRI cross-linking and IL-3 protect human basophils from intrinsic apoptotic stress  Lionel Rohner, MSc, Ramona Reinhart, PhD, Björn Hagmann, PhD, Andrea.
FLC treatment results in an increase in ploidy in a significant fraction of cells. FLC treatment results in an increase in ploidy in a significant fraction.
STING stimulation in T cells inhibits cell cycle progression.
Palbociclib increases proteasome activity and the clearance of protein aggregates without significant effects on autophagy Palbociclib increases proteasome.
Fig. 1 LB100 and LB102 specifically inhibit PP2A phosphatase activity and the growth of BCR-ABL+ cells. LB100 and LB102 specifically inhibit PP2A phosphatase.
Alpha-synuclein induces autophagy in microglial cells.
Evaluation of LC3 and ATG13 dynamics in AS-stimulated microglial cells using live-imaging. Evaluation of LC3 and ATG13 dynamics in AS-stimulated microglial.
Inducible DM1 model displays increased autophagy.
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. Proportion of motile objects and track length
Mitochondrial membrane potential is lost during apoptin treatment, and anti-apoptotic Bcl-2 family members block apoptin-induced death. Mitochondrial membrane.
Blockage of peroxisomal FAO induces differentiation on activated satellite cells. Blockage of peroxisomal FAO induces differentiation on activated satellite.
De novo WASP expression restores the defective MK differentiation of WASP-KO cells. De novo WASP expression restores the defective MK differentiation of.
IFN-γ and TNF-α cause an upregulation of Fas expression in human ESCs
Caspase 8 is expressed in human ESCs but is not regulated by IFN-γ, TNF-α or hCG. Caspase 8 is expressed in human ESCs but is not regulated by IFN-γ, TNF-α.
Fig. 3. Effect of substrate orientation on growth rate for bottom-dwelling tadpoles with similar oral configuration. Effect of substrate orientation on.
BMP signalling is dispensable for early gastruloid patterning.
Fig. 5. Combination of SAHA and ML produces augmented suppression of cellular proliferation with impaired cell cycle progression, enhanced apoptotic.
An inhibitor of HSP90β reduces the level of HNF4A protein in hepatic progenitor cells. An inhibitor of HSP90β reduces the level of HNF4A protein in hepatic.
Averages from seven separate experiments of primary myoblast cultures grown in HS-2; HS-2+GAL-M; HS-2+COS-1; FCS-20; FCS-20+GAL-M; or FCS-20+COS-1. Averages.
FAK/Src activity is required to trap PTP1BDA in adhesions.
ArfGAP1 expression alters GBF1 recruitment to Golgi membranes.
Effect of the plastid translation inhibitor Spec on LR development
Fig. 1. Phenotypic characterisation of primary human tubular epithelial cells and human renal fibroblasts. Phenotypic characterisation of primary human.
Transbilayer distribution of cholesterol in the plasma membrane is defective in staurosporine-treated cells. Transbilayer distribution of cholesterol in.
Fig. 4. Perinuclear dynein regulators are not required for primary ciliogenesis.RPE cells were transfected with siRNA and either nocodazole-treated, fixed,
Volume 3, Issue 5, Pages (May 2001)
Effect of γ-secretase inhibition on the vulnerability of primary neurons to OGD. (A) Experimental design. Effect of γ-secretase inhibition on the vulnerability.
Fig. 3. Effects of Tec on IL-1β-induced apoptosis in chondrocytes.
Ibm1 and edm2 mutants generate more stomatal divisions in the leaf epidermis. ibm1 and edm2 mutants generate more stomatal divisions in the leaf epidermis.
Graf-dependent GEEC endocytosis is required for EGFR internalization and degradation at high Spi. Graf-dependent GEEC endocytosis is required for EGFR.
Regulation of lipid droplet formation by PI3-kinase activity.
WASP deficiency produces aberrant F-actin distribution, increased adhesion and downregulation of CD43 during megakaryocytic differentiation. WASP deficiency.
Mark J Hickman, Leona D Samson  Molecular Cell 
Fig. 2. Acetylation stiffens primary cilia.
The influence of SHIP2 on cell migration in breast cancer cells.
MK-8628 augments T lymphocyte apoptosis.
