Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DIA-Brain-aged- target gene knockout mice

ABSTRACT: The differences between wild-type mice and target gene knockout mice were analyzed by proteomic tests.

ORGANISM(S): Mus Musculus

SUBMITTER: Xiaozhi Liu

PROVIDER: PXD059745 | iProX | Mon Jan 13 00:00:00 GMT 2025

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Publications

Downregulation of Hmox1 and Rpgrip1l Expression Linked to Risk-Taking Behavior, Reduced Depressive Symptoms, and Diminished Novelty Socialization in SUMO1 Knockout Mice.

Dai Qiwei Q Wang Yuxiang Y Xu Hongbin H Dong He H Nie Fang F Zhang Lianxue L Liu Xiaozhi X Li Zhiqing Z

Cellular and molecular neurobiology 20250401 1

SUMO1 is involved in the normal physiological functions of the nervous system and is also associated with the development of neurodegenerative diseases. Whereas, the effects and underling mechanisms of SUMO1 knockout (SUMO1- KO) on emotion- and cognition -related behaviors remain unexplored. We investigated changes in depression-like behaviors, social interaction, and cognition in SUMO1-KO mice compared to wild-type (WT) controls using the open-field test, tail suspension test, three-chamber tes ...[more]

PMID: 40169460

Similar Datasets

Analyzing gene expression profiles in the brain of miR-137 knockout mice versus wild-type mice

Project description:We conducted this experiment using mice with a systemic knockout of miR-137. At 14 days post-birth, we sacrificed the mice and extracted key organs, including the brain. To assess the impact of miR-137 knockout on brain gene expression, we extracted RNA from the livers of both wild-type and knockout mice and analyzed it using microarray.

2025-05-15 | GSE248675 | GEO

Proteomic analysis of removed hippocampal and cortex brain regions in control and conditional gene knockout mice

Project description:Hippocampaus and cortex brain regions of control mice and conditional knockout mice were removed to do the test

2024-12-31 | PXD059322 |

PD-1 Knockout Engineered T Cells for Advanced Colorectal Cancer with MSI high expression

Project description:Interventions: experimental group :PD-1 Knockout Engineered T Cells Primary outcome(s): Number of participants with Adverse Events and/or Dose Limiting Toxicities as a Measure of Safety and tolerability of dose of PD-1 Knockout T cells using Common Terminology Criteria for Adverse Events (CTCAE v4.0) in patients Study Design: historical control

| 2662961 | ecrin-mdr-crc

AQP8 knockout project - 2DE of wild and AQP8 knockout mice colon

Project description:2DE of wild and AQP8 knockout mice colon

2010-07-01 | PRD000252 | Pride

Gene expression changes in Dhcr7 knockout brain, lung and liver at E18.5 compared to wild-type embryos

Project description:The genetic defect underlying the human Smith-Lemli-Opitz dysmorphological disorder is loss-of-function mutations affecting the cholesterol synthesis enzyme dehydrocholesterol delta7 reductase, DHCR7. Dhcr7 knockout mice recapitulate the biochemical characteristics, but all knockout pups die within 14h of birth. Tissues of knockout mice accumulate the precursor sterol, 7-dehydrocholesterol, and show reduced levels of cholesterol (J. Clin. Invest. (2001) 108: 905-915). We compared the global gene expression changes in lung, liver and brain from knockout mice to those seen from organs harvested from same-pregnancy wild-type embryos, harvested before birth (E18.5). Since the P0 knockout pups die, we expected that there would be significant changes in gene expression between knockout and wild-type organs, and further comparing the altered genes in common to brain, lung and liver would point to a common mechanistic pathway where disruption of normal sterol synthesis in all cells leads to pathophysiology. Remarkably, these data show that the global gene expression between knockout and wild-type organs is hardly altered, despite the complete loss of cholesterol synthesis. There are so few genes that are altered, and furthermore, those that are altered are very limited in sharing similarities in all three tissues. This suggests that disorganized gene expression is not the cause of the early neonatal lethality.

2012-08-02 | GSE39811 | GEO

Effect of aryl hydrocarbon receptor (Ahr) gene knockout on expression profiles of aged (18-month-old) murine hematopoietic stem cells

Project description:As part of a study of the role of the aryl hydrocarbon receptor (Ahr) in maintenance and senescence of hematopoietic stem cells (HSC), global gene expression profiling was done with HSC isolated from 18-month-old Ahr-knockout and wild-type mice. HSC from aged AhR-KO mice had changes in expression of many genes related to HSC maintenance, consistent with the phenotype observed in aging Ahr-KO mice: decreased survival rate, splenomegaly, increased circulating white blood cells, hematopoietic cell accumulation in tissues, anemia, increased numbers of stem/progenitor and lineage-committed cells in bone marrow, decreased erythroid progenitor cells in bone marrow, and decreased self-renewal capacity of HSC. 10 samples: 5 Ahr knockout, 5 wild-type

2015-03-28 | E-GEOD-67378 | biostudies-arrayexpress

Gene expression changes in Dhcr7 knockout brain, lung and liver at E18.5 compared to wild-type embryos

2012-08-01 | E-GEOD-39811 | biostudies-arrayexpress

Proteomic analysis of UCHL1 conditional knockout mice

Project description:Proteomic analysis of osteoclast precursor cells of UCHL1 conditional knockout mice and wild-type mice was performed

2024-08-14 | PXD052578 |

Hippocampal gene expression in aged and young HSD1 knockout mice

Project description:Mice deficient in the glucocorticoid-regenerating enzyme 11β-HSD1 resist age-related spatial memory impairment. To investigate the mechanisms/pathways involved, we used microarrays to identify differentially expressed hippocampal genes that associate with cognitive ageing and 11β-HSD1. Aged wild-type mice were separated into memory-impaired and unimpaired relative to young controls according to their performance in the Y-maze. All individual aged 11β-HSD1-deficient mice showed intact spatial memory. The majority of differentially expressed hippocampal genes were increased with ageing (e.g. immune/inflammatory response genes) with no genotype differences. However, the neuronal-specific transcription factor, Npas4 and immediate early gene, Arc were reduced (relative to young) in the hippocampus of memory-impaired but not unimpaired aged wild-type or aged 11β-HSD1-deficient mice. Quantitative RT-PCR and in situ hybridization confirmed reduced Npas4 and Arc mRNA expression in memory-impaired aged wild-type mice. These findings suggest that 11β-HSD1 may contribute to the decline in Npas4 and Arc mRNA levels associated with memory impairment during ageing, and that decreased activity of synaptic plasticity pathways involving Npas4 and Arc may, in part, underlie the memory deficits seen in cognitively-impaired aged wild-type mice.

2015-11-23 | GSE68515 | GEO

Gene expression in brain of interleukin-18 knockout mice at 6 and 12 weeks of age

Project description:Interleukin-18 knockout mice had metabolic syndromes after 24 weeks of age. We examined gene expression profiles in mice brain using genome-wide microarray technology, and compared gene expression profiles between wild-type and interleukin-18 knockout mice. To verify responsible molecules involved in metabolic syndromes such as obesity, we compared the gene expression levels at 6 and 12 weeks of age, and picked up them whose expression was more than 2-fold increase or less than 1/2-fold decrease.

2019-12-20 | GSE64307 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data