Hordeum
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB12902 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR342060.fastq.gz | Fastqsanger.gz | |||
| DRR342061.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 2 of 2 |
Similar Datasets
Project description:Isolation of AVR-Pias recognized by the rice resistance gene, Pias
| PRJDB12884 | ENA
Project description:Activation of the serine/threonine kinase Akt contributes to the formation, maintenance, and therapeutic resistance of cancer, which is driving development of compounds that inhibit Akt. Phosphatidylinositol ether lipid analogues (PIAs) are analogues of the products of PI3K that inhibit Akt activation, translocation, and the proliferation of a broad spectrum of cancer cell types. To gain insight into the mechanism of PIAs, time-dependent transcriptional profiling of 5 active PIAs and the PI3K inhibitor LY294002 (LY) was performed in non-small cell lung cancer (NSCLC) cells using high-density oligonucleotide arrays. Gene ontology analysis revealed genes involved in apoptosis, wounding response, and angiogenesis were upregulated by PIAs, while genes involved in DNA replication, repair and mitosis were suppressed. Genes that exhibited early differential expression were partitioned into 3 groups; those induced by PIAs only (DUSP1, KLF6, CENTD2, BHLHB2, PREX1), those commonly induced by PIAs and LY (TRIB1, KLF2, RHOB and CDKN1A), and those commonly suppressed by PIAs and LY (IGFBP3, PCNA, PRIM1, MCM3 and HSPA1B). Increased expression of the tumor suppressors RHOB (RhoB), KLF6 (COPEB) and CDKN1A (p21Cip1/Waf1) was validated as an Akt-independent effect that contributed to PIA-induced cytotoxicity. Despite some overlap with LY, active PIAs have a distinct expression signature that contributes to their enhanced cytotoxicity.
2011-03-23 | GSE27911 | GEO
Project description:The purpose of this study was to assess the impact of sex on gene expression in LV of AS patients at the time of AVR. LV samples of men (n = 9; age: 75 M-1 8 y) and women (n = 10; age: 72 M-1 9 y) undergoing AVR were used for RNA isolation. Genome-wide expression profiling was performed using the Affymetrix platform and the data were analyzed with R and Bioconductor. Diseased samples were compared with LV samples of men (n = 10; age: 56 M-1 4 y) and women (n = 8; age: 56 M-1 5 y) with no apparent cardiovascular disorder.
2014-09-04 | E-MEXP-3684 | biostudies-arrayexpress
Project description:Disease resistance is mediated by specific recognition of pathogen avriulence effectors (AVR) by nucleotide-binding leucine-rich repeat (NLR) receptors. The barley (Hordeum vulgare) mildew locus A (mla) resistance gene homolog 1 (RGH1) encoded NLRs (MLAs) confer isolate-specific resistance to the widespread mildew fungus Blumeria graminis forma specialis hordei (Bgh). In barley, MLA has been subject to extensive functional diversification, resulting in allelic resistance specificities, each recognizing a cognate Bgh AVRa. The by genetic association isolated AVRa1 and AVRa13 effectors belong to the candidate secreted effector protein (CSEP) gene family (Lu et al., 2016). To unravel the complex mechanisms underlying MLA functional diversification in barley and wheat, isolation of numerous Bgh AVRa genes and recognition of their gene products by MLA is necessary. Our here deployed higher resolution genetic association approach identified the Bgh avirulence gene candidate loci AVRa7, AVRa9, AVRa22 and AVRa10 by associating of transcript polymorphisms and AVRa phenotypes from a collection of 27 Bgh isolates. We collected 10 Bgh isolates from a local Bgh population in Cologne in addition to our previous collection of 17 Bgh isolates (Lu et al., 2016).
2019-02-19 | GSE110266 | GEO
Project description:Activation of the serine/threonine kinase Akt contributes to the formation, maintenance, and therapeutic resistance of cancer, which is driving development of compounds that inhibit Akt. Phosphatidylinositol ether lipid analogues (PIAs) are analogues of the products of PI3K that inhibit Akt activation, translocation, and the proliferation of a broad spectrum of cancer cell types. To gain insight into the mechanism of PIAs, time-dependent transcriptional profiling of 5 active PIAs and the PI3K inhibitor LY294002 (LY) was performed in non-small cell lung cancer (NSCLC) cells using high-density oligonucleotide arrays. Gene ontology analysis revealed genes involved in apoptosis, wounding response, and angiogenesis were upregulated by PIAs, while genes involved in DNA replication, repair and mitosis were suppressed. Genes that exhibited early differential expression were partitioned into 3 groups; those induced by PIAs only (DUSP1, KLF6, CENTD2, BHLHB2, PREX1), those commonly induced by PIAs and LY (TRIB1, KLF2, RHOB and CDKN1A), and those commonly suppressed by PIAs and LY (IGFBP3, PCNA, PRIM1, MCM3 and HSPA1B). Increased expression of the tumor suppressors RHOB (RhoB), KLF6 (COPEB) and CDKN1A (p21Cip1/Waf1) was validated as an Akt-independent effect that contributed to PIA-induced cytotoxicity. Despite some overlap with LY, active PIAs have a distinct expression signature that contributes to their enhanced cytotoxicity. H157 cells were plated at 2x10^6 in T-75 flasks in RPMI medium 1640 containing 10% FBS and incubated for 24h. The media was then changed to RPMI medium 1640 with 0.1% FBS and the cells were incubated overnight. The following morning, cells were treated with 10 microM PIA6 dissolved in DMSO for 0h, 2h, 6h or 12h, and an equal volume of DMSO was added to control samples. For the PIA comparison, 10 microM PIAs (5, 6, 7, 23, 24, 25) or 10 microM LY294002 (LY) were incubated with the cells for 6h. In the PIA comparison experiment, the same concentration of PIA7 (an inert analog consisting of only the lipid side chain) was used as a control. Following incubation, the alterations in cellular morphology were photographed, and cells from 6-well plates were harvested for immunoblot analysis. Total RNA was extracted from cells treated in T-75 flasks using TRIzol reagent (Invitrogen) and chloroform, and purified according to the RNeasy midiprep spin kit protocol (Qiagen). Oligonucleotide microarray was performed with dye-swap. Microarray chips were generated from the 34,580 longmer probe set Human Genome Oligo Set Version 3.0 (Qiagen). Protocols for cDNA labeling, hybridization, and scanning are available through the National Human Genome Research Institute microarray core.
