Project description:BioID2 Zebrafish Interaction Proteomics analyzed by nanoscale capillary LC coupled to a Fusion Lumos OT with label-free quantitation.
Project description:Antimicrobial-induced DNA damage, and subsequent repair via upregulation of DNA repair factors, including error-prone translesion polymerases, can lead to the increased accumulation of mutations in the microbial genome, and ultimately increased risk of acquired mutations associated with antimicrobial resistance. While this phenotype is well described in bacterial species, it is less thoroughly investigated amongst microbial fungi. Here, we monitor DNA damage induced by antifungal agents in the fungal pathogen Candida albicans, and find that commonly used antifungal drugs are able to induce DNA damage, leading to the upregulation of transcripts encoding predicted error-prone polymerases and related factors. We focus on REV1, encoding a putative error-prone polymerase, and find that while deleting this gene in C. albicans leads to increased sensitivity to DNA damage, it also unexpectedly renders cells more likely to incur mutations and evolve resistance to antifungal agents. We further find that deletion of REV1 leads to a significant depletion in the uncharacterized protein Shm1, which itself plays a role in fungal mutagenesis. Together, this work lends new insight into previously uncharacterized factors with important roles in the DNA damage response, mutagenesis, and the evolution of antifungal drug resistance.
Project description:we report a novel nanomedicine (Gd@C82(OH)22 ) effectively inhibit human breast tumor growth by antiangiogenesis in vivo. To further identify which angiogenic factor(s) were affected on mRNA level, the "RT² Profiler™ PCR Array Mouse Angiogenesis (APMM-024, SuperArray Bioscience Corporation)" was used. Keywords: nanomedicine, Gd@C82(OH)22, angiogenesis, MCF-7, breast cancer In the experimental group, the tumor bearing mice were administered intraperitoneally (i.p.) [Gd@C82(OH)22]n saline solution once a day at the dose of 2.5mM/kg, after the tumor tissue implantation into the animal for 7 days, continuing until the mice were sacrificed. The 0.9% saline soultion was used as control. At the end of the experiment, parts of the tumor tissue was collected, and further be analyzed by PCR-array.
Project description:Medulloblastoma is the most frequent malignant primary brain tumor in children. Despite recent advances in integrated genomics, the prognosis in children with high-risk medulloblastoma remains devastating, and new tumor-specific therapeutic approaches are needed. Here, we present an atlas of naturally presented T-cell antigens in medulloblastoma. We mapped the human leukocyte antigen (HLA)-presented peptidomes of 28 tumors and performed comparative immunopeptidome profiling against an in-house benign database. Medulloblastoma proved to be a rich source of novel tumor-associated antigens, naturally presented on HLA class I and II molecules. Remarkably, most tumor-associated peptides and proteins were subgroup-specific, whereas shared presentation among all subgroups of medulloblastoma (WNT, SHH, Group 3 and Group 4) was rare. Functional testing of top-ranking novel candidate antigens demonstrated the induction of peptide-specific T-cell responses, supporting their potential for T-cell immunotherapy. This study is an in-depth mapping of naturally presented T-cell antigens in medulloblastoma. Integration of immunopeptidomics, transcriptomics, and epigenetic data led to the identification of a large set of actionable targets that can be further used for the translation into the clinical setting by facilitating the informed design of immunotherapeutic approaches to children with medulloblastoma.