MECHANISM OF ISOMEROREDUCTASE INDUCTION IN ESCHERICHIA COLI

Abstract not availabl

Induction of HFR formation in F[raised +] males of Escherichia coli treated with MNNG

N-methyl-N'-nitro-N-nitrosoguanidine, MNNG, was shown to stimulate the formation of Hfr males in a F[raised +] population of Escherichia coli. The frequency of Hfrs is raised 23.3 fold, with MNNG treatment, above that of spontaneous Hfr formation. At least twelve different sites of F factor integration were found in MNNG induced Hfrs. Several possible mechanisms of the MNNG induced F factor integration process were studied. A model for Hfr formation has been discussed.Biology and Biochemistry, Department o

Electroporation buffer composition and method of use

The subject invention concerns an electroporation buffer that allows for enhanced transfection efficiency and cell viability of cells during application of an electric current. Buffers of the invention provide for maximum transfer of target particles into cells while maintaining the health and growth potential of the cell population. Compositions of the invention comprise electroporation buffers of approximately physiological ionic strength and pH, and having serum or purified proteins, such as serum albumin, added thereto. The subject invention is suitable for use with any cell type. The subject invention also concerns methods of electroporation using an electroporation buffer of the invention

Ras Pathway Activation and MEKi Resistance Scores Predict the Efficiency of MEKi and SRCi Combination to Induce Apoptosis in Colorectal Cancer

Colorectal cancer (CRC) is the second leading cause of cancer death in the United States. The RAS pathway is activated in more than 55% of CRC and has been targeted for therapeutic intervention with MEK inhibitors. Unfortunately, many patients have de novo resistance, or can develop resistance to this new class of drugs. We have hypothesized that much of this resistance may pass through SRC as a common signal transduction node, and that inhibition of SRC may suppress MEK inhibition resistance mechanisms. CRC tumors of the Consensus Molecular Subtype (CMS) 4, enriched in stem cells, are difficult to successfully treat and have been suggested to evade traditional chemotherapy agents through resistance mechanisms. Here, we evaluate targeting two pathways simultaneously to produce an effective treatment by overcoming resistance. We show that combining Trametinib (MEKi) with Dasatinib (SRCi) provides enhanced cell death in 8 of the 16 tested CRC cell lines compared to treatment with either agent alone. To be able to select sensitive cells, we simultaneously evaluated a validated 18-gene RAS pathway activation signature score along with a 13-gene MEKi resistance signature score, which we hypothesize predict tumor sensitivity to this dual targeted therapy. We found the cell lines that were sensitive to the dual treatment were predominantly CMS4 and had both a high 18-gene and a high 13-gene score, suggesting these cell lines had potential for de novo MEKi sensitivity but were subject to the rapid development of MEKi resistance. The 13-gene score is highly correlated to a score for SRC activation, suggesting resistance is dependent on SRC. Our data show that gene expression signature scores for RAS pathway activation and for MEKi resistance may be useful in determining which CRC tumors will respond to the novel drug combination of MEKi and SRCi