Fig. 6 PPAR-γ is a direct target of Suv420h.

Slides:

Advertisements

Similar presentations

Fig. 5 Correlation of RNA expression and protein abundance.

Advertisements

Fig. 4 The extracellular domain of sortilin is sufficient for BDNF/TrkB signaling. The extracellular domain of sortilin is sufficient for BDNF/TrkB signaling.

Fig. 1 KCC2 down-regulation is prevented in sortilin-deficient mice.

Fig. 1 TET2 is a coactivator of ERα.

Fig. 2 Global production, use, and fate of polymer resins, synthetic fibers, and additives (1950 to 2015; in million metric tons). Global production, use,

Fig. 3 Oil, gas, and FP water variations with time.

Fig. 5 Thermal conductivity of n-type ZrCoBi-based half-Heuslers.

Fig. 1 Characterization of Suv420h dKO mice.

Fig. 1 Map of water stress and shale plays.

Fig. 4 p100/TSN enables E2F1 to interact with alternatively spliced transcripts. p100/TSN enables E2F1 to interact with alternatively spliced transcripts.

Biological consequence of SENP7 alternative splicing for E2F1 activity

Fig. 1 Examples of experimental stimuli and behavioral performance.

Fig. 1 meR marks on E2F1 confer genome-wide effects.

Fig. 6 Comparison of properties of water models.

Single-base validation using ligation-amplification method and qPCR

Adipose tissue dysfunction induces increased liver HIF-1α expression

Fig. 2 Reference-fixing experiment, results.

Distinct enhancer binding of CEBPA in WT GMPs versus p30 L-GMPs

Fig. 4 CEBPA-p30 mediated activation of Nt5e expression.

Fig. 1 Experimental apparatus used to train and test free-flying bees on their capacity to learn addition and subtraction. Experimental apparatus used.

Motif enrichment analysis of p42, common, and p30 CEBPA-bound regions

Fig. 3 Rotation experiment, setup.

Fig. 1 Product lifetime distributions for the eight industrial use sectors plotted as log-normal probability distribution functions (PDF). Product lifetime.

Fig. 5 Transcriptional changes in dKO mice after HFD regimen.

Fig. 5 EGLN2-mediated HIF1A down-regulation promotes ferroptosis.

Fig. 5 Conceptual diagram of the impact of acid deposition on calcium cycling and subsequent plant water use. Conceptual diagram of the impact of acid.

Fig. 1 Distribution of total and fake news shares.

Fig. 6 RUNX/CBFB interaction inhibitor, Ro5-3335, significantly decreases mouse neurofibroma growth in vivo. RUNX/CBFB interaction inhibitor, Ro5-3335,

Fig. 2 Expressions of cll, abd-A, and Abd-B by qRT-PCR.

Fig. 2 2D QWs of different propagation lengths.

Fig. 4 Cdc42 enhances the cellular uptake of EVs.

Fig. 4 DFT ωB97x/def2-TZVPP atomic charges on the sulfur atom of substituted thioaldehyde and AIMNet prediction with a different number of iterative passes.

Fig. 5 Simultaneous absence of caspase-3 and -7 is required for significant decrease of caspase-8 and -9 activation in intrinsic apoptosis. Simultaneous.

Fig. 4 Activation of mitochondrial apoptosis pathway by n-HA.

Fig. 1 A time-course RNA-seq analysis reveals prominent IRF8 expression in the spinal cord during the recovery phase after SCI. A time-course RNA-seq analysis.

Fig. 5 Schematic phase diagrams of Ising spin systems and Mott transition systems. Schematic phase diagrams of Ising spin systems and Mott transition systems.

Fig. 2 Suv420h dKO mice have improved metabolic parameters.

Fig. 4 Bcl11b regulates expression of key Treg cell genes while suppressing inflammatory and innate genes. Bcl11b regulates expression of key Treg cell.

Fig. 3 Transcriptional changes in dKO mice.

Fig. 4 OER performance of ACoO3 (A = Ca, Sr) in alkaline solutions with different pH. OER performance of ACoO3 (A = Ca, Sr) in alkaline solutions with.

Fig. 3 Loss of SBP2 in obesity exacerbated insulin resistance and adipogenesis. Loss of SBP2 in obesity exacerbated insulin resistance and adipogenesis.

Fig. 3 Production of protein and Fe(II) at the end of growth correlated with increasing concentrations of ferrihydrite in the media that contained 0.2.

Fig. 2 NH3, NOx, SO2, and NMVOC emission changes triggered by the JJJ clean air policy. NH3, NOx, SO2, and NMVOC emission changes triggered by the JJJ.

Fig. 4 Differential histone modifications at promoters in various brain cell populations. Differential histone modifications at promoters in various brain.

Compensatory metabolic pathways during long-term selegiline treatment

Fig. 2 Viperin promotes methionine oxidation of KSHV helicase.

Fig. 5 Comparison of the liquid products generated from photocatalytic CO2 reduction reactions (CO2RR) and CO reduction reactions (CORR) on two catalysts.

Fig. 5 Enzyme activity of PE-DNase I/Pt tuned by changing temperature or NIR light. Enzyme activity of PE-DNase I/Pt tuned by changing temperature or NIR.

Fig. 1 Location of the Jirzankal Cemetery.

