Molecular Neurobiology of Loss Part 2
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA858032 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20096904_1.fastq.gz | Fastqsanger.gz | |||
| SRR20096904_2.fastq.gz | Fastqsanger.gz | |||
| SRR20096905_1.fastq.gz | Fastqsanger.gz | |||
| SRR20096905_2.fastq.gz | Fastqsanger.gz | |||
| SRR20096906_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Molecular Neurobiology of Loss Part 1
| PRJNA858031 | ENA
Project description:Molecular Neurobiology of Loss
| PRJNA858028 | ENA
Project description:Psychological loss is a common experience that erodes well-being and negatively impacts quality of life. The molecular underpinnings of loss are poorly understood, making it challenging to develop treatment strategies. Here, we investigate the mechanisms of loss using an enrichment removal (ER) paradigm in rats. RNA-seq was used to investigate the molecular landscape of the basolateral amygdala (BLA), a region previously implicated in loss, in adult male Sprague-Dawley rats following ER. Rats were subjected to standard housing (SH) for 6 weeks, environmental enrichment (EE) for 6 weeks, or enrichment removal (ER), consisting of 4 weeks of EE followed by 2 weeks of removal into impoverished conditions (n=10/pool/group). Rats were then perfused and micropunches were collected from the basolateral amygdala (BLA) for bulk RNA-seq.
2022-07-15 | GSE208028 | GEO
Project description:Psychological loss is a common experience that erodes well-being and negatively impacts quality of life. The molecular underpinnings of loss are poorly understood, making it challenging to develop treatment strategies. Here, we investigate the mechanisms of loss using an enrichment removal (ER) paradigm in rats. RNA-seq was used to investigate the molecular landscape of the basolateral amygdala (BLA), a region previously implicated in loss, in adult male Sprague-Dawley rats following ER. Rats were subjected to standard housing (SH) for 6 weeks, environmental enrichment (EE) for 6 weeks, or enrichment removal (ER), consisting of 4 weeks of EE followed by 2 weeks of removal into impoverished conditions (n=6/group). Rats were then perfused and micropunches were collected from the basolateral amygdala (BLA) for bulk RNA-seq.
2022-07-15 | GSE208026 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-07-15 | GSE208029 | GEO
Project description:Psychological loss is a common experience that erodes well-being and negatively impacts quality of life. The molecular underpinnings of loss are poorly understood. Here, we investigate the mechanisms of loss using an environmental enrichment removal (ER) paradigm in male rats. The basolateral amygdala (BLA) was identified as a region of interest, demonstrating differential Fos responsivity to ER and having an established role in stress processing and adaptation. A comprehensive multi-omics investigation of the BLA, spanning multiple cohorts, platforms, and analyses, revealed alterations in microglia and the extracellular matrix (ECM). Follow-up studies indicated that ER decreased microglia size, complexity, and phagocytosis, suggesting reduced immune surveillance. Loss also substantially increased ECM coverage, specifically targeting perineuronal nets surrounding parvalbumin interneurons, suggesting decreased plasticity and increased inhibition within the BLA following loss. Behavioral analyses suggest that these molecular effects are linked to impaired BLA salience evaluation, leading to a mismatch between stimulus and reaction intensity. These loss-like behaviors could be rescued by depleting BLA ECM during the removal period, helping us understand the mechanisms underlying loss and revealing novel molecular targets to ameliorate its impact.
| S-EPMC10914625 | biostudies-literature
Project description:To gain molecular insight into the prenatal neurobiology of DS, we performed single-nucleus sequencing, spatial transcriptomics, and proteomics on mid-gestational prenatal human brain tissue. We captured altered expression dynamics of lineage commitment genes in DS neural progenitor cells, which suggest changes to the fate and functionality of neuronal and glial cells.
2025-07-11 | GSE280175 | GEO
Project description:To gain molecular insight into the prenatal neurobiology of DS, we performed single-nucleus sequencing, spatial transcriptomics, and proteomics on mid-gestational prenatal human brain tissue. We captured altered expression dynamics of lineage commitment genes in DS neural progenitor cells, which suggest changes to the fate and functionality of neuronal and glial cells.
2025-07-11 | GSE280170 | GEO
Project description:Distinct genetic abnormalities such as TP53 deletion at 17p13.1, have been identified as having an adverse prognostic relevance in B-cell chronic lymphocytic leukemia (B-CLL). Conventional cytogenetic studies have shown that TP53 deletion in B-CLL is associated predominantly with 17p loss resulting from complex chromosomal rearrangements. We performed genome-wide DNA (SNPs arrays), fluorescence in situ hybridization (FISH) and gene expression profiling (GEP) analyses to investigate the significance of 17p loss in a panel of 71 genetically well-characterized B-CLLs in Binet stage A, 18 of which carried a TP53 monoallelic deletion. Combined SNP arrays and FISH approaches showed 17p loss in all of the TP53-deleted cases, with breakpoints scattered along the 17p11.2 region. Mutations in exons 5 to 9 of TP53 were found in 9/12 deleted samples. GEP of 60 B-CLLs, including 7 patients with 17p loss, identified 40 differentially expressed genes in 17p- versus 17p normal samples, 35 of which were down-regulated in 17p- tumors. The majority (30/35) of these transcripts, including putative tumor suppressor genes, mapped to 17p. Overall, these data indicate that, beside TP53 deletion, the concomitant loss of 17p arm may contribute to the strong negative prognostic impact known to be associated with this lesion in B-CLL. This SuperSeries is composed of the following subset Series: GSE9992: Molecular and transcriptional characterization of chromosome 17p loss in chronic lymphocytic leukemia, experiment A GSE11036: Molecular and transcriptional characterization of chromosome 17p loss in chronic lymphocytic leukemia, experiment B Keywords: SuperSeries Refer to individual Series
2008-11-11 | E-GEOD-11038 | biostudies-arrayexpress
Project description:Molecular and transcriptional characterization of chromosome 17p loss in chronic lymphocytic leukemia
| PRJNA107133 | ENA