Fig. 5 Analysis of metabolite changes in M

Slides:

Advertisements

Similar presentations

Fig. 8. Recurrent copy number amplification of BRD4 gene was observed across common cancers. Recurrent copy number amplification of BRD4 gene was observed.

Advertisements

Fig. 1. NS1 protein alignment and linear epitope mapping of the 10 antibodies used to run the DENV serotype–specific NS1 rapid tests, pan-DENV NS1 test,

Fig. 7. Intrapatient variation in key contact signatures for PGDM1400 and PGT121. Intrapatient variation in key contact signatures for PGDM1400 and PGT121.

Representation of the evolutionary model.

Untargeted metabolomics profiling by GC-TOF-MS reveals a human PCa-associated metabolic phenotype in Zn-deficient middle-aged Wistar-Unilever rat prostates.

Fig. 1. Generation of ERY974. Generation of ERY974. (A) Schematic illustration of ERY974 structure and the introduced mutations. The two Fab arms share.

Fig. 6. dAST directly from clinical samples using dPCR and dLAMP for quantification. dAST directly from clinical samples using dPCR and dLAMP for quantification.

Fig. 1. The cell-intrinsic fibroblast circadian proteome contains numerous cytoskeletal regulators. The cell-intrinsic fibroblast circadian proteome contains.

Regional genome association plots for the GWAS results of the FADS1/2/3 region of chromosome 11. Regional genome association plots for the GWAS results.

Extension of the GlyRβ binding site on gephyrin.

Fig. 2. Mutational signature exposures in Taiwan HCCs and summary of AA signature mutations. Mutational signature exposures in Taiwan HCCs and summary.

Fig. 3. Structure of ALS-associated RNA binding proteins.

Effects of highly concentrated SFN provided as BSE in T2D patients

Fig. 8. Gene and protein changes in ALK-dependent STING pathways in human sepsis. Gene and protein changes in ALK-dependent STING pathways in human sepsis.

Fig. 3. Antimicrobial activity is detected in diverse strains of CoNS and not predictable at the species level. Antimicrobial activity is detected in diverse.

Fig. 5. Correlation of tail and long bone growth velocities with Cxm serum concentrations in mice. Correlation of tail and long bone growth velocities.

β-ARs signal cooperatively with mutant EGFR and inactivate LKB1

Fig. 4. Liver HBV mRNA paired-end sequencing reads in HBeAg-positive and HBeAg-negative chimpanzees. Liver HBV mRNA paired-end sequencing reads in HBeAg-positive.

Fig. 2. Engraftment of CART-EGFRvIII and cytokine modulation in the peripheral blood. Engraftment of CART-EGFRvIII and cytokine modulation in the peripheral.

Fig. 2. dAST using dPCR is robust to the presence of high concentrations of commensal bacteria due to the specificity of NA amplification. dAST using dPCR.

Fig. 1. Associations between fecal amino acids and their derivatives with disease in pediatric patients with Crohn’s disease compared to healthy subjects.

Fig. 4. Functional annotation of VUS in EGFR.

Fig. 1. Schematic representation of the MANO method.

Fig. 2. Mutant KRAS mediates resistance to PARPi and sensitivity to PARPi and MEKi Mutant KRAS mediates resistance to PARPi and sensitivity to PARPi and.

Fig. 2. Associations between bacterial taxa abundance ascertained by fecal shotgun metagenomic sequencing and the fecal metabolome in healthy pediatric.

Mattia Zampieri, Michael Zimmermann, Manfred Claassen, Uwe Sauer

Fig. 3. Frequencies of amino acids at critical PGT121 and contact sites in the SHIV-SF162P3 challenge stock. Frequencies of amino acids at critical.

Fig. 3. BET inhibition reduces homologous recombination.

Fig. 2 Maraba treatment results in complete responses in the window of opportunity setting. Maraba treatment results in complete responses in the window.

Fig. 6 Bimodal treatment results in reduced tinnitus loudness and reduced TFI scores in human patients. Bimodal treatment results in reduced tinnitus loudness.

Fig. 1. Identification of SE-associated lncRNAs.

Fig. 2. GPC3 expression in normal and tumor tissues.

Bio-AMS enhances the activity of rifampicin and ethambutol in vitro

Fig. 4. Specific versus nonspecific NP accumulation.

Fig. 4. In vivo analysis of slpA mutant in the Syrian Golden hamster.

Dot plots of trisomic versus fetal fractions for cohorts 1 and 2

The MSP domain of MOSPD2 binds the FFAT motif

Fig. 7 Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors. Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors.

Fig. 3 Pairwise similarity of antimicrobials with respect to metabolic changes induced in M. smegmatis. Pairwise similarity of antimicrobials with respect.

Fig. 6. Epitope mapping of C12G6.

Fig. 6. Safety assessment in cynomolgus monkey.

Fig. 4 Nanocages captured multiple TB-related analytes.

