Project description:Efficient processing of target antigens by the ubiquitin-proteasome-system (UPS) is essential for treatment of cancers by T cell therapies. However, immune escape due to impaired expression of IFN-γ-inducible components of the antigen presentation machinery and consequent inefficient processing of HLA-dependent tumor epitopes can be one important reason for failure of such therapies. Here, we show that repeated short-term co-cultures of Melan-A/MART-1 tumor antigen-expressing melanoma cells with Melan-A/MART-1 (26-35)-specific CTL led to the generation of clones resistant to CTL-mediated cell death. To determine which of the UPS components and its associated pathways was responsible for CTL escape; three UKRV-Mel-15a clones were subjected to microarray gene expression analysis. Three UKRV-Mel-15a-derived melanoma clones were isolated following three repeated short-term exposures to Melan-A/MART (26-35) CTL and harvested for RNA extraction and hybridization on Affymetrix microarrays.
Project description:This experiment evaluates quick (alarm) response to chilling in chilling-sensitive maize plants.<br>Maize inbred line cm109 were grown in optimal conditions until third leaf was fully developed. <br>At this stage plants were divided into three experimental variants: k0 - control plants, frozen<br>at the beginning of daylight, k4 - control plants kept in the same conditions and frozen after 4 hours<br>since beginning of daylight, c4 - plants kept in 14 deg. C for 4 hours since "dawn". At the mentioned<br>moments, leaves were harvested and frozen in liquid nitrogen for RNA isolation.
Project description:Global transcriptomics analysis of the Desulfovibrio vulgaris change from syntrophic growth with Methanosarcina barkeri to sulfidogenic metabolism
Project description:To study the composition of mRNPs containing TcDhh1, we carried out immunoprecipitation assays with anti-TcDhh1 and epimastigotes lysates. Pre-immune serum was used as control. We also carried out a ribonomic approach to identify the mRNAs present within the TcDhh1 immunoprecipitated complexes. For this purpose, competitive microarray hibridizations were performed against negative controls, the non-precipitated fraction.
Project description:Exploration of transcriptome expression in 5 control and 4 familial dysautonomia (FD) human olfactory ecto-mesenchymal stem cells (hOE-MSCs) at very early (P1 and P2) and later (P5 and P9) cell passages.
Project description:<br><br>Annual heart allograft failure in humans rates about 3-5%. The main reason after the first postoperative year is chronic rejection. Myointimal hyperplasia, the hellmark of chronic rejection, results in a specific type of ischemic heart disease. The lack of angina pectoris symptoms allow ventricular arrythmias, sudden cardiac death or heart failure to occur without warning. In addition, diagnostic tools such as endomyocardial biopsy, coronary angiography or intracoronary ultrasound fail to predict the individual risk for myocardial dysfunction.<br><br>The mechanisms responsible for chronic rejection are predominantly alloimmune mediated with activated T cells, macrophages, B cell mediated antibody formation and secreted cytokines responding to HLA and other endothelial cell antigens. In addition, non immunologic risk factors such as recipient age, metabolic factors, hypertension and ischemia contribute to development of this disease. Previous studies have demonstrated that ischemia has a profound influence on short term allograft survival but the underlaying mechanisms remain largely unknown. Apoptosis seems to play a crucial role in ischemia/reperfusion injury and several mechanisms for programmed cell death have been described. However, consequences on long term cell function of viability have not been investigated. <br><br>The aim of this study was to investigate the implication and the mechanism of prolonged cold organ storage as a non immunologic risk factor in the pathogenesis of chronic rejection in a cardiac allograft model. <br><br>We aimed for answering the following specific questions:<br><br>How does cold ischemia affect the alloimmue response short and long term? <br><br>How does prolonged cold ischemia affect gene expression at later time points after transplantation? <br><br>Does it influence gene expression during chronic rejection?<br><br><br><br>