Similar Datasets
Project description:The experiment was designed to investigate the regulatory landscape of H3K27me3, a histone methylation form, in the hippocampal neurons upon lead exposure. It reveals that the targeting pathways were altered and migrated throughout the genome, indicating that H3K27me3's sophisticated alterations are responsible for lead-led impairment of hippocampal neurons. Besides, the causes leading to its adaptive changes were figured out.
2018-11-17 | E-MTAB-6837 | biostudies-arrayexpress
Project description:Transcriptome profiling of rat primary hippocampal neurons when the dyslexia candidate gene DCDC2 is overexpressed using transient transfections.<br><br>Additional processed data files and their associated custom CDF are available on the FTP site for this experiment.
2011-03-01 | E-MTAB-518 | biostudies-arrayexpress
Project description:To understand how cells communicate with each other, it is essential to define the cellular secretome, a collection of proteins including soluble secreted, unconventionally secreted and proteolytically-shed proteins. Quantitative methodologies to decipher the secretome are challenging, due to the requirement of large cell numbers and abundant serum proteins that interfere with the detection of low-abundant cellular secretome proteins. Here, we have use the highe perfomance secretome-protein-enrichment-with-click-sugars method (hiSPECS) for glyco-secretome analysis. We applied this method to investigate differences of hippocampal and cortical murine neurons. Additionally, we have inhibited the Alzheimer related protease BACE1 to identify potential substrates in the secretome of hippocampal neurons.
2020-09-25 | PXD020503 | Pride
Project description:Neurons express Phactr1 at high level (Allen et al., 2004), and Phactr1 mutations are associated with morphological and functional developmental defects in cortical neurons (Hamada et al., 2018). To identify targets of the Phactr1/PP1 phosphatase holoenzyme, we cultured hippocampal and cortical neurons from wildtype and Phactr1-null animals, treated them either with Latrunculin B or Cytochalasin D to inhibit or activate formation of the Phactr1/PP1 complex (Wiezlak et al., 2012), and analysed phosphorylation profiles using TMT phosphoproteomics. Among over 9000 phosphorylation sites quantified, we found numerous phosphorylation sites that differed significantly in their response to these stimuli in wildtype as opposed to Phactr1-null neurons.
2020-10-28 | PXD019882 | Pride
Project description:A central hallmark of brain aging is the alteration of neuronal functions in the hippocampus, leading to a progressive decline in learning and memory. Multiple reports have shown the importance of blood-borne factors in inter-tissue communication for the maintenance of cognitive fitness and proper regulation of neuronal homeostasis throughout life. Among these blood-borne factors, we identified Osteocalcin (OCN), a bone-derived hormone. OCN induces autophagy machinery in hippocampal neurons which is essential for activity-dependent synaptic plasticity. However, the way in which blood-borne factors like OCN communicate with neurons, including their regulatory mechanisms, remains largely elusive. Here, we show the importance of a core primary cilium (PC)-proteins/autophagy machinery axis in hippocampal neurons that mediate the effects of the pro-youthful blood factor OCN on neuronal homeostasis and cognitive fitness. We found that OCN’s receptor, GPR158, is present at the PC of hippocampal neurons and mediates the regulation of autophagy machinery by OCN. During aging, PC-core proteins are reduced in hippocampal neurons and associated with neuronal PC morphological abnormalities. Restoring their levels is sufficient to improve neuronal autophagy and cognitive impairments in aged mice. Mechanistically, we found that OCN promotes neuronal autophagy in the hippocampus by the induction of PC-dependent cAMP response element-binding protein (CREB) signaling pathway. Altogether, this study proposes a novel paradigm for blood factor-neuron communication dependent on a neuronal PC/autophagy axis by identifying a novel regulatory pathway fostering cognitive fitness and providing the foundation for autophagy-based therapeutic strategies to treat age-related cognitive dysfunction.
