Project description:Ex vivo colorectal adenocarcinoma samples were analysed by desorption electrospray ionisation using an Orbitrap mass spectrometer. The samples were analysed in negative mode over the m/z range 600-1000. Some of the samples presented in this dataset were analysed as part of [1]. The study makes available imzML files of profile and centroid mode data, as well as low- and high- resolution optical image files of H&E-stained sections. These files can be found in the zip file named after each tissue section. </p> Ref:</br> [1] Gerbig S, Golf O, Balog J, Denes J, Baranyai Z, Zarand A, Raso E, Timar J, Takats Z. Analysis of colorectal adenocarcinoma tissue by desorption electrospray ionization mass spectrometric imaging. Anal Bioanal Chem. 2012 Jun;403(8):2315-25. doi:10.1007/s00216-012-5841-x. PMID:22447214</br>
Project description:Taking the advantage that B16F10 cells retain the wild-type p53, we introduced the p53 partner into these cells, the p19Arf. Also, in order to induce a immune stimulation in experiments *in vivo*, we introduced the interferon-beta cDNA. This combination induced several benefits when compared to the use of these factors alone, as seen by propidium iodide staining, tunel staining, several gene expression analysis, tumor growth, mice survival, among others. Because of this, we had the interest to study the effects of the combination of p19Arf plus interferon-beta upon gene regulation of B16F10 cells, compared to the effects of these transgenes alone. Previous works from our group that show several benefits of p19Arf plus interferon-beta combination upon B16F10 cells are described in Merkel et al (2010) doi: 10.1186/1471-2407-10-316, Merkel et al (2013) doi:10.1038/cgt.2013.23 and Medrano et al (2016) doi: 10.1007/s00262-016-1807-8 .
Project description:Fungal effectors play important roles in inciting disease development on host plants. We identified an effector (Secreted in Xylem4, SIX4) in an Arabidopsis infecting isolate (Fo5176) of the root-infecting fungal pathogen Fusarium oxysporum and demonstrated this effector is required for full virulence. To explore the role of Fo5176_SIX4 we use whole transcriptome profiling of root tissues from plants overexpressing this effector (35sSIX4) versus wild-type (Col-0) plants after F. oxysporum infection. Published in DOI:10.1007/978-3-319-42319-7_4. Belowground Defence Strategies in Plants.
Project description:Soil cultivation of spring wheat cultivar Remus. <br>
Hydroponic sampling of exudates to search for the BNI MBOA (and related compounds)<br>
Quantify MBOA<br>
Search for other known BNIS<br>
Characterize exudate<br>
<br>
LC-HRMS according to 10.1007/s00216-025-05818-y<br>
Project description:Soil cultivation of 11 winter/summer/mixed wheat cultivars. <br>
Collection of irrigation water (leachates). <br>
Hydroponic sampling of exudates to search for the BNI MBOA (and related compounds)<br>
<br>
Aims: <br>
- Quantify MBOA<br>
- Search for other known BNIS<br>
- Characterize exudate<br>
<br>
LC-HRMS according to 10.1007/s00216-025-05818-y<br>
Project description:A functional genetic screen to identify genes causing tamoxifen resistance in an estrogen-dependent human breast cancer cell model was performed. By insertion of defective retrovirus into the genome, individual genetic changes were introduced at random in ZR-75-1 cells. Subsequently, infected cells were selected for their ability to proliferate while being exposed to tamoxifen, and from these cultures stable cell lines were established. The retrovirus insertion sites were mapped enabling the identification of several candidate breast cancer anti-estrogen resistance (BCAR) genes. By cDNA transfection of estrogen-dependent cells resulting in their transformation into a tamoxifen-resistant phenotype, proof was provided for the causative role of BCAR genes.A functional genetic screen to identify genes causing tamoxifen resistance in an estrogen-dependent human breast cancer cell model was performed. By insertion of defective retrovirus into the genome, individual genetic changes were introduced at random in ZR-75-1 cells. Subsequently, infected cells were selected for their ability to proliferate while being exposed to tamoxifen, and from these cultures stable cell lines were established. The retrovirus insertion sites were mapped enabling the identification of several candidate breast cancer anti-estrogen resistance (BCAR) genes identified. By cDNA transfection of estrogen-dependent cells resulting in their transformation into a tamoxifen-resistant phenotype, proof was provided for the causative role of BCAR genes (Van Agthoven et al, Breast Cancer Res Treat DOI:10.1007/s10549-008-9969-5, 2008). To elucidate the mechanisms how these individual BCAR genes induce cell proliferation in growth-arrested ZR-75-1 cells, we assessed the gene expression patterns between the different groups of cell lines. Keywords: Expression profiling, reference design RNA was isolated from two independent cultures of 69 tamoxifen-resistant cell lines. Detailed information regarding these cell lines with respect to the viral integration sites, was described previously (Van Agthoven et al, Breast Cancer Res Treat DOI:10.1007/s10549-008-9969-5, 2008). Each sample was hybridized in duplicate/triplicate and once in a dye-swap. The mixture of cell lines used as a reference was detailed previously (Jansen et al, J Clin Oncol 23, 732, 2005).
Project description:Processed and raw enteric adenovirus protein microarray reactivity data from 119 year-1 infant serum samples from a Bangladeshi birth cohort, with sample-level metadata aligned to Table 1 of the associated manuscript (Hendrick J, et al. J Infect Dis. 2025; jiaf558. doi:10.1093/infdis/jiaf558).
Project description:Dilute + Shoot: Sample Preparation + Measurement<br>
500 uL of each samples were mixed with 500 uL MeOH + 0.2% FA<br>
Samples were vortexed<br>
Samples were centrifuged at 4000 rpm and 4C for 20 min<br>
Supernatents were transferred into a 2 mL HPLC glass vial with insert<br>
Measurement of 2 uL (or 20uL) with LC-HRMS (Q Exactive HF; Standard Metabolomics Method; FPS)<br>
for further details on the analytical method refer to 10.1007/s00216-025-05818-y<br>