Purpose: This study aimed to identify a novel biomarker or a target of treatment for colorectal cancer (CRC).
Clinical significance of osteoprotegerin expression in human colorectal cancer.
Specimen part
View SamplesHepatocyte IKK deficiency worsens HCFD-induced NASH in male but not female mice.
Gender difference in NASH susceptibility: Roles of hepatocyte Ikkβ and Sult1e1.
Sex, Specimen part
View SamplesWe aimed to identify a reprogramming factor in mammalian oocytes. DJ-1 is one candidate gene of the factor. Inhibition of DJ-1 function in nuclear transfer embryos affected developmental abilities. The downstream effect of this DJ-1 inhibition was examined using microarrays.
Identification and characterization of an oocyte factor required for development of porcine nuclear transfer embryos.
Disease
View SamplesThe differentiation of preadipocytes into adipocytes is controlled by several transcription factors, including peroxisome proliferator-activated receptor (PPAR) and CCAAT/enhancer-binding protein (C/EBP), which are known as master regulators of adipogenesis. BCL11B is a zinc finger-type transcription factor that regulates the development of the skin and central nervous and immune systems. Here, we found that BCL11B was expressed in the white adipose tissue (WAT), particularly the subcutaneous WAT and that BCL11B/ mice had a reduced amount of subcutaneous WAT. During adipogenesis, BCL11B expression transiently increased in 3T3-L1 preadipocytes and mouse embryonic fibroblasts (MEFs). The ability for adipogenesis was reduced in BCL11B knockdown 3T3-L1 cells and BCL11B/ MEFs, whereas the ability for osteoblastogenesis was unaffected in BCL11B/ MEFs. Luciferase reporter gene assays revealed that BCL11B stimulated C/EBP activity. Furthermore, the expression of downstream genes of the Wnt/-catenin signaling pathway was not suppressed in BCL11B/ MEFs during adipogenesis. Thus, this study identifies BCL11B as a novel regulator of adipogenesis, which works, at least in part, by stimulating C/EBP activity and suppressing the Wnt/-catenin signaling pathway.
Identification of BCL11B as a regulator of adipogenesis.
Specimen part
View SamplesThe Toll-like receptor 4 (TLR4) pathway is important for tumor-initiating cells. We used microarrays to obtain gene profiling data in order to increase understanding of the pathways.
Reciprocal regulation by TLR4 and TGF-β in tumor-initiating stem-like cells.
Sex, Specimen part
View SamplesMice with homozygous null mutations in the HDL receptor (SR-BI) and apoE genes (SR-BI KO/apoE double KO (dKO) mice) spontaneously develop occlusive, atherosclerotic coronary artery disease (CAD) and die prematurely (50% mortality at 42 days of age) on standard chow diet feeding. Microarray analysis was performed to investigate the changes in gene expression profiles during the development of spontaneous severe CAD, which includes myocardial infarction and heart failure. These data will provide new insights in understanding the pathophysiology of CAD.
Identification of apolipoprotein D as a cardioprotective gene using a mouse model of lethal atherosclerotic coronary artery disease.
Age, Specimen part
View SamplesExpression of key transcription factors Klf4, Oct3/4, Sox2, and c-Myc (KOSM) in embryonic stem cells can reprogram somatic cells into pluripotent cells. We found that two histone variants, TH2A and TH2B, and histone chaperone Npm enhance the KOSM-dependent generation of induced pluripotent cells (iPSCs) and produce iPSCs only with Klf4 and Oct3/4. To identify directly affected genes by these histone variants during reprogramming, we carried out gene expression profiling of MEFs overexpressing TH2A/TH2B/Npm and TH2A/TH2B deficient MEFs after infection with retroviruses expressing KOSM.
Histone variants enriched in oocytes enhance reprogramming to induced pluripotent stem cells.
Specimen part
View SamplesGene expression of Ethanol-treated hepatocytes from WT and transglutaminase 2 knockout mice
Role of transglutaminase 2 in liver injury via cross-linking and silencing of transcription factor Sp1.
No sample metadata fields
View SamplesTo clarify the downstream signal pathway of EML4-ALK in NSCLC, we performed Affymetrix GeneChip analysis using ALK inhibitor CH5424802-treated NCI-H2228 xenograft tumors, and comprehensively characterized the gene expression regulated by inhibition of activated ALK.
CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant.
Specimen part
View SamplesGene expression profiling was carried out in six (wild type, ß2SP+/-, ß2SP-/-, SMAD3+/-, SMAD3-/- and ß2SP+/-/ SMAD3+/-) different mouse knockout embryonic fibroblast (MEF) cells. Beta-2-spectrin (ß2SP) is a dynamic intracellular non-pleckstrin homology (PH)-domain protein that belongs to a family of polypeptides that have been implicated in conferring cell polarity. Spectrins have been linked to multiple signaling pathways, including cell cycle regulation, DNA repair and TGFß signaling. In this study, we report a major role of the TGFß/Smad3 adaptor ß2-Spectrin in conserving genomic integrity from alcohol-induced DNA damage and describe a novel pathway that protects genomes from genotoxic stresses. To determine the mechanism for the oncogenic switch, and whether it is related to the role of ß2SP in TGF-ß signaling transduction or secondary to its cytoskeletal functions, we analyzed disruption of two elements of the TGF-ß pathway by generating double heterozygous Sptbn1+/-/Smad3+/- mice. Overall design: Whole-transcriptome RNA sequencing MEF cells of the following genotypes was carried out on an Illumina HiSeq 2000 sequencer: wildtype, heterozygous Beta-2-spectrin knockout (ß2SP+/-), homozygous Beta-2-spectrin knockout (ß2SP-/-), heterozygous SMAD3 (Mothers against decapentaplegic, Drosophila, Homolog of 3, SMAD3+/-), homozygous knockout SMAD3-/-, and double heterozygous mutation of Beta-2-spectrin and SMAD3 (ß2SP+/-/ SMAD3+/-).
TGF-β/β2-spectrin/CTCF-regulated tumor suppression in human stem cell disorder Beckwith-Wiedemann syndrome.
No sample metadata fields
View Samples