Posttranslational phosphorylation of p53 by platinum drugs in ovarian tumor cells. Posttranslational phosphorylation of p53 by platinum drugs in ovarian.

Slides:



Advertisements
Similar presentations
Neal et al.Supplementary Figure S1
Advertisements

DNA damage induces complex signal activation dynamics across many signaling pathways. DNA damage induces complex signal activation dynamics across many.
MEL23 and MEL24 inhibit Mdm2 and p53 ubiquitination in cells.
Pirh2 promotes p73 ubiquitination in vivo.
Knock-down of endogenous PINK1 abrogates Parkin Ser65 phosphorylation.
Proline supplementation during P5CS protein knockdown suppressed GCN2 activation. Proline supplementation during P5CS protein knockdown suppressed GCN2.
Pioglitazone inhibits aromatase expression in human preadipocytes.
Inhibition of FGFR signaling and tumor growth in SNU-16 xenograft model by administration of E7090. Inhibition of FGFR signaling and tumor growth in SNU-16.
Downregulation of SPRY4 expression is associated with FGFR1–FRS2 activation. Downregulation of SPRY4 expression is associated with FGFR1–FRS2 activation.
Collagen-dependent phosphorylation of eIF4E in PDAC cells.
Role of HER2 in mediating acquired resistance to EGFR inhibition.
Leto et al., Supplementary Figure S3
ONC201 activates the ATF4 pathway through the eIF2α kinases HRI and PKR. ONC201 activates the ATF4 pathway through the eIF2α kinases HRI and PKR. (A) Western.
HIPK2 decreases the stability of Notch1-IC through proteasome-dependent degradation. HIPK2 decreases the stability of Notch1-IC through proteasome-dependent.
Knocking down Wnt3 increases the cells' response to trastuzumab and reduces cells' invasiveness. Knocking down Wnt3 increases the cells' response to trastuzumab.
Oral administration of CX-4945 suppresses Tau phosphorylation in DYRK1A-overexpressing mice. Oral administration of CX-4945 suppresses Tau phosphorylation.
JAK3A572V mutation causes constitutive JAK3 activity and IL-2–independent proliferation of NKTCL cells. JAK3A572V mutation causes constitutive JAK3 activity.
Time-dependent effects of IL-6 on tyrosine phosphorylation of IRS-1.
SYCE2 potentiates the steady-state ATM activity.
The p53 pathway is involved in the inhibition of cell proliferation observed in 15-LOX-1-overexpressing cells. The p53 pathway is involved in the inhibition.
CO-1686 does not inhibit WT EGFR signaling in vivo and is active in EGFR-mutant transgenic mouse lung cancer models. CO-1686 does not inhibit WT EGFR signaling.
BEZ235 induces MAPK signaling in a FOXO3A-dependent manner.
eNOS regulated IR-induced NO generation and EGFR signal activation.
Curcumin-generated ROS activates Chk1 and Chk2 kinases.
The sesquiterpene lactone PN up-regulates MDM2 and p53 proteins.
MEL23 and MEL24 inhibit Mdm2 and p53 ubiquitination through the Mdm2-MdmX hetero-complex. MEL23 and MEL24 inhibit Mdm2 and p53 ubiquitination through the.
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.
FOXO3a phosphorylation and expression.
CDCP1 is required for invadopodia formation and ECM degradation by human breast cancer cells. CDCP1 is required for invadopodia formation and ECM degradation.
PTENP1 sensitizes renal cancer cells to chemotherapy.
The role of p53 in H2O2-mediated cell death of hOGG1-deficient H1299 lung carcinoma p53 null cells. The role of p53 in H2O2-mediated cell death of hOGG1-deficient.
Identification of NSC as a FADD-kinase inhibitor.
BME treatment increases granzyme B expression in NK 3.3 cells.
DNA damage signaling regulates mutant p53 ubiquitination.
Mcl-1 knockdown promotes cleavage of caspase-3 in nonadherent melanoma cells. Mcl-1 knockdown promotes cleavage of caspase-3 in nonadherent melanoma cells.
Expression of versican in mammary tumor stem/progenitor cells.
Inhibition of stress-associated MAPK signaling attenuates SASP expression in CAFs. A, N-CAFs were treated with 100 nmol/L GEM plus DMSO or the above-listed.