2011-03-22 | E-GEOD-27911 | biostudies-arrayexpress
Project description:The quadruple mutant avr-14(vu47); glc-3(ok321) avr-15(vu227) glc-1(pk54) with avr-15 rescued with a myo-2 promoter for pharynx-specific expression (strain LRB269) was used. This allowed worms to perceive food but not eat it when the drug ivermectin is added.
2018-09-20 | GSE114955 | GEO
Project description:Protein inhibitor of activated STAT (PIAS) are E3 SUMO ligases playing important roles in protein stability and signaling transduction pathways. PIAS proteins are overexpressed in the triple-negative breast cancer cell line MDA-MB-231, and PIAS knockout (KO) results in a reduction in cell proliferation and cell arrest in S phase. However, the molecular mechanisms underlying PIAS functions in cell proliferation and cell cycle remain largely unknown. Here, we used quantitative SUMO proteomics to explore the regulatory role of PIAS SUMO E3 ligases upon CRISPR/Cas9 KO of individual PIAS. A total of 1422 sites were identified, and around 10% of SUMO sites were regulated following KO of one or more PIAS genes. We identified protein substrates that were either specific to individual PIAS ligase or regulated by several PIAS ligases. Ki-67 and TOP2A, which are involved in cell proliferation and epithelial-to-mesenchymal transition, are SUMOylated at several lysine residues by all PIAS ligases, suggesting a level of redundancy between these proteins. Confocal microscopy and biochemical experiments revealed that SUMOylation regulated TOP2A protein stability, while this modification is involved in the recruitment of Ki-67 nucleolar proteins containing SUMO interacting motif. These results provide novel insights into both the redundant and specific regulatory mechanisms of cell proliferation and cell cycle mediated by PIAS SUMO E3 ligases.
2023-02-02 | PXD023841 | Pride
Project description:affy_riz_2011_7 - affy_riz_2011_7 - The Bacterial Leaf Blight disease of rice is due to Xanthomonas oryzae pv. oryzae. As for many pathogenic bacteria, it relies on a type 3 secretion system (TTSS) that is devoted to the injection of type 3 effectors (T3Es) into the eukaryotic host cell. These proteins are meant to suppress host basal defense responses and/or mimic some host regulatory function promoting bacterial survey in the plant. During an incompatible interaction, T3Es may act as Avr proteins and stimulate Effector-Triggered-Immunity. We aim at evaluating the transcriptomic response of rice leaves challenged with avirulent strains of Xoo BAI3 and MAI1 on resistant lines IR64 and IRBB4 versus the reference susceptible rice line Nipponbare. In addition, we investigated the transcriptomic response of rice leaves upon inoculation of an XoohrcC mutant strain affected in the production of a functional TTSS.-The goal of the experiment is to characterize the rice leaf transcriptome response, upon the inoculation of susceptible and resistant rice leaves 24 hours post-infection. To that end, the experimental design includes the inoculation of susceptible Nipponbare rice leaves with Xoo strains BAI3 (race A1) and MAI1 (race A3), that will be compared to the response of resistant lines IRBB4 and IR64 rice lines. In addition, Nipponbare rice leaves will also be challenged with the BAI3hrcC mutant that is affected in the production of a functional TTSS. 18 arrays - rice; avirulent vs virulent
2012-10-15 | E-GEOD-34192 | biostudies-arrayexpress
Project description:affy_riz_2011_7 - affy_riz_2011_7 - The Bacterial Leaf Blight disease of rice is due to Xanthomonas oryzae pv. oryzae. As for many pathogenic bacteria, it relies on a type 3 secretion system (TTSS) that is devoted to the injection of type 3 effectors (T3Es) into the eukaryotic host cell. These proteins are meant to suppress host basal defense responses and/or mimic some host regulatory function promoting bacterial survey in the plant. During an incompatible interaction, T3Es may act as Avr proteins and stimulate Effector-Triggered-Immunity. We aim at evaluating the transcriptomic response of rice leaves challenged with avirulent strains of Xoo BAI3 and MAI1 on resistant lines IR64 and IRBB4 versus the reference susceptible rice line Nipponbare. In addition, we investigated the transcriptomic response of rice leaves upon inoculation of an XoohrcC mutant strain affected in the production of a functional TTSS.-The goal of the experiment is to characterize the rice leaf transcriptome response, upon the inoculation of susceptible and resistant rice leaves 24 hours post-infection. To that end, the experimental design includes the inoculation of susceptible Nipponbare rice leaves with Xoo strains BAI3 (race A1) and MAI1 (race A3), that will be compared to the response of resistant lines IRBB4 and IR64 rice lines. In addition, Nipponbare rice leaves will also be challenged with the BAI3hrcC mutant that is affected in the production of a functional TTSS.
2012-10-15 | GSE34192 | GEO