Ontology highlight
ABSTRACT:
PROVIDER: PRJNA544972 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: RARRES1 is proposed as tumor suppressor gene but its function is not clear yet. To elucidate RARRES1 function in carcinogenesis, we examine phenotype and genetic characteristics of the RARRES1 genetically knockout mice lung. Methods: Genetic profiles of RARRES1 wild type and knockout mouse lung tissues of embryonic day 19.5, 10-month-old, and 18-month-old mice were analyzed by whole genome and RNA sequencing in triplicate, using Illumina Hiseq X ten. Additionally, three lung tumors originated from RARRES1 knockout mice also examine using same platform. Results: RARRES1 knockout accelerate spontaneous lung carcinogenesis, with pluripotency of stem cells, Hippo signaling pathway, Wnt signaling pathway, and cell cycle related genes are significantly activated including Nanog, CDK1, Cyclin E. In addition, RARRES1 knockout induced lung cancer had rare oncogenic mutations, on the contrary, lung tissue progenitor cell, lung bipotent progenitor cell and AT2 type cell popularity increased. Conclusions: RARRES1 knockout accelerate spontaneous lung carcinogenesis through organ stem cell population enhancement with various stemness related gene set activation beside rare mutational driving.
2024-02-02 | GSE131161 | GEO
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
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. Dhcr7+/- females were mated with Dhcr+/- males, and timed pregnancy obtained. At E18.5, pregnant dams were sacrificed, and embryos harvested, organs removed and RNA extracted, and all embryos were genotyped. Matching wild-type and knockout embryos were taken from each pregnancy, and two females yielded all genotypes used herein.
2012-08-01 | E-GEOD-39811 | biostudies-arrayexpress
Project description:Proteomics of gastric mucosal tissues of H.pylori-infected DDIT4 knockout mice and wild-type mice
2023-12-25 | PXD048124 | iProX
Project description:Ctcf heterozygous knockout mice are susceptible to neoplasia in a broad range of tissues, including lymphoma, endometrial cancer, and non-small cell lung cancer. Retention of the wild type Ctcf allele in these tumors establishes CTCF as a haploinsufficient tumor suppressor gene. Both human tumors and normal murine tissues with CTCF disruption are characterized by genome-wide differences in DNA methylation relative to CTCF wild type tissues, indicating even modest disruption of CTCF broadly destabilizes DNA methylation in vivo. This cross species functional analysis identifies CTCF as a commonly mutated tumor suppressor gene and establishes a central role for DNA methylation stability in tumor suppression. RRBS sequencing of transgenic Ctcf heterozygous mice and wild-type litter mate whole lung tissue.
2014-07-30 | E-GEOD-48975 | biostudies-arrayexpress
Project description:Striatal and hippocampal tissues were dissected out from wild type and helios knockout mice to perform comparisions by pairs of genotypes. First the comparision between wild type and helios knockout mice using striatal tissues and the second comparision was made between wild type and helios knockout hippocampal tissues
2019-01-04 | GSE124641 | GEO
Project description:RNA-Seq of unseparated lung cells and primary mouse lung fibroblasts from wild-type and ST2 gene knockout mice
2023-01-04 | GSE197398 | GEO
Project description:Ventilator-induced lung injury in wild-type and jnk1 knockout mice
| PRJNA99853 | ENA
Project description:This study aims to compared RNA expression profiles between the skin tissues of IRF1 knockout (IRF-/-) mice and wild-type mice by microarray analysis. Male IRF1 knockout (IRF-/-) mice and wild-type mice (8 weeks old) were irradiated with a single 35-Gy dose of irradiation was administered to the treatment area at a rate of 750 cGy/min using a 6-MeV electron beam accelerator (Clinac 2100EX, Varian Medical Systems, Inc., CA). Skin tissues from irradiated areas were collected and subjected to RNA expression analysis.
2019-01-11 | GSE124895 | GEO
Project description:Gene Expression in wild type and CCR5 knockout mice with lung metastasis
| PRJNA224557 | ENA