2024-11-07 | PXD056975 | Pride
Project description:To investigate the possible roles on mitotic/microtubule-related genes during hippocampal neuron differentiation, we dissected E18.5 mouse embryonic hippocampi, cultured neurons in vitro and collected total RNA samples from different timepoints of differentiation.
2018-06-03 | GSE113680 | GEO
Project description:To investigate if Fibcd1 mediates CSPG signalling to neurons, we established a primary mouse hippocampal neuron culture plated +/- a coating of CSPGs. After determining that Fibcd1 KO neurons are partially resistant to CSPG signals, we sought to identify the transcriptional finger print of CSPG-Fibcd1 signalling by nulk RNA-seq.
2022-04-25 | GSE201289 | GEO
Project description:We report genome-wide binding targets of REF6, a H3K27me3 demethylase and also high-throughput profiling of histone modifications of H3K27me3 in Arabidopsis flowers. Using chromatin-immunoprecipitation followed by high-throughput sequencing, we mapped thousands of binding targets of REF6 in flowers and in addition, we used a second fixative, DSG to capture more indirect targets of REF6. In order to investigate the function of indirect binding of REF6 represented H3K27me3 demethylase, the binding targets of DNA binding domain deleted REF6 were identified in the triple mutant background in which REF6 and its two homologs were mutated. Meanwhile, the H3K27me3 marked regions in both wild type and triple mutant flowers were defined. By analyzing the differentially enriched H3K27me3 region and REF6 binding profile, we found that REF6 functions to determine the boundary of H3K27me3 regions. Comparison of binding profiles of REF6 in flowers and in seedlings (ref) revealed a tissue-specific binding manner. More importantly, we found that the indirect binding of REF6 is mediated by trans factors and this indirect binding is crucial for REF6 function, especially in reproductive organs in Arabidopsis. Our results provide novel molecular insights into REF6 functions.
2018-07-09 | GSE106942 | GEO
Project description:We induced over-expression and under-expression of Camk2b in cultured rat hippocampal neurons through transfection with lentivirus plasmids. Then isobaric tag for relative and absolute quantitation (iTRAQ)-based quantitative proteomics followed by bioinformatics analyses were carried out to explore the impacts of Camk2b dysexpression on the proteome of the neurons.
2022-07-27 | PXD033931 |
Project description:Ongoing neuronal activity during development and plasticity acts to refine synaptic connections and contributes to the induction of plasticity and ultimately long term memory storage. Activity-dependent post-transcriptional control of mRNAs occurs through transport to axonal and dendritic compartments, local translation, and mRNA stability. We have identified a mechanism that contributes to activity-dependent regulation of mRNA stability during synaptic plasticity. In this study we demonstrate rapid, post-transtriptional control over process-enriched mRNAs by neuronal activity. Systematic analysis of the 3'-UTRs of destablized transcripts, identifies enrichment in sequence motifs corresponding to miRNA binding sites. The miRNAs that were identified, miR-326-3p/miR-330-5p, miR-485-5p, miR-666-3p, and miR-761 are predicted to regulate networks of genes important in plasticity and development. We find that these miRNAs are developmentally regulated in the hippocampus, many increasing by postnatal day 14. We further show that miR-485-5p controls NGF-induced neurite outgrowth in PC12 cells, tau expression, and axonal development in hippocampal neurons. miRNAs can function at the synapse to rapidly control and affect short- and long-term changes at the synapse. These processes likely occur during refinement of synaptic connections and contribute to the induction of plasticity and learning and memory. 12 hippocampal cell culture samples analysed, 3 coverslips pooled per sample. Treatments are as follows: Block: an inhibitor cocktail containing 50 µM D-APV, 40 µM CNQX, and 100 nM TTX for 3 hrs Activity: 50 µM bicuculline (BiC)/500 µM 4-Aminopyridine ActD: 25 µM actinomycin D
2014-03-12 | E-GEOD-55780 | biostudies-arrayexpress