Effects of visfatin on the cell proliferation and phosphorylation of ERK, Akt, and GSK-3β proteins in HCC cells. Effects of visfatin on the cell proliferation.
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.
TFAP2A knockdown inhibits cell growth by targeting HIF-1α signaling.
Effect of IL24 on phosphorylation of eIF2α and proliferation in cancer cells. Effect of IL24 on phosphorylation of eIF2α and proliferation in cancer cells.
IGF-IR in human head and neck cancer.
KPT-9274 shows specificity for attenuation of PAK4 targets preferentially in RCC cells. KPT-9274 shows specificity for attenuation of PAK4 targets preferentially.
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.
Changes in signal transduction pathway induced by gefitinib.
Characterization of DNA-PK and PARP-1 levels and activities in the cell lines studied. Characterization of DNA-PK and PARP-1 levels and activities in the.
Met is expressed in Her2-overexpressing cell lines and Her2 (+) breast tumors. Met is expressed in Her2-overexpressing cell lines and Her2 (+) breast tumors.
FGFR1 is dominantly expressed in mesenchymal-like KRAS-mutant lung cancer cell lines. FGFR1 is dominantly expressed in mesenchymal-like KRAS-mutant lung.
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.
The effects of AZD1775 and olaparib on DNA damage response signaling.
Induction of PARP cleavage (A) and activation of caspases (B) after treatment with a combination of TRAIL and cisplatin. Induction of PARP cleavage (A)
P53 restoration in a syngeneic transplant model of Mdm2Tg p53Neo/Neo CreER angiosarcoma. p53 restoration in a syngeneic transplant model of Mdm2Tg p53Neo/Neo.
Double knockdown of HER2/EGFR abolishes HPSE nucleolar localization in 231BR3 cells. Double knockdown of HER2/EGFR abolishes HPSE nucleolar localization.
Effect of MIF siRNA on the production of MMP-13 induced by LPA
PARP1 suppresses the transcription of PD-L1 in cancer cells.
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.
Association of TCTP with Pim-3 in human pancreatic cancer cell lines.
Elevated STAT3 phosphorylation and RANTES levels in tamoxifen-treated breast cancer cells. Elevated STAT3 phosphorylation and RANTES levels in tamoxifen-treated.
Ceritinib is a potent ALK inhibitor in crizotinib-naïve models.
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.
Knockdown of NR4A1 induces endoplasmic reticulum stress–mediated apoptosis by increasing ROS production in pancreatic cancer cells. Knockdown of NR4A1.
I3C reduces the level of Cdc25A protein in breast 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.
Time course of NMT knockdown.
Presentation transcript:

Posttranslational phosphorylation of p53 by platinum drugs in ovarian tumor cells. Posttranslational phosphorylation of p53 by platinum drugs in ovarian tumor cells. A2780, 2780CP/Cl-16, and 2780CP/Cl-24 cells were treated with increasing concentrations of cisplatin, DAP, or oxaliplatin for 24 hours, and lysates were then prepared for Western blot analysis using the Ser20 phospho-specific antibody for direct comparison of effects of the three drugs in each cell line (A). The lysates from cells similarly treated with cisplatin (B), DAP (C), or oxaliplatin (D) were analyzed using the indicated antibodies to compare the effects of each drug in the three cell lines. The Ser15 and Ser20 signals in the immunoblots were quantified by densitometry and the ratios of Ser15:total p53 and Ser20:total p53 determined and plotted against concentration using linear regression analysis. In an independent study, 2780CP/Cl-24 cells transfected with control- or MDM4-siRNA were then treated with cisplatin, DAP, or oxaliplatin for 24 hours. Cells were then harvested and subjected to Western blot using the indicated antibodies (E). In some cases, “short” and “long” exposures were used to visualize the proteins. Xiaolei Xie et al. Mol Cancer Res 2017;15:328-339 ©2017 by American Association for Cancer Research