Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27251374_1.fastq.gz | Fastqsanger.gz | |||
| SRR27251374_2.fastq.gz | Fastqsanger.gz | |||
| SRR27251375_1.fastq.gz | Fastqsanger.gz | |||
| SRR27251375_2.fastq.gz | Fastqsanger.gz | |||
| SRR27251376_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Gestational and perinatal disruption of neural development increases the risk of developing schizophrenia (SCZ) later in life. Embryonic day 17 (E17) methylazoxymethanol (MAM) treatment leads to histological, physiological and behavioural abnormalities in post-puberty rats resembling those described in SCZ patients. However, the validity of E17 MAM-exposed mice as a SCZ model has not been explored. Here we treated E17 C57BL/6 mouse dams with various dosages of MAM. We found that this mouse strain was more vulnerable to MAM treatment than rats and there were gender difference in behavioural abnormalities, histological changes and prefrontal cortical gene expression profiles in MAM (7.5 mg/kg)-exposed mice. Both male and female MAM-exposed mice had deficits in prepulse inhibition but were normal in social interaction and novel object recognition tasks. Female MAM-exposed mice were hyperactive in spontaneous locomotion while male mice were normal. Consistently, only female MAM-exposed mice exhibited reduced brain weight, decreased size of prefrontal cortex (PFC) and enlarged lateral ventricles. Transcriptome analysis of the PFC revealed that there were more differentially expressed genes in female MAM-exposed mice than those in male mice. Moreover, expression of Pvalb, Arc and genes in their association networks were downregulated in the PFC of female MAM-exposed mice. These results show that E17 MAM-exposure in C57BL/6 mice leads to behavioural changes that mimic positive symptoms and sensorimotor gating deficits associated with SCZ. MAM-exposed female mice may be used to study gene expression changes, inhibitory neural circuit dysfunction and glutamatergic synaptic plasticity deficits related to SCZ.
2019-01-09 | GSE108925 | GEO
Project description:Methylazoxymethanol (MAM), the genotoxic metabolite of the cycad azoxyglucoside cycasin, induces genetic alterations in bacteria, yeast, plants, insects and mammalian cells, but adult nerve cells are thought to be unaffected. We show that the brains of young adult mice treated with a single systemic dose of MAM display DNA damage (O6-methylguanine lesions) that peaks at 48 hours and decline to near-normal levels at 7 days post-treatment. By contrast, at this time, MAM-treated mice lacking the gene encoding the DNA repair enzyme O6-methylguanine DNA methyltransferase (MGMT), showed persistent O6-methylguanine DNA damage. The DNA damage was linked to cell-signaling pathways that are perturbed in cancer and neurodegenerative disease. These data are consistent with the established carcinogenic and developmental neurotoxic properties of MAM in rodents, and they support the proposal that cancer and neurodegeneration share common signal transduction pathways. They also strengthen the hypothesis that early life exposure to the MAM glucoside cycasin has an etiological association with a declining, prototypical neurodegenerative disease seen in Guam, Japan, and New Guinea populations that formerly used the neurotoxic cycad plant for medicine and/or food. Exposure to environmental genotoxins may have relevance to the etiology of related tauopathies, notably, Alzheimer’s disease, as well as cancer. Mouse brains from eleven-week-old male C57BL6 wild-type and Mgmt-/- mice were exposed to either MAM or Vehicle for 6 hr, 24 hr, 48 hr, 168 hr. Five or six mice per group for a total of 94 mice.
2013-01-10 | E-GEOD-26600 | biostudies-arrayexpress
Project description:Macrophages form a primary immune cells population in tumor tissues and malignant ascites microenvironment (MAM). They can be activated and polarized into tumor-associated macrophages (TAM) by the embedded environment and promote tumor progression and metastasis However, the molecular mechanisms of MAM in macrophage polarization and the effects on epithelial ovarian cancer (EOC) metastatic progression remain elusive. Here, we found that that MAM modulates RhoA-GTPase-F-actin-Hippo signaling cascade in facilitating M2-like macrophage polarization that, in turn, promotes tumor dissemination. PUFA enriched magligant ascites microenvironment promote macrophage lipid oxidative phosphorylation and supression RhoA-GTPase-Yap1 axis. Genetic ablation Yap1 in macrophage exhibited M2-like polarization and enhanced ovrian tumor dissemination. Pharmacology inhibit Mst1/2 could rescue M2-like TAM polarization in MAM and alter the lipid oxidation of macrophages in MAM, more importantly, inhibit ovarian metastatic properties. Through comparasion primary TAM (P-TAM) and metastasis TAM (M-TAM), we proved that Hippo-Yap1 siganl results M-TAM with high M2/M1 ratio. These findings implicate critical functions of PUFA modulate RhoA-Hippo axis in facility TAM polarization and also suggest manipulation of PUFA metabolism or RhoA-Hippo siganl as a therapeutic strategy aganist EOC metastasis.
