A model system of Potyvirus turnip mosaic virus and Arabidopsis was used in this experiment. GFP-tagged virus supplied a visualized marker for us to localize the viral infection foci and its expansion on leaf under UV light. Initially, we dissect an individual infection focus and its adjacent region into four parts and define those four parts as zone 0, 1, 2, and 3, which represented different viral infection stages respectively. Corresponding fours parts were also dissected from control plant treated with turnip leaf sap only. This process was replicated three times totally.
Spatial analysis of arabidopsis thaliana gene expression in response to Turnip mosaic virus infection.
Age, Specimen part
View SamplesA large-scale parallel expression analysis was conducted to elucidate Mla-specified responses to powdery mildew infection using 22K Barley1 GeneChip probe arrays. Our goal was to identify genes differentially expressed in incompatible (resistant) vs. compatible (susceptible) and Mla-specified Rar1-dependent vs. -independent interactions. A split-split-plot design with 108 experimental units (3 replications x 2 isolates x 3 genotypes x 6 time points) was used to profile near-isogenic lines containing the Mla1, Mla6, and Mla13 resistance specificities in response to inoculation with the Blumeria graminis f. sp. hordei (Bgh) isolates 5874 (AvrMla1, AvrMla6) and K1 (AvrMla1, AvrMla13).
Interaction-dependent gene expression in Mla-specified response to barley powdery mildew.
Age, Specimen part, Disease, Disease stage, Cell line, Time
View SamplesGlycine max and Phytophthora sojae infected Glycine max Transcriptome
No associated publication
Specimen part
View SamplesThe project was aim of search the different mechanism of resoonse to soybean cyst nematode and mining the candidate resisitance genes from next generation sequencing
No associated publication
Specimen part, Disease, Disease stage
View SamplesExpression profiling in Rpp2-resistant (PI230970) and susceptible (Embrapa-48) plant lines to soybean rust from infection to symptom development
Distinct Biphasic mRNA Changes in Response to Asian Soybean Rust Infection
Specimen part, Time
View SamplesTranscriptome seqeunecing on 16 paired HCCs and non-tumorous livers to investigate the effect of HBV integration
No associated publication
No sample metadata fields
View Samplesold and young human cardiac fibroblasts plus those treated with rapamycin and methionine restriction or a combination of both
No associated publication
Sex, Specimen part
View SamplesNo description.
No associated publication
No sample metadata fields
View SamplesPTEN encodes a lipid phosphatase that is underexpressed in many cancers owing to deletions, mutations or gene silencing. PTEN dephosphorylates phosphatidylinositol 3,4,5-triphosphate (PIP3), thereby opposing the activity of class I phosphatidylinositol 3-kinases (PI3Ks) that mediate growth and survival factors signaling through PI3K effectors such as AKT and mTOR. To determine whether continued PTEN inactivation is required to maintain malignancy, we generated an RNAi-based transgenic mouse model that allows tetracycline-dependent regulation of PTEN in a time- and tissue-specific manner. Postnatal PTEN knockdown in the hematopoietic compartment produced highly disseminated T-cell leukemia (T-ALL). Surprisingly, reactivation of PTEN mainly reduced T-ALL dissemination but had little effect on tumor load in hematopoietic organs. Lymphoma infiltration into the intestine was dependent on CCR9 G-protein coupled receptor (GPCR) signaling, which was amplified by PTEN loss. Our results suggest that in the absence of PTEN, GPCRs may play an unanticipated role in driving tumor growth and invasion in an unsupportive environment. They further reveal that the role of PTEN loss in tumor maintenance is not invariant and can be influenced by the tissue microenvironment, thereby producing a form of intratumoral heterogeneity that is independent of cancer genotype.
No associated publication
No sample metadata fields
View SamplesObesity, an immense epidemic affecting approximately half a billion adults, has doubled in prevalence in the last several decades. Epidemiological data support that obesity due to intake of a high-fat, western diet increases the risk of colon cancer; however, the mechanisms underlying this risk remain unclear. Here, utilizing next generation RNA sequencing, we aimed to determine the high-fat diet mediated gene expression profile in mouse colon and the AOM/DSS model of colon cancer.
No associated publication
Sex, Specimen part, Disease, Cell line, Treatment
View Samples