Project description:To explore the mechanism of action upon addition of MMC to oBHV therapy, unbiased transcriptional profiling was conducted on B16-C10 tumors treated with PBS, oBHV or MMC+oBHV harvested at day 5.
Project description:During mammalian pregnancy, immune cells are vertically transferred from mother to fetus. The functional role of these maternal microchimeric cells (MMc) is largely unknown. We show that MMc induce a preferential differentiation of hematopoietic stem and progenitor cells towards myelopoiesis in bone marrow of fetal mice, and improves resilience against cytomegalovirus infection in neonates. In humans, low MMc counts in cord blood are associated with an increased number of infections in the first year of life primarily in male newborns. Taken together, MMc boost neonatal immunity in mice and humans to mitigate the risk for early life infections.
Project description:Transcriptional profiling of A. baumannii ATCC 17978 comparing treated-MMC cultures with non-MMC treated cultures Two-condition experiment A. baumannii 17978 MMC+ vs A. baumannii 17978 MMC-. Biological replicates:3, Technical replicates:2
Project description:Transcriptional profiling of Deinococcus radiodurans comparing control wild type cells with bphPR deletion mutant were treated with MMC (5 μg/ml)
Project description:LexA is a transcriptional repressor for genes requiring expression primarily during SOS response in response to stress such as that caused by DNA alkylating agent Mitomycin C (MMC). LexA undergoes self-cleavage under stress conditions thereby lifting the repression on genes whose expression is required for stress response. In our experiment LexA binding sites in the genome were determined in untreated and MMC treated (overnight, 14h) cultures using a LexA-3xFLAG strain and anti-FLAG monoclonal antibodies. Wild type Streptomyces venezuelae (unFLAGged LexA) cultures, with and without MMC treatment were used as negative controls.
Project description:Spinal muscular atrophy (SMA) is a neurodegenerative disease which exhibits selective motor neuron death caused by a ubiquitous deficiency of the survival motor neuron (SMN) protein. It remains unclear how the ubiquitous reduction of SMN lead to death in selective motor neuron pools. Medial motor neuron columns (MMC) are vulnerable, whereas lateral motor columns (LMC) are resistant to motor neuron death in SMA. Here we performed microarray and pathway analysis comparing cholera toxin subunit B (CTb) labeled vulnerable MMC and resistant LMC of pre-symptomatic SMA with corresponding motor neuron columns of control mice to identify pathways involved in selective motor neuron death in SMA. WT is FVB. SMN is Delta7 (SMNΔ7;SMN2;Smn-) on a FVB background.