Fig. 4 CO2 emission changes triggered by the JJJ clean air policy.

Fig. 2 Tissue-specific transcriptomic alterations in response to acute sleep loss in healthy humans. Tissue-specific transcriptomic alterations in response.

Multiplexed four- and eight-channel devices for rapid processing

Fig. 6 The combined therapeutic efficacy of N-pepABS and low dose of Dox on MDA-MB-231 xenografts. The combined therapeutic efficacy of N-pepABS and low.

Fig. 2 Mean field results. Mean field results. (A) Solutions P(x) to Eq. 4 for a range of T and wc = (B) Modulus ∣pk∣ of order parameters versus.

Fig. 6 Stabilization of hippocampal signaling over sleep.

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 The increase in CD90+ mSSC abundance in fractured bones following local COX-2 overexpression depended on MCP-1. The increase in CD90+ mSSC abundance.

Fig. 1 Schematic depiction of a paradigm for rapid and guided discovery of materials through iterative combination of ML with HiTp experimentation. Schematic.

Fig. 2 ITGA5 knockdown attenuates hPSC activation, differentiation, and functions. ITGA5 knockdown attenuates hPSC activation, differentiation, and functions.

Fig. 4 Spatial mapping of the distribution and intensity of industrial fishing catch. Spatial mapping of the distribution and intensity of industrial fishing.

Fig. 4 Single-particle contact angle measurements.

Fig. 3 Performance of the generative model G, with and without stack-augmented memory. Performance of the generative model G, with and without stack-augmented.

Fig. 4 Behavior of resistance peak near density nm = 5.

Fig. 4 Systemic AAV9 delivery of gene editing components to ΔEx44 mice rescues dystrophin expression. Systemic AAV9 delivery of gene editing components.

Fig. 1 Doping schematics and optical properties.

Fig. 3 Gene expression analysis in 48-plex drug treatment experiments.

Fig. 2 Combined transcriptome profiling, ChIP-seq, and ATAC-seq analysis identifies 14 highly plausible direct targets of Runx. Combined transcriptome.

Fig. 2 hTERT induces expression of heat shock protein genes through HSF1 and interacts with Hsp70-1. hTERT induces expression of heat shock protein genes.

Fig. 3 Calculated electronic structure of ZrCoBi.

Cxxc1-deficient TH17 cells exhibit a Treg cell–like expression profile

Presentation transcript:

Fig. 6 PPAR-γ is a direct target of Suv420h. PPAR-γ is a direct target of Suv420h. (A) GSEA of PPAR-γ targets in the ChIP-PET (pair end-tagging) experiment in mouse from the ChEA database for RNA-seq Young (left) and RNA-seq Diet (right). (B) Venn diagram showing the overlap of genes up-regulated in Suv420h dKO with a comprehensive dataset of PPAR-γ targets as defined in Materials and Methods. (C to E) RT-qPCR for PPAR-γ expression in the indicated experimental condition [n = 3 controls and n = 7 dKO in (C); n = 6 for both genotypes and feeding conditions in (D); n = 6 for both conditions in (E)]. (C) RT-qPCR for PPAR-γ expression in iBAT from control and dKO mice. (D) RT-qPCR for PPAR-γ expression in iBAT from mice used in the DIO (see Fig. 4) experiment, after 14 weeks of HFD regimen. Control mice were fed with standard chow (ND, normal diet). (E) RT-qPCR for PPAR-γ expression in iBAT from mice with or without cold exposure (see Fig. 2, E and F). (F and G) ChIP assays using the indicated antibodies analyzed by qPCR using primers located on the PPAR-γ and glyceraldehyde phosphate dehydrogenase (GAPDH) (used as negative control) genomic regions as shown by the scheme above each graph (n = 3). (F) ChIP-qPCR performed in iBAT dissected from mice with or without cold exposure. The day before the experiment, mice were grouped in cages with water and bedding, and starved overnight. On the day of the experiment, mice were placed either at room temperature or at 4°C for 6 hours. At the end of the treatment, mice were euthanized, and iBAT was isolated. Chromatin was extracted from iBAT as described in Materials and Methods and used for ChIP. (G) ChIP-qPCR performed in proliferating brown pre-adipocytes treated for 7 days with either the Suv420h inhibitor A-196 (10 mM) or DMSO, as control. IgG, immunoglobulin G. (H) RT-qPCR for PPAR-γ expression in brown pre-adipocytes treated for 7 days with the Suv420h-specific inhibitor A-196 (10 mM) (n = 4) (left). Representative Western blot showing decrease of H4K20me3 upon treatment (right). (I) RT-qPCR expression analysis of the indicated PPAR-γ target genes in brown pre-adipocytes treated with A-196 (10 mM) alone or in combination with the iPPAR-γ (10 μM) (n = 3). For A to I, values are expressed as mean ± SEM; t test. (L) Oxygen Consumption Rate (OCR) measurement in proliferating brown pre-adipocytes treated with A-196 (10 μM) alone or in combination with the iPPAR-γ (10 mM) (mean ± SEM; one-way ANOVA) (n = 5). *P < 0.05, **P < 0.01, ***P < 0.001, ++P < 0.01 relative to A-196; +++P < 0.001 relative to A-196. Simona Pedrotti et al. Sci Adv 2019;5:eaav1472 Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).