The regulatory domain of HSF1 is involved in the pro-apoptotic response to TNF. (A) Upper panel, functional domains and potential DAPK phosphorylation.
Figure 1. Effects of Gal-4 on apoptosis and proliferation of monocytes
Expression of IP3R subtypes in HEK cells.
Aplf downregulation does not induce cellular arrest.
Distinct mitochondrial membrane potential, ATP-to-ADP ratio and NAD(P)H responses to glucose and methylsuccinate. Distinct mitochondrial membrane potential,
TRIM17 and Beclin 1 colocalize with the anti-autophagy factor Mcl-1.
A, ATP production by PC3 prostate cancer cells after treatment with oligonucleotide/Lipofectin complexes. a, ATP production by PC3 prostate cancer cells.
Fig. 6 Caspase-3– and -7–deficient cells maintain mitochondrial membrane polarity following intrinsic or extrinsic apoptotic stimuli. Caspase-3– and -7–deficient.
Mcl-1 knockdown promotes cleavage of caspase-3 in nonadherent melanoma cells. Mcl-1 knockdown promotes cleavage of caspase-3 in nonadherent melanoma cells.
The Akt/Mcl-1 pathway plays a prominent role in mediating antiapoptotic signals downstream of the B-cell receptor in chronic lymphocytic leukemia B cells.
Fig. 3 Regulation of CD73 and CD39 cell membrane expression and extracellular adenosine levels by ERs in osteoclasts. Regulation of CD73 and CD39 cell.
Tipifarnib combined with bortezomib induces cell death in diverse multiple myeloma and AML cell lines. Tipifarnib combined with bortezomib induces cell.
IGF-I partially protects Rh30 cells from apoptosis despite simultaneous inhibition of PI3K-Akt and MAP kinase pathways. IGF-I partially protects Rh30 cells.
Fig. 2 BX795 is nontoxic to HCE cells at therapeutic concentration.
WEE1 inhibition followed by TRAIL treatment results in apoptotic cell death in MB231 cells. WEE1 inhibition followed by TRAIL treatment results in apoptotic.
Presentation transcript:

Effects of fAS stimulation on cathepsin-B activity, mitochondrial quality and microglial cell survival after autophagy inhibition. Effects of fAS stimulation on cathepsin-B activity, mitochondrial quality and microglial cell survival after autophagy inhibition. (A,B) BV2 (A) or primary (B) microglial cells were left untreated or treated with spautin-1 (10 µM) for 24 h or FIP200 siRNA for 48 h. Cells were then stimulated with fAS (5 μM) for 24 h and cell death was evaluated using propidium iodide (PI) combined with Annexin V–FITC staining and subsequent flow cytometric analysis. Mean±s.e.m. percentages of Annexin V–FITC/IP double-positive dead cells are shown. (C) BV2 microglial cells were treated and stimulated as described in A and BCL-2, BCL-xL and cleaved caspase-3 protein levels were evaluated using flow cytometry. Graphs show representative histograms for each protein. (D,E) BV2 microglial cells were left untreated or treated with spautin-1 (SP-1, 10 µM) for 24 h or FIP200 siRNA for 48 h and stimulated with fAS (5 μM) for 24 h. Untreated (control) and scramble (scr) siRNA as controls also shown. Cathepsin-B activity (D) and mitochondrial mass and membrane potential (E) were measured as described in Fig. 5H and I, respectively. (F–H) BV2 cells were treated with the autophagy inhibitors spautin-1 (SP-1, 10 µM) for 24 h or FIP200 siRNA for 48 h (si) and stimulated with fAS (5 μM) at the indicated time points. (F) GAL-3 immunostaining. (G,H) Mean±s.e.m. quantification of GAL-3 puncta (G) and LysoTracker Red DND-99 staining (H). LysoTracker staining was evaluated using flow cytometry and results are relative to the mean fluorescence intensity (Gmean) of the control condition. Results were analysed by one-way ANOVA followed by post-hoc Dunnet's test; n=3. *P<0.05, **P<0.01, ***P<0.001; #P<0.05, ##P<0.01 when comparing fAS with fAS plus SP-1 or FIP200 siRNA treatment. Claudio Bussi et al. J Cell Sci 2018;131:jcs226241 © 2018. Published by The Company of Biologists Ltd