Transcriptional profile of injured hearts treated with the cholinesterase inhibitor pyridostigmine (PYR) at Day 5
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PROVIDER: PRJNA480795 | ENA |
REPOSITORIES: ENA
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2014-08-25 | GSE58168 | GEO
Project description:In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing human cancer cells. 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline
2014-08-25 | E-GEOD-58168 | biostudies-arrayexpress
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2021-10-01 | E-MTAB-10860 | biostudies-arrayexpress
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2007-11-23 | E-GEOD-4710 | biostudies-arrayexpress
Project description:Unveiling the signal transduction of phytohormone abscisic acid (ABA) will be greatly helpful to improve plant responses to stressful environment. ABA signaling is perceived and mediated by multi-member receptor PYR/PYLs, while whose post-translational modification, especially phosphorylation, is largely unknown. Here we demonstrated that Arabidopsis EL1-like (AEL), a casein kinase that regulates various physiological processes, phosphorylates PYR/PYLs and stimulates whose ubiquitination and degradation, leading to the suppressed ABA responses. Arabidopsis ael triple mutants display hypersensitive responses to ABA treatment, which is consistent with the suppressed degradation of PYR/PYL proteins. PYR/PYLs are phosphorylated in vivo and mutation of the conserved AEL-phosphorylation sites results in the reduced phosphorylation, ubiquitination, and degradation of PYR/PYLs, and hence the enhanced ABA responses. Our studies demonstrate the crucial roles of AEL-mediated phosphorylation in regulating the stability and function of PYR/PYLs and provide informative clues for elucidating the functional mechanism of ABA through regulating PYR/PYL receptors.
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Project description:Abscisic acid (ABA) is a key hormone for plant growth, development and stress adaptation. Perception of ABA through four types of receptors has been reported. We show here that impairment of ABA perception through the PYR/PYL/RCAR branch reduces vegetative growth and seed production, and leads to a severely open stomata and dramatic ABA insensitive phenotype, even though other branches for ABA perception remain functional. Arabidopsis sextuple mutant impaired in 6 PYR/PYL receptors, namely PYR1, PYL1, PYL2, PYL4, PYL5 and PYL8, was able to germinate and grow even on 100 mM ABA. Whole-rosette stomatal conductance (Gst) measurements revealed that leaf transpiration in the sextuple pyr/pyl mutant was higher than in the ABA-deficient aba3-1 or ABA-insensitive snrk2.6 mutants. The gradually increasing Gst values of plants lacking three, four, five and six PYR/PYLs indicate quantitative regulation of stomatal aperture by this family of receptors. The sextuple mutant lacked ABA-mediated activation of SnRK2s and ABA-responsive gene expression was dramatically impaired as was reported in snrk2.2/2.3/2.6. In summary, these results show that ABA perception by PYR/PYLs plays a major role to regulate seed germination and establishment, basal ABA signaling required for vegetative and reproductive growth, stomatal aperture and transcriptional response to the hormone.
2012-11-30 | GSE36692 | GEO
Project description:Purpose: To analyze gene expression in calcific (C3H) and non-calcific (B6) hearts Methods: B6 and C3H mice were induced cardiac injury by rapid freeze thaw of cardiac tissue (cryo-injury). A left thoracotomy was performed at the level of 2nd intercostal space and the exposed beating heart was frozen for 10 seconds by gently pressing a pre-cooled steel rod of 1mm diameter in dry ice. Freezing of cardiac tissue was confirmed by the rapid discoloration of the tissue. Seven days after injury, injured and uninjured regions from same heart were used for RNA sequence. Results: In contrast to only 70 odd genes that were differentially upregulated following injury in non-calcified mouse hearts (B6) about 960 genes were upregulated in C3H hearts following injury induced calcification. Out of the 960 differentially upregulated genes, only 35 were found to be common or upregulated in both C3H and B6 hearts after injury illustrating of the overlapping but dramatically different magnitude of the injury response. Families of genes regulating diverse aspects of an injury response including inflammation, extracellular matrix proteins, cell proliferation and collagen production were differentially expressed between the calcific and non-calcific hearts after injury. The mean expression of osteogenic genes (osteogenic signature) was significantly higher in injured C3H hearts compared to uninjured C3H hearts. The osteogenic signature was not higher in injured B6 hearts compared to control uninjured B6 hearts. Conclusions: Calcific hearts compared to non-calcific hearts responded to injury with a dramatically different transcriptional program.
2016-11-07 | GSE87837 | GEO