(A) ZR75-1 cells were treated with 1 μM 5-aza-2′-deoxycytidine (5-Aza) for 4 d. (A) ZR75-1 cells were treated with 1 μM 5-aza-2′-deoxycytidine (5-Aza)

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B Supplementary Fig S1. (A) ZR75- and MCF7-PELP1 knockdown cells were generated as described in methods section. Pooled colonies were analyzed for PELP1.

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Cell Physiol Biochem 2013;32: DOI: /

From: MicroRNA let-7 Regulates 3T3-L1 Adipogenesis

Rab11-FIP3 silencing impairs T cell activation events.

Rab11-FIP3 silencing upregulates TCR-CD3 cell surface expression in an Lck-dependent manner. Rab11-FIP3 silencing upregulates TCR-CD3 cell surface expression.

An siRNA screen identifies LIMT as an ERK‐dependent negative regulator of mammary cell migration An siRNA screen identifies LIMT as an ERK‐dependent negative.

Expression of α5β1-integrin enhances EboV GP-mediated infection of GD25 cells. Expression of α5β1-integrin enhances EboV GP-mediated infection of GD25.

NF1 silencing confers resistance of PC9 lung adenocarcinoma cells to erlotinib (erl). NF1 silencing confers resistance of PC9 lung adenocarcinoma cells.

PPARγ signaling correlates with LATS2 in human and mouse tumors and promotes cell death in a LATS2-dependent manner. PPARγ signaling correlates with LATS2.

BRD4 is associated with poor patient survival and constitutes a promising target for NRASMut melanoma BRD4 is associated with poor patient survival and.

A B 20% O2 5% O2 C 5% O2 + NAC DAPI gH2AX pLKO.1 GFP-SOD1 S 0.1Gy

Expression and regulation of MD-2s.

DNAPKcs is required for DNA repair in the presence of androgen.

LATS2 is a tumor suppressor in a mouse lumB breast cancer model.

(A) Schematic representation of the conditional Lats1 locus.

B7-H4 expression correlates with MHC-I expression and improved prognosis in patients with breast cancer. B7-H4 expression correlates with MHC-I expression.

Expression of SYCE2 activates the DSB repair pathway.

Deletion of Lats1 is phenotypically distinct from Lats2 deletion in PyMT tumors. Deletion of Lats1 is phenotypically distinct from Lats2 deletion in PyMT.

LATS2 promotes death of lumB cells.

A, left: indicated MEFs were transfected as described in the Methods section. A, left: indicated MEFs were transfected as described in the Methods section.

(A) Genotyping of the Lats2 and Cre alleles in the PyMT-derived cell lines (see primers location in Fig S2A). (A) Genotyping of the Lats2 and Cre alleles.

Knockdown of DAO inhibits DNA damage–induced senescence.

Fold Change of hsa-miR-3687 (T/N)(log2)

DNMT3A variants cause unique DNAm signatures.

Supplementary Fig. S1 BCL2 5’flanking ctrl siRNA luc

Down-regulation of LATS1 promotes the formation of tumors enriched in basal-like features. Down-regulation of LATS1 promotes the formation of tumors enriched.

BRD4 is associated with poor patient survival and constitutes a promising target for NRASMut melanoma BRD4 is associated with poor patient survival and.

UPF1 depletion specifically up-regulates components of the PERK/IRE1 ER stress response pathways. UPF1 depletion specifically up-regulates components of.

Hairpin & reporter systems.

LATS2-associated gene expression pattern is down-regulated specifically in lumB breast tumors. LATS2-associated gene expression pattern is down-regulated.

Selective abrogation of endogenous MHCII expression in LNSCs.

Metascape Tripathi et al 2015pathways enrichment analysis (Tripathi et al 2015, of differentially expressed genes (counts > 5, FC.

(A) Schematic representation of the conditional Lats2 locus.

No correlation between the distance of the duplicated alleles and the transcription levels on each of the alleles. No correlation between the distance.

(A) Distribution of LATS2 mRNA expression levels in different breast cancer subtypes (PAM50, METABTIC dataset); ***P-value < 0.001, t test comparing lumB.

SYCE2 potentiates the steady-state DNA repair activity without affecting the cell cycle checkpoint. SYCE2 potentiates the steady-state DNA repair activity.

