Ccnyl1 is a newly identified genes, but the founction of which remained unclear, here we used the Ccnyl1 knockout mice to finding clues for its functional roles
CCNYL1, but Not CCNY, Cooperates with CDK16 to Regulate Spermatogenesis in Mouse.
Specimen part
View SamplesTo find out genes regulated by geranylgeraniol (GGOH) treatment in peritoneal macrophage, we compared gene expression of cells treated with 200ng ml LPS and 250 micromolar compactin versus 200ng ml LPS, 250 micromolar compactin and 100micromolar GGOH.
Sufficient production of geranylgeraniol is required to maintain endotoxin tolerance in macrophages.
Specimen part, Treatment
View SamplesMyoblasts harvested from a postnatal day 2 WT and Foxj3 KO litter.
No associated publication
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View SamplesInitially, we had compared gene expression differences in the embryonic gonads (E13.5) of the 129 and M19 strains by performing microarray analysis. These studies allowed us to identify downregulation of expression of the D19Bwg1357e, Zfp162 and Cox15 genes in the M19 strain.
No associated publication
Sex, Specimen part
View SamplesWe have determined the consequences of ICN1 overexpression from retroviral vectors introduced into bone marrow cells.
No associated publication
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View Samplesgamma delta intraepithelial lymphocytes were isolated from the colons of DSS-treated and untreated mice. Total RNAs were isolated and compared by Affymetrix DNA microarray.
No associated publication
No sample metadata fields
View SamplesThe mammalian gastrointestinal tract harbors thousands of bacterial species that include symbionts as well as potential pathogens. The immune responses that limit access of these bacteria to underlying tissue remain poorly defined.
Gammadelta intraepithelial lymphocytes are essential mediators of host-microbial homeostasis at the intestinal mucosal surface.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Combined Gene Expression and RNAi Screening to Identify Alkylation Damage Survival Pathways from Fly to Human.
Specimen part, Treatment
View SamplesDespite the high toxicity, alkylating agents are still at the forefront of several clinical protocols used to treat cancers. In this study, we investigated the mechanisms underlying alkylation damage responses, aiming to identify novel strategies to augment alkylating therapy efficacy. In this pursuit, we compared gene expression profiles of evolutionary distant cell types (D. melanogaster Kc167 cells, mouse embryonic fibroblasts and human cancer cells) in response to the alkylating agent methyl-methanesulfonate (MMS). We found that many responses to alkylation damage are conserved across species independent on their tumor/normal phenotypes. Key amongst these observations was the protective role of NRF2-induced GSH production primarily regulating GSH pools essential for MMS detoxification but also controlling activation of unfolded protein response (UPR) needed for mounting survival responses across species. An interesting finding emerged from a non-conserved mammalian-specific induction of mitogen activated protein kinase (MAPK)-dependent inflammatory responses following alkylation, which was not directly related to cell survival but stimulated the production of a pro-inflammatory, invasive and angiogenic secretome in cancer cells. Appropriate blocking of this inflammatory component blocked the invasive phenotype and angiogenesis in vitro and facilitated a controlled tumor killing by alkylation in vivo through inhibition of alkylation-induced angiogenic response, and induction of tumor healing.
Combined Gene Expression and RNAi Screening to Identify Alkylation Damage Survival Pathways from Fly to Human.
Specimen part, Treatment
View SamplesNutritional and genetic risk factors for intestinal tumors are additive on mouse tumor phenotypes, demonstrating that diet and genetic factors impact risk by distinct combinatorial mechanisms. We analyzed expression profiles of small intestine crypts and villi from mice with nutritional and genetic risk factors. The results advanced our understanding of the mechanistic roles played by major risk factors in the pathogenesis of intestinal tumors.
Paneth cell marker expression in intestinal villi and colon crypts characterizes dietary induced risk for mouse sporadic intestinal cancer.
Age, Specimen part
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