2024-05-01 | GSE175552 | GEO
Project description:Methylazoxymethanol (MAM), the genotoxic metabolite of the cycad azoxyglucoside cycasin, induces genetic alterations in bacteria, yeast, plants, insects and mammalian cells, but adult nerve cells are thought to be unaffected. We show that the brains of young adult mice treated with a single systemic dose of MAM display DNA damage (O6-methylguanine lesions) that peaks at 48 hours and decline to near-normal levels at 7 days post-treatment. By contrast, at this time, MAM-treated mice lacking the gene encoding the DNA repair enzyme O6-methylguanine DNA methyltransferase (MGMT), showed persistent O6-methylguanine DNA damage. The DNA damage was linked to cell-signaling pathways that are perturbed in cancer and neurodegenerative disease. These data are consistent with the established carcinogenic and developmental neurotoxic properties of MAM in rodents, and they support the proposal that cancer and neurodegeneration share common signal transduction pathways. They also strengthen the hypothesis that early life exposure to the MAM glucoside cycasin has an etiological association with a declining, prototypical neurodegenerative disease seen in Guam, Japan, and New Guinea populations that formerly used the neurotoxic cycad plant for medicine and/or food. Exposure to environmental genotoxins may have relevance to the etiology of related tauopathies, notably, Alzheimer’s disease, as well as cancer.
2013-01-10 | GSE26600 | GEO
Project description:To determine the role of the hepatic microenvironment in HCC metastasis, we compared the gene expression profiles of 20 noncancerous surrounding hepatic tissues from two HCC patient groups, those with primary HCC together with venous metastasis which we termed a metastasis-inclined microenvironment (MIM) and those with HCC without detectable metastasis, which we termed a metastasis-averse microenvironment (MAM). There were a total of 20 cDNA microarrays performed, comparing 9 MIM or 11 MAM HCC patient samples to a common reference pool of 8 normal liver tissues.
2010-07-01 | E-GEOD-5093 | biostudies-arrayexpress
Project description:Input control for ChIP-seq on transgenic flies expressing mam-eGFP fusion proteins. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2024-02-27 | GSE258034 | GEO
Project description:ChIP-seq on transgenic flies expressing mam-eGFP fusion proteins. The IP was performed using an anti-GFP antibody. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2024-02-27 | GSE258572 | GEO
Project description:Background: The present study investigated a role of proteins from BET family (epigenetic readers) in schizophrenia-like abnormalities in MAM-E17 model of schizophrenia. Methods: An inhibitor of BET proteins, JQ1, was given during adolescence in postnatal days (P) 23-P30, and behavioral response (sensorimotor gating, recognition memory) and prefrontal cortex (mPFC) function (long-term potentiation (LTP), molecular and proteomic studies) were performed in adult males and females. Results: Deficits in sensorimotor gating and recognition memory were observed only in MAM-treated males. However, adolescent JQ1 treatment affected control, but MAM-treated groups in both sexes. Electrophysiological study showed an LTP impairment only in male MAM-treated animals, and JQ1 did not have any effect on LTP in the mPFC. In contrast, MAM did not affect immediate early gene expression (markers of neuronal and synaptic activity), but JQ1 altered them in both sexes. Proteomic study revealed alterations in MAM-treated groups only in males, while JQ1 affected both sexes. Conclusions: Prenatal MAM administration induced schizophrenia-like abnormalities only in males. In contrast, adolescent JQ1 treatment affected both sexes and induced behavioral changes in control groups, altered a markers of neuronal and synaptic activity and proteomic landscape in the mPFC of both groups (VEH- and MAM-treated). Thus, adolescent inhibition of BET family might change neuroplasticity in the mPFC.
2021-09-07 | PXD027050 | Pride
Project description:MAM (Microbial-Anti-Inflammatory Molecule) is a 14,5 kDa protein that is one of the best-known effector molecules with anti-inflammatory properties in Faecalibacterium duncaniae, a critical species in the human gut microbiota. Despite its importance, MAM function and molecular features remain poorly understood. Therefore, in this study, we sought to elucidate MAM's physiological importance. We investigated MAM localization using mass-spectrometry, immunogold labeling, and peptide secretion dynamics during bacterial growth. Bioinformatic analysis and microscopy further supported our understanding of MAM protein domain organization, interactions, and putative macromolecular assembly. Our results identified MAM as the most abundant protein in the cell envelope, and the second most abundant one in the overall proteome of F. duncaniae, with confirmed localization at the bacterial surface through immunogold labeling. Bioinformatics analysis highlights that MAM could comprise an N-terminal 21 residue leader peptide whose sequence contains all the motifs to be recognized and cleaved by a peptidase, followed by a 114 residue cargo peptide. Appropriately, in silico modeling suggests that the MAM leader peptide nicely accommodates the peptidase-domain-containing ABC transporter (PCAT) that is adjacent to MAM in the genome of F. duncaniae. After N-terminal excision, the cargo protein could be transported to the cell envelope via this PCAT, where it could assemble into a hexameric, pore-like structure, as revealed by AlphaFold3 modeling. Electron microscopy images of In situ F.duncaniae cells revealed a highly ordered lattice with repetitive units of hexamers. Moreover, an enriched fraction of MAM protein was obtained with in vitro LiCl extraction, exhibiting the same organizational pattern as the predicted hexameric organization. These findings provide the first comprehensive characterization and molecular export mechanisms of MAM as a key protein component of the F. duncaniae cell envelope, suggesting roles in cell structure, permeability, and communication with the host environment. It reveals a novel, lattice-like organization on the F. duncaniae cell envelope that may play a critical role in maintaining bacteria structure. This work introduces a novel discussion about the unique organization of the F.duncaniae cell envelope, having MAM as a key component for the bacteria, supporting the understanding of the unique biology of F. duncaniae and its potential as a next-generation probiotic or Live Biotherapeutics
2025-06-30 | PXD057939 | Pride
Project description:By isolating mitotic mitochondria-associated membrane (MAM) components and analysing them with mass spectrometry (MS), we identified 3,741 MAM components.
2024-07-30 | PXD041607 |