De novo WASP expression restores the defective MK differentiation of WASP-KO cells. De novo WASP expression restores the defective MK differentiation of.

Fig. 3. Coilin levels correlate with altered nascent U2 snRNA, hTR and rRNA levels.RNA isolated from HeLa or WI-38 cells following RNAi targeting coilin.

Integrin binding of soluble GRGDSP and fibronectin.

CREB1 promotes the induction of endogenous ERα target genes.

Kinetics of GFP secretion from CHO cells.

DRAM, a p53-Induced Modulator of Autophagy, Is Critical for Apoptosis

(A) Relative expression levels of the top most down-regulated genes in LATS2L breast tumors (TCGA-BRCA dataset, see Fig 1) in the panel of breast cancer.

Ectopic expression of caveolin-1 in ZR75 human breast cancer cells downregulated survivin and decreased cell proliferation. Ectopic expression of caveolin-1.

Association of NM-HA and NM-GFP with SGs is transient.

LATS2 augments oxidative phosphorylation.

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

Fig. 6 Overexpression of constitutively activated S6K2 or S6K1 is capable of rescuing cell defects due to mEAK-7 knockdown. Overexpression of constitutively.

Fig. 4 HRI regulates BCL11A levels.

JAK inhibitors suppress IL-17–induced expression of IκB-ζ.

Fig. 4 Cdc42 enhances the cellular uptake of EVs.

Induction of CDCP1 is regulated by Ras in NSCLC cells.

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.

Bone marrow stroma partially protects multiple myeloma and AML cell lines from tipifarnib- and bortezomib-induced cell death. 8226/S myeloma cells were.

ARID1A promotes DSB end resection.

Fig. 2 Viperin promotes methionine oxidation of KSHV helicase.

RUNX3 depletion induces cellular senescence and inflammatory cytokine expression in cells undergoing TGFβ-mediated EMT. A, Cells were transfected with.

Anti-CD40 activates TAMs and recruits inflammatory monocytes.

AS1411 alters subcellular distribution of PRMT5 in a time-dependent, dose-dependent, and nucleolin-dependent manner. AS1411 alters subcellular distribution.

Fig. 4 Dcr-2 binds to the 3′UTR of Toll mRNA.

Volume 26, Issue 11, Pages e6 (March 2019)

LDL cholesterol inhibits Vγ9Vδ2 T-cell activation and cytokine production. LDL cholesterol inhibits Vγ9Vδ2 T-cell activation and cytokine production. Preexpanded.

PARP1 suppresses the transcription of PD-L1 in cancer cells.

Fig. 3 Effects of ASO and eGLP1-ASO conjugates on gene expression and protein levels in vitro in cell lines and primary mouse islet cells. Effects of ASO.

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

Curcumin decreases viability and proliferation of Bcr-Abl-expressing cells. Curcumin decreases viability and proliferation of Bcr-Abl-expressing cells.

BRCA1 sequence variants classified as pathogenic do not restore HR

IL-17 signaling upregulates ABIN-1 mRNA but downregulates protein.

Wnt5A and ROR2 contribute to intrinsic resistance to BRAF inhibitors.

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.

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(A) ZR75-1 cells were treated with 1 μM 5-aza-2′-deoxycytidine (5-Aza) for 4 d. (A) ZR75-1 cells were treated with 1 μM 5-aza-2′-deoxycytidine (5-Aza) for 4 d. PPARG and LPL mRNA levels were analyzed by RT-qPCR; mean ± SD of two technical replicates. (B) Scatter plot depicting PPARG and LATS1 mRNA expression levels in luminal tumors (TCGA BRCA dataset, n = 613). (C) ZR75-1 cells were transfected with either control vector (GFP only) or GFP-LATS2 expression plasmid and treated with 100 μM RGZ for 4 d. Cell death was measured as in Fig 3D. Values were normalized relative to nontreated cells transfected with vector only. (D) ZR75-1 cells were transfected with the indicated siRNA oligonucleotides and treated with 100 μM RGZ for 4 d. The percentage of dead cells was measured by PI exclusion followed by flow cytometry analysis, and values were normalized to nontreated siControl cells. Noa Furth et al. LSA 2018;1:e201800171 © 2018 Furth et al.