Dual apoptotic signaling pathways triggered by IMMU-140: Anti–HLA-DR- and SN-38–mediated signals. Dual apoptotic signaling pathways triggered by IMMU-140:

Slides:



Advertisements
Similar presentations
Supplemental Figure S2. Location and H 2 O 2 -dependent binding of RBPs to biotinylated MKP-1 transcripts. (A) Schematic of the MKP-1 mRNA showing the.
Advertisements

DNA damage induces complex signal activation dynamics across many signaling pathways. DNA damage induces complex signal activation dynamics across many.
by Rong Chen, Michael J. Keating, Varsha Gandhi, and William Plunkett
A FOXO3a-BIM cascade mediates sensitivity to PARP and MEK inhibition
Figure S1 Nil + CK Nil CK C BIM BCLXL Pro-caspase 3 Cleaved caspase 3
Proline supplementation during P5CS protein knockdown suppressed GCN2 activation. Proline supplementation during P5CS protein knockdown suppressed GCN2.
Stimulation of the B-cell receptor activates the JAK2/STAT3 signaling pathway in chronic lymphocytic leukemia cells by Uri Rozovski, Ji Yuan Wu, David.
Volume 23, Issue 1, Pages (July 2006)
NF1 downregulation activates MAPK pathway signaling.
NM-3 induces p21 levels and down-regulation of Cdk2 activity.
Validation of proteins identified by mass spectrometry.
AMPK induces VEGF-A production by upregulating ERK signaling.
Protein expression profiling of small cell lung carcinoma treated with valproic acid (VPA) and VAC (mafosfamide, doxorubicin and vindesine). Protein expression.
GF103209X attenuates PKC, MEK and ERK 1/2 phosphorylation in laminarin-challenged haemocytes. GF103209X attenuates PKC, MEK and ERK 1/2 phosphorylation.
ATM function in repair of double-stranded DNA breaks.
PARP cleavage is detected in TA cells, but not in KSC
Fig. 6. Effect of SAHA and ML on histone acetylation, BAX, and p21CDKN1A expression.PANC-1 and BxPC-3 cells were incubated for 48 hours with 5 µM.
JAK3A572V mutation causes constitutive JAK3 activity and IL-2–independent proliferation of NKTCL cells. JAK3A572V mutation causes constitutive JAK3 activity.
TNFα is an important survival and growth signal for melanoma.
pERK ERK pSTAT1 STAT1 pSTAT3 STAT3 pAKT AKT
Tyrosine phosphorylation of proteins in podocyte lysates following exposure to healthy or lupus nephritis plasma. Tyrosine phosphorylation of proteins.
Aβ-mediated Ras-MAPK signaling and Cyclin D1 expression in B103 cells are dependent on APP expression and can be reversed with MEK or Ras inhibition. Aβ-mediated.
Effect of M-cadherin RNAi on apoptosis in confluent C2C12 myoblasts.
The sesquiterpene lactone PN up-regulates MDM2 and p53 proteins.
The effects of the FASN blocker C75 on cell growth and survival (A, E, and F), on expression/phosphorylation of PI3K and MAPK signaling proteins and on.
Quantification of NMT knockdown.
A, IGFBP-3 knockdown via siRNA using real-time qRT-PCR analysis.
Variation in dUTPase expression in cell lines.
FOXO3a phosphorylation and expression.
Synergistic effect of CNP and doxorubicin (DOX) on thiol oxidation.
Silencing hOGG1 triggers caspase-3 and caspase-7 activation in response to H2O2 in GM00637 cells. Silencing hOGG1 triggers caspase-3 and caspase-7 activation.
Identification of NSC as a FADD-kinase inhibitor.
Effect of LY on phosphorylation of various MAP kinase substrates in HeLa cells in vitro. Effect of LY on phosphorylation of various MAP kinase.
AG1024 reduced the level of tyrosyl-phosphorylated proteins, including Erk2. AG1024 reduced the level of tyrosyl-phosphorylated proteins, including Erk2.
Imatinib mesylate inhibits PDGF-mediated ERK and Akt activation.
Mcl-1 knockdown promotes cleavage of caspase-3 in nonadherent melanoma cells. Mcl-1 knockdown promotes cleavage of caspase-3 in nonadherent melanoma cells.
Effect of other nucleoside analogues on p38 MAPK phosphorylation levels. Effect of other nucleoside analogues on p38 MAPK phosphorylation levels. A, MM.1S.
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.
MiR-200c is a PI3K–AKT signaling pathway regulator in CRC
TDP1 and TOP1 protein levels correlate positively with TDP1 and TOP1 mRNA levels in colorectal cancer cell lines. TDP1 and TOP1 protein levels correlate.
Curcumin suppresses the expression of antiapoptotic proteins in multiple myeloma cells. Curcumin suppresses the expression of antiapoptotic proteins in.
A. A. Honokiol inhibits TNF-induced NF-κB activation, IκBα phosphorylation, and IκBα degradation. Honokiol inhibits TNF-induced activation of NF-κB. H1299.
Effect of SFN on the protein expression of Nrf2, HO-1, and NQO1 in JB6-shMock and JB6-shNrf2 cells. Effect of SFN on the protein expression of Nrf2, HO-1,
Src expression in a panel of human TCC cell lines.
FACS analyses of the inhibitory effect induced by mixed docetaxel, gefitinib, and cyclopamine on EGF plus SHHNp–stimulated PC3 cells. FACS analyses of.
Effect of coapplication of dexrazoxane and doxorubicin on DSB formation, TOP2A protein level, and apoptosis. Effect of coapplication of dexrazoxane and.
Staurosporine induces changes in MMP
DNA demethylation reactivates GSN expression in gastric cancer cells.
Induction of DNA strand breaks by artesunate.
PKCζ is tyrosine phosphorylated by EGF and contributes to EGF-induced activation of ERK in Mef cells. PKCζ is tyrosine phosphorylated by EGF and contributes.
Localization of oxidated thiols in A375 melanoma cells.
Effects of EGCG on the anchorage-independent growth of EFT cells.
PTPH1 depends on its catalytic activity to increase ER nuclear accumulation and to enhance breast cancer sensitivity to TAM. A, effects of PTPH1 and PTPH1/DA.
A, expression of p53 downstream mediator p21.
Changes in signal transduction pathway induced by gefitinib.
WP1066 induces caspase-dependent apoptosis.
The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. Serum-starved.
Effects of UVB on AKT in SKH-1 mouse epidermis.
AS1411 alters subcellular distribution of PRMT5 in a time-dependent, dose-dependent, and nucleolin-dependent manner. AS1411 alters subcellular distribution.
SAHA blocks IR-induced increase of RAD51 protein in MM cells.
Effect of bevacizumab on the proliferation of A2780 cells.
Induction of PARP cleavage (A) and activation of caspases (B) after treatment with a combination of TRAIL and cisplatin. Induction of PARP cleavage (A)
Posttranslational phosphorylation of p53 by platinum drugs in ovarian tumor cells. Posttranslational phosphorylation of p53 by platinum drugs in ovarian.
RA-9 induces G2–M cell-cycle arrest and caspase-mediated apoptosis in ovarian cancer cells. RA-9 induces G2–M cell-cycle arrest and caspase-mediated apoptosis.
AR promotes DNA double-strand break resolution.
FGF19 amplification in liver cancer cell lines is associated with response to NVP-BGJ398. FGF19 amplification in liver cancer cell lines is associated.
Effect of SFN on the total activity and protein expression of HDACs in JB6 P+ cells. Effect of SFN on the total activity and protein expression of HDACs.
Effects of NMT siRNAs on MARCKS and c-Src.
Identification and characterization of activated integrin pathway module by signal transduction representation (A) and unsupervised hierarchical clustering.
Time course of NMT knockdown.
Presentation transcript:

