Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15606735_1.fastq.gz | Fastqsanger.gz | |||
| SRR15606735_2.fastq.gz | Fastqsanger.gz | |||
| SRR15606736_1.fastq.gz | Fastqsanger.gz | |||
| SRR15606736_2.fastq.gz | Fastqsanger.gz | |||
| SRR15606737_1.fastq.gz | Fastqsanger.gz |
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Project description:Analysis of leaves of wild-type and rice COI mutants treated with methyl jasmonate (MeJA). Results provide the role of rice COI on response to jasmonic acid.
2022-06-11 | GSE205750 | GEO
Project description:Aim: To improve risk stratification in patients with stable coronary artery disease (CAD), we aimed to identify genes in monocytes predictive of new ischemic events in patients with CAD and determine to what extent expression of these transcripts resembles expression in acute myocardial infarction (AMI). Results: COX10 and ZNF484 distinguished between AMI and the whole group of stable CAD patients with an accuracy of 90%. COX10 and ZNF484 together with MT-COI and WNK1 distinguished AMI patients from stable CAD patients with and without a new event with a sensitivity of 89% and a specificity of 98%. MT-COI and COX10 increased the accuracy for separating stable CAD patients with and without a new coronary event from 68 to 80% in addition to age, gender, BMI, diabetes, lipids, blood pressure and hs-CRP. Interestingly, expression of MT-COI, COX10 and WNK1 (but not ZNF484) in PBMCs paired with that in monocytes; COX10 in whole blood was similar to that in monocytes. Conclusions: This work showed that COX10 and ZNF484, eventually combined with MT-COI and WNK1 have the potential to accurately discriminate between AMI and stable CAD patients, and may improve the risk assessment of stable CAD patients.
2019-08-13 | GSE129935 | GEO
Project description:Coilin is a scaffold protein essential for the structural integrity of Cajal Bodies, which are non-membranous nuclear organelles that are thought to facilitate assembly and maturation of nuclear RNPs, including spliceosomal snRNPs. To investigate further coilin’s functions in plant cells, and to identify proteins that may functionally interact with coilin, we performed a genetic suppressor screen in Arabidopsis thaliana using a coilin (coi) mutant displaying altered splicing of a GFP pre-mRNA. The modified splicing pattern results in a ‘hyper-GFP’ phenotype in young coi seedlings relative to the intermediate level of GFP in wild-type seedlings. Additionally, in newly emerging leaves of older coi seedlings, the GFP gene frequently undergoes abrupt siRNA-associated posttranscriptional gene silencing that persists during growth. In the suppressor screen, we searched for mutations that subdue one or both of these GFP phenotypes and identified several understudied factors in plants: WRAP53, a putative Cajal body protein; SMU2, a predicted splicing-related factor; and ZC3HC1, an uncharacterized zinc finger protein. All three mutations return the hyper-GFP phenotype of the coi mutant to approximately the intermediate wild-type level. The zc3hc1 mutations in particular induce premature and more extensive posttranscriptional gene silencing similar to mutations in SOP1 and DCL4, which are known modifiers of posttranscriptional gene silencing. Candidate coilin-interacting proteins identified by immunoprecipitation-mass spectrometry include many splicing-related factors, nucleolar proteins, and mRNA export factors. Our results demonstrate the usefulness of the coi mutant to identify new modifiers of alternative splicing and posttranscriptional gene silencing, and suggest diverse roles for coilin in plant cells.
2023-07-27 | PXD027146 | Pride
Project description:In recent years, several small molecule cytotoxic drugs have been identified as potential inhibitors of ribosome biogenesis (Drygin et al., 2011; Peltonen et al., 2014a; Peltonen et al., 2014b). CX-5461 is one such drug that has also demonstrated anticancer potential for a wide range of malignancies (Bywater et al., 2012; Cornelison et al., 2017; Devlin et al., 2015; Drygin et al., 2011; Hald et al., 2019; Hein et al., 2017; Ismael et al., 2019; Lawrence et al., 2018; Lee et al., 2017; Negi and Brown, 2015; Taylor et al., 2019; Xu et al., 2017; Yan et al., 2017) (Haddach et al., 2012), and is presently under phase I trials for the treatment of both hematological cancers and solid tumours (Group, 2016; Khot et al., 2019). CX-5461 was initially characterized as an inhibitor of RNA Polymerase I (RPI/PolR1/PolI) that is responsible for the synthesis of the major ribosomal RNAs and the initial step in ribosome biogenesis (Drygin et al., 2011). Since RPI and its corresponding core transcription factors are dedicated to this task alone, they present ideal molecular targets by which to modulate ribosome biogenesis. However, the specificity of CX-5461 has been questioned and it has been suggested that this drug may also act by stabilizing DNA G-quadruplexes or by “poisoning” topoisomerase II (Topo II). Thus, the primary target of this drug and its mode of action are still in doubt. Here we used Deconvolution-ChIP-Seq in NIH3T3 and HEK293T cells treated for different times with CX-5461. The data show that the primary target of CX5461 is the initiation of ribosomal RNA gene (rDNA) transcription. CX-5461 blocks transcription initiation in vitro and in vivo by arresting RNA polymerase I (RPI/Pol1) within the preinitiation complex. In contrast to previous suggestions, CX-5461 does not effect recruitment of the TBP-TAF complex SL1 to the rDNA promoter, the recruitment of the initiation competent RPI-Rrn3 complex or ongoing transcription elongation, arguing against a role for G-quadruplex stabilization or topoisomerase II poisoning. Inhibition of transcription by CX-5461 is not reversible, the RPI-Rrn3 complex remains arrested in the preinitiation complex even after drug removal. This leads to nucleolar stress, extensive DNA damage and cell senescence. Our data show that the cytotoxicity of CX-5461 is the downstream result of the highly specific inhibition of rDNA transcription. The observation that this inhibition is irreversible will be important for the future design of chemotherapeutic strategies and the avoidance of drug resistance.
2021-04-07 | E-MTAB-9242 | biostudies-arrayexpress