Similar Datasets
Project description:mRNAseq of wild type and ets-5 mutant C. elegans BAG neurons
| PRJNA680272 | ENA
Project description:The gene expression profile of WT (N2) C. elegans were compared to that of ets-4(ok165) and ets-4(uz1) mutant animals
2010-05-15 | GSE21851 | GEO
Project description:The extent to which behavior is shaped by experience varies between individuals. Genetic differences contribute to this variation but the neural mechanisms are not understood. In this study, we identify a natural genetic variant of the dendritic scaffolding protein ARCP-1 that modifies individual behavioral flexibility in C. elegans. Disrupting ARCP-1 alters how previous oxygen experience modulates escape behavior in response to carbon dioxide. ARCP-1 normally suppresses CO2 aversion by inhibiting signaling from the BAG CO2-sensing neurons. To further investigate how disrupting ARCP-1 alters BAG function, we specifically labeled these neurons with GFP, used FACS to isolate the fluorescent cells from acutely dissociated arcp-1 mutant and control animals, and profiled their gene expression using RNA-Seq. We find transcriptional changes for a broad range of gene classes and link altered neuropeptide expression to increased CO2 aversion in the arcp-1 mutant.
2019-11-19 | GSE135687 | GEO
Project description:Purpose: The goals of this study are to identify cellular pathways to recover a-syn aggregation-mediated toxicity induced in response to CDC or BAG treatment on PD-iPSC derived mDA neurons. Methods: mRNA profiles of 30-day-old PD-mDA neurons with CDC or BAG treatment for 1 day were generated by deep sequencing, in duplicate, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Conclusions: Our study represents the detailed analysis of mDA neuronal transcriptomes in response to CDC or BAG treatments, with biologic replicates, generated by RNA-seq technology. Our results show that CDC or BAG treatment could rescue the toxcity from a-syn aggregation via purine metabolism / ion transport pathways.
2021-06-30 | GSE153325 | GEO
Project description:Targeting the activation function-1 (AF-1) at the N-terminus of the androgen receptor (AR) is an attractive therapeutic alternative to the current approaches to inhibit AR action in prostate cancer (PCa). Here we show that the AR AF-1 is bound by the BAG domain of the cochaperone Bag-1L. Mutations in this domain or loss of Bag-1L abrogates AR signaling and reduces PCa growth. Correspondingly, Bag-1L protein levels increase with progression of primary prostate tumors to castration-resistant PCa, correlating inversely with patient response to abiraterone therapy. Intriguingly, BAG domain residues important for its interaction with the AR AF-1 overlap a potentially druggable pocket of this protein. Bag-1L is therefore a putative therapeutic target for the inhibition of AR AF-1 activity.
2017-08-23 | GSE102183 | GEO
Project description:The BF-3 pocket of the androgen receptor (AR) has been identified as an allosteric modulator of the transactivation function of the AR. We now demonstrate that a duplicated GARRPR motif at the N-terminus of the cochaperone Bag-1L functions through this BF-3 domain. Amino acid exchanges in these two motifs impair binding of Bag-1L to the AR but increase the androgen-dependent activation of a subset of AR-target genes. We have therefore identified GARRPR as a novel BF-3 regulatory sequence important for fine-tuning the activity of the receptor. LNCaP cells stably expressing the empty vector construct (=control), or wild-type or N-terminal GARRPR mutant Bag-1L were cultured under hormone-starvation conditions for 72 h and then treated with vehicle or 10 nM DHT for 4 h. Biological triplicate samples were analyzed for each cell line.
2014-02-18 | E-GEOD-51524 | biostudies-arrayexpress
Project description:The BF-3 pocket of the androgen receptor (AR) has been identified as an allosteric modulator of the transactivation function of the AR. We now demonstrate that a duplicated GARRPR motif at the N-terminus of the cochaperone Bag-1L functions through this BF-3 domain. Amino acid exchanges in these two motifs impair binding of Bag-1L to the AR but increase the androgen-dependent activation of a subset of AR-target genes. We have therefore identified GARRPR as a novel BF-3 regulatory sequence important for fine-tuning the activity of the receptor.
2014-02-18 | GSE51524 | GEO
Project description:Herein, we explore the druggability of BAG-1S (the smallest isoform) with a specific emphasis on its interaction with C-RAF. We firstly characterize the higher order structure of BAG-1S structure to determine druggable sites by HDX-MS. We then map the BAG-1S:c-Raf interface – identifying a 20 amino acid region likely to interact with c-Raf. Following which, we use mutational analysis of BAG-1S to show specific amino acids that disrupt the BAG-1S:c-Raf interaction, downstream signaling and cell growth. Finally, we develop a BAG-1S interacting peptide (from c-Raf) that disrupts BAG-1 protein:protein interactions (including C/B-RAF, CHIP and HSP70) and modified with a cell-penetrating motif which inhibits the growth of cancer cells with associated signaling inhibition and induction of apoptosis.
2024-12-17 | PXD058656 | Pride
Project description:Targeting the activation function-1 (AF-1) at the N-terminus of the androgen receptor (AR) is an attractive therapeutic alternative to the current approaches to inhibit AR action in prostate cancer (PCa). Here we show that the AR AF-1 is bound by the BAG domain of the cochaperone Bag-1L. Mutations in this domain or loss of Bag-1L abrogates AR signaling and reduces PCa growth. Correspondingly, Bag-1L protein levels increase with progression of primary prostate tumors to castration-resistant PCa, correlating inversely with patient response to abiraterone therapy. Intriguingly, BAG domain residues important for its interaction with the AR AF-1 overlap a potentially druggable pocket of this protein. Bag-1L is therefore a putative therapeutic target for the inhibition of AR AF-1 activity.
2017-08-23 | GSE89938 | GEO
Project description:Targeting the activation function-1 (AF-1) at the N-terminus of the androgen receptor (AR) is an attractive therapeutic alternative to the current approaches to inhibit AR action in prostate cancer (PCa). Here we show that the AR AF-1 is bound by the BAG domain of the cochaperone Bag-1L. Mutations in this domain or loss of Bag-1L abrogates AR signaling and reduces PCa growth. Correspondingly, Bag-1L protein levels increase with progression of primary prostate tumors to castration-resistant PCa, correlating inversely with patient response to abiraterone therapy. Intriguingly, BAG domain residues important for its interaction with the AR AF-1 overlap a potentially druggable pocket of this protein. Bag-1L is therefore a putative therapeutic target for the inhibition of AR AF-1 activity.
2017-08-23 | GSE89917 | GEO