The cross-talk between PARylation and phosphorylation.

Slides:



Advertisements
Similar presentations
SCLCs and LCNECs are sensitive to PARP inhibition in vitro.
Advertisements

PGAM5 dephosphorylates ASK1.
MEL23 and MEL24 inhibit Mdm2 and p53 ubiquitination in cells.
Pirh2 promotes p73 ubiquitination in vivo.
SREBP-1 pathway is involved in MPST-regulated fat accumulation in hepatocytes. SREBP-1 pathway is involved in MPST-regulated fat accumulation in hepatocytes.
A FOXO3a-BIM cascade mediates sensitivity to PARP and MEK inhibition
Partial knockdown of MPST upregulates CSE by interacting with CSE
Expression and regulation of MD-2s.
HES1 is a novel interactor of the Fanconi anemia core complex
DNAPKcs is required for DNA repair in the presence of androgen.
UUKV NSs interacts with MAVS
A20 inhibits caspase-8 cleavage and TRAIL-induced apoptosis.
HRTV and SFTSV NSs, but not UUKV NSs, inhibits JAK/STAT IFN signaling.
Collagen-dependent phosphorylation of eIF4E in PDAC cells.
BRAF inhibitor-resistant BRAF-mutant melanoma cells show increased invasion and metastatic potential. BRAF inhibitor-resistant BRAF-mutant melanoma cells.
Role of HER2 in mediating acquired resistance to EGFR inhibition.
Mechanism of Smad1/5 activation by rapamycin.
Effect of expression of constitutively active CAMKK2 on AMPK activation and the cell cycle in G361 cells. Effect of expression of constitutively active.
A, analysis of cytoplasmic histone-associated DNA fragmentation in LNCaP cells following 24-h cotreatment with the indicated concentrations of SFN and.
Expression of the mutants of HP1α and the mutant of SYCE2 in MCF7 cells or RPE cells. Expression of the mutants of HP1α and the mutant of SYCE2 in MCF7.
HIPK2 decreases the stability of Notch1-IC through proteasome-dependent degradation. HIPK2 decreases the stability of Notch1-IC through proteasome-dependent.
JAK3A572V mutation causes constitutive JAK3 activity and IL-2–independent proliferation of NKTCL cells. JAK3A572V mutation causes constitutive JAK3 activity.
SYCE2 potentiates the steady-state ATM activity.
Wild-type NSD3 is required for the blockade of differentiation in BRD4–NUT-expressing NMC cells. Wild-type NSD3 is required for the blockade of differentiation.
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.
JAK inhibitors suppress IL-17–induced expression of IκB-ζ.
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.
co-IP of LEDGF/p75 and MeCP2.
TFAP2A is highly expressed in nasopharyngeal carcinoma cells and tumor tissues. TFAP2A is highly expressed in nasopharyngeal carcinoma cells and tumor.
Key functional sites of SPINDLIN1 could be phosphorylated by Aurora-A.
CDCP1 is required for invadopodia formation and ECM degradation by human breast cancer cells. CDCP1 is required for invadopodia formation and ECM degradation.
Induction of CDCP1 is regulated by Ras in NSCLC cells.
The SFKs confer BRAF inhibitor resistance in BRAF-mutant melanoma cells. The SFKs confer BRAF inhibitor resistance in BRAF-mutant melanoma cells. A, phospho-protein.
Mapping the Pirh2 and p73 interaction sites.
Activation of CHOP and DR5 by DIM-C-pPhtBu.
Phosphorylation of TET2 by JAK2 in response to hematopoietic cytokines
Selective delivery of pIC/PPHAffibody decreases the survival of HER2-overexpressing cells. Selective delivery of pIC/PPHAffibody decreases the survival.
Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. A.
Sensor siRNAs can be used in high-order combinations.
CXCR4 expression levels of MDA-MB-231 cells at 48 hours posttransfection of CXCR4 siRNAs. CXCR4 expression levels of MDA-MB-231 cells at 48 hours posttransfection.
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.
Discovery of Gö6976-related potent reversible EGFR T790M inhibitors.
Knockdown of PKM2 suppressed TPA-induced skin cell transformation.
N-3 PUFAs promote endometrial cancer cell apoptosis in vitro and in vivo. n-3 PUFAs promote endometrial cancer cell apoptosis in vitro and in vivo. HEC-1-A.
KPT-9274 shows specificity for attenuation of PAK4 targets preferentially in RCC cells. KPT-9274 shows specificity for attenuation of PAK4 targets preferentially.
Role of MAPKs on DPP-23-induced autophagy and apoptosis.
CDCP1 links Ras and SFK signaling and regulates anoikis resistance, cell migration, and invasion in NSCLC cells. CDCP1 links Ras and SFK signaling and.
CLIC1 supports invadopodia formation in vitro and metastasis in vivo.
Pirh2 represses p73-dependent transactivation.
Cellular localization of Panx1 and altered membrane morphology in stable Panx1-transfected C6 glioma cells. Cellular localization of Panx1 and altered.
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.
Activation of multiple RTKs in chondrosarcoma cells.
The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. The combination of trastuzumab and SU11274 abrogate Akt phosphorylation. Serum-starved.
Signal Transducer and Activator of Transcription 3 as Molecular Therapy for Non–Small- Cell Lung Cancer  Cheng-Yi Wang, MD, Ting-Ting Chao, PhD, Wei-Tien.
AS1411 alters subcellular distribution of PRMT5 in a time-dependent, dose-dependent, and nucleolin-dependent manner. AS1411 alters subcellular distribution.
BCR/ABL expression, tyrosine phosphorylation, and signaling in dasatinib- and imatinib-resistant cell lines and the ubiquitin inhibitor lactacystin modifies.
Differential effects of the RAF inhibitor PLX4032 in BRAF-mutant melanoma, thyroid, and colorectal cancer cell lines. Differential effects of the RAF inhibitor.
Fig. 6 The C9ORF72/SMCR8 complex regulates ULK1.
The interaction of PALB2 with BRCA1 is required for the assembly of PALB2, BRCA2, and RAD51 nuclear foci. The interaction of PALB2 with BRCA1 is required.
Interaction of NHEJ and HR pathways in PCO cultures.
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
Posttranslational phosphorylation of p53 by platinum drugs in ovarian tumor cells. Posttranslational phosphorylation of p53 by platinum drugs in ovarian.
PARP1 suppresses the transcription of PD-L1 in cancer cells.
Elevated STAT3 phosphorylation and RANTES levels in tamoxifen-treated breast cancer cells. Elevated STAT3 phosphorylation and RANTES levels in tamoxifen-treated.
Effect of 6-SHO on mouse prostate cancer HMVP2 cells.
The inverse correlation between PARP1 and PD-L1, PAR, and p-STAT3 expression in surgical specimens of ovarian cancer. The inverse correlation between PARP1.
D-GM3 promotes uPAR clustering on the cell surface and activates p38 MAPK. A, uPAR expression in cells was either knocked down by treatment with 4 independent.
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.
Presentation transcript:

The cross-talk between PARylation and phosphorylation. The cross-talk between PARylation and phosphorylation. A, 3 × 105 SKOV3 and OVCAR8 cells were treated with PARP1 siRNA (siPARP1) for 24 hours, and the phosphorylation of STAT3 was analyzed by Western blot. B, OVCAR8 cells were treated with various PARP inhibitors for 24 hours, and the phosphorylation of STAT3 was analyzed by Western blot. C, The analysis of STAT3 distribution by confocal microscopy. SKOV3 cells were stained with anti-STAT3 and DAPI. Scale bar, 25 μm. D, PARP1 siRNA-treated OVCAR8 cells were transfected with siRNA-resistant wild Flag-PARP1 or mutant Flag-PARP1 (H862 or E988), and the phosphorylation of STAT3 was assessed by Western blot. E, SKOV3 and OVCAR8 cells were treated with siPARP1 for 24 hours, and the phosphorylation of JAK2 was analyzed by Western blot. F, OVCAR8 cells were first transfected with Flag-PARP1 for 24 hours, and then 500 μmol/L vanadate was added for 25 minutes, and the phosphorylation of STAT3 was analyzed by Western blot, GA: GAPDH. G, HEK 293T cells were transfected with Flag-PARP1, together with HA-STAT3, a constitutively active STAT3 (HA-STAT3C), or the activation mutant HA-STAT3Y705F. The cells were subjected to immunoprecipitation with anti-HA, followed by Western blot to detect poly(ADP-ribosyl)ated STAT3. IB, immunoblotting. H, HEK 293T cells were transfected with Flag-PARP1 and HA-STAT3 followed by treatment with 5 μmol/L AZD1480 (JAK2 inhibitor) for 12 hours. Western blot was used to detect poly(ADP-ribosyl)ated STAT3. NC: siRNA-negative control; CON, DMSO treated. Ling Ding et al. Cancer Immunol Res 2019;7:136-149 ©2019 by American Association for Cancer Research