Dual apoptotic signaling pathways triggered by IMMU-140: Anti–HLA-DR- and SN-38–mediated signals. Dual apoptotic signaling pathways triggered by IMMU-140: Anti–HLA-DR- and SN-38–mediated signals. Cells were plated and IMMU-114 and IMMU-140 were added as described in Materials and Methods and Supplementary Data. Both IMMU-114 and IMMU-140 were added at equal 10 nmol/L protein doses for the indicated times before cells were harvested for Western blot analysis. All incubation times shown in blue indicate IMMU-114 and those in red indicate IMMU-140. A, JVM-3 (CLL), MN-60 (ALL), GDM-1 (AML), MOLM-14 (AML), and A-375 (melanoma) cell lines analyzed for full-length PARP (PARP FL), cleaved PARP fragment (Cleaved), and phosphorylated ERK1/2 (p-ERK1/2) levels. Total ERK1/2 and β-actin served as protein loading controls. B, Levels of dsDNA breaks were determined by release of phosphorylated histone H2A.X (p-H2A.X). Assessment of changes in dsDNA breaks was calculated as ratios relative to untreated control, normalized to β-actin protein loading control (Δp-H2A.X). Thomas M. Cardillo et al. Mol Cancer Ther 2018;17:150-160 ©2018 by American Association for Cancer Research