Fig. 4. Actin polymerization rhythms are required for circadian regulation of adhesion and wound-healing efficacy by fibroblasts. Actin polymerization.

Metabolic pathway changes of intracellular M. tuberculosis.

Fig. 1. Experimental workflow of the dAST method and computationally estimated operational space. Experimental workflow of the dAST method and computationally.

Conformational ensembles of apo and ligated FimH variants in solution

Fig. 6. FGFR1 and CCND1 amplification–mediated resistance to estrogen deprivation is therapeutically actionable. FGFR1 and CCND1 amplification–mediated.

Antiproliferative effects of JQ-EZ-05 on VHL−/− ccRCC are on-target

Fig. 2. Pathways differentially regulated in patients with early Lyme disease and STARI. Pathways differentially regulated in patients with early Lyme.

Fig. 3. The effects of DCA on hemodynamic and functional end points and their association with genetic factors (variants of the SIRT3 and UCP2 genes) that.

Workflow of a sample-to-answer AST performed in less than 30 min

Fig. 4 Effect of LRRK2 mutations on protein kinase activity and GTPase activity. Effect of LRRK2 mutations on protein kinase activity and GTPase activity.

Fig. 1 A single amino acid difference in the ATP-binding domain of GSK3α and GSK3β results in structural and topological differences. A single amino acid.

Fig. 2 Analysis of CLL lymph nodes.

Fig. 2 Genotype-induced differential gene expression is different in MDMi cells compared to monocytes. Genotype-induced differential gene expression is.

Adrian I. Campos, Mattia Zampieri

Fig. 2 ALRN-6924 rapidly increases transcription at the p21 locus and affects its bursting dynamics. ALRN-6924 rapidly increases transcription at the p21.

Log- to stationary-phase growth results in differential acetyl abundance on specific proteins. Log- to stationary-phase growth results in differential.

Fig. 1 Antibiotic-induced metabolome responses in M. smegmatis.

IIV induces CD21hiCD27+ and CD21loCD27+ influenza-specific B cells

Fig. 5 Early and modest immune response at day 3 after exposure in Delayed animals. Early and modest immune response at day 3 after exposure in Delayed.

Fig. 2. Clinically actionable somatic genomic alterations in various tumor types. Clinically actionable somatic genomic alterations in various tumor types.

Biochemical and behavioral assessment of GRIN2B(P553T) patient after l-serine dietary supplementation. Biochemical and behavioral assessment of GRIN2B(P553T)

Fig. 7 Bacterial dependency networks in IgA deficiency and HDs.

Fig. 4 Deorphanization of quinine and mefloquine protein targets.

BACE2 substrates in mouse CSF.

Misfolding mutations impair the BRCA1 nuclear aggregation in yeast and the BRCA1 nuclear localization in human cells. Misfolding mutations impair the BRCA1.

Structural insights based on chimeric Alp4-GCP2 analysis.

Untargeted LC/MS metabolite profiling of DFMO-treated HT-29 colorectal cancer cells. Untargeted LC/MS metabolite profiling of DFMO-treated HT-29 colorectal.

Fig. 8 Immune correlates of protection.

Presentation transcript:

Fig. 5 Analysis of metabolite changes in M Fig. 5 Analysis of metabolite changes in M. smegmatis after treatment with the GSK compound GSK2623870A. Analysis of metabolite changes in M. smegmatis after treatment with the GSK compound GSK2623870A. (A) Pairwise similarity between M. smegmatis metabolome response profiles to 16 GSK compounds with no similarity to known MoAs. (B) Schematic representation of trehalose monomycolate exporter protein MmpL3. Transmembrane segments are represented in violet. Circles indicate the locations of amino acid changes associated with resistance of M. tuberculosis to antimycobacterial lead compounds previously found to select for resistance mutations in MmpL3. These compounds include SQ109 (blue), THPP (orange), and SPIROS (purple). The black star indicates the amino acid change associated with resistance to the GSK compound GSK2623870A. The genomes of the M. tuberculosis H37Rv and Beijing GC1237 mutant strains contain an A to G SNP at position 755, which resulted in a tyrosine to cysteine missense mutation at position 252 of the MmpL3 protein. (C) Results from limited proteolysis analysis. Each dot in the volcano plot represents the relative difference in peptide abundance between the treated and untreated proteome extracts. Proteins highlighted in red are known to physically interact with fatty acid synthase FAS-I (figs. S17 and S18). For each protein, the size of the dot reflects the number of interacting partners (80) with significant conformational changes. (D) Rapid metabolic changes induced by the GSK antimicrobial compound GSK2623870A. Each dot corresponds to the R2 and Z-score values of the metabolite 5 min after exposure of M. smegmatis to the antimicrobial compound. Metabolites highlighted in red are involved in fatty acid metabolism. Mattia Zampieri et al., Sci Transl Med 2018;10:eaal3973 Published by AAAS