Chromosulfine, a novel cyclopentachromone sulfide produced by a marine-derived fungus after introduction of neomycin resistance

RSC Advances ◽  
2016 ◽  
Vol 6 (50) ◽  
pp. 43975-43979 ◽  
Author(s):  
Le Yi ◽  
Cheng-Bin Cui ◽  
Chang-Wei Li ◽  
Ji-Xing Peng ◽  
Qian-Qun Gu
Keyword(s):  
Neomycin Resistance

The discovery of chromosulfine, a novel cyclopentachromone sulfide generated by activating silent fungal pathways in a marine-derived fungus, was reported.

Inhibition of retroviral replication by anti-sense RNA

1986 ◽  
Vol 6 (12) ◽  
pp. 4758-4762
Author(s):  
R Y To ◽  
S C Booth ◽  
P E Neiman
Keyword(s):  
Steady State ◽  
Cultured Cells ◽  
Host Cells ◽  
Rna Molecules ◽  
Sense Orientation ◽  
Steady State Levels ◽  
Rna Inhibition ◽  
Retroviral Replication ◽  
Retroviral Infections ◽  
Neomycin Resistance

We tested the effect of anti-sense RNA on the replication of avian retroviruses in cultured cells. The replication of a recombinant retrovirus carrying a neomycin resistance gene (neor) in the anti-sense orientation was blocked when the cells expressed high steady-state levels of RNA molecules with neor in sequence in the sense was blocked when the cells expressed high steady-state levels of RNA molecules with neor sequences in the sense orientation, i.e., complementary to the viral sequence. Viral DNA bearing neor sequences was not detected specifically in host cells where this anti-sense RNA inhibition of viral replication occurred. These observations suggest that anti-sense RNA inhibition may be a useful strategy for the inhibition of retroviral infections.

Targeted disruption of the murine Nhe1 locus induces ataxia, growth retardation, and seizures

1999 ◽  
Vol 276 (4) ◽  
pp. C788-C795 ◽  
Author(s):  
Sheila M. Bell ◽  
Claire M. Schreiner ◽  
Patrick J. Schultheis ◽  
Marian L. Miller ◽  
Richard L. Evans ◽  
...  
Keyword(s):  
Cell Volume Regulation ◽  
Ventral Surface ◽  
Postnatal Growth ◽  
Particulate Material ◽  
Ph Homeostasis ◽  
Targeted Disruption ◽  
Cellular Processes ◽  
Sequence Encoding ◽  
Neomycin Resistance ◽  
Postmortem Examinations

In most cells, the ubiquitously expressed Na+/H+exchanger isoform 1 (NHE1) is thought to be a primary regulator of pH homeostasis, cell volume regulation, and the proliferative response to growth factor stimulation. To study the function of NHE1 during embryogenesis when these cellular processes are very active, we targeted the Nhe1 gene by replacing the sequence encoding transmembrane domains 6 and 7 with the neomycin resistance gene. NHE activity assays on isolated acinar cells indicated that the targeted allele is functionally null. Although the absence of NHE1 is compatible with embryogenesis, Nhe1 homozygous mutants (−/−) exhibit a decreased rate of postnatal growth that is first evident at 2 wk of age. At this time, Nhe1 −/− animals also begin to exhibit ataxia and epileptic-like seizures. Approximately 67% of the −/− mutants die before weaning. Postmortem examinations frequently revealed an accumulation of a waxy particulate material inside the ears, around the eyes and chin, and on the ventral surface of the paws. Histological analysis of adult tissues revealed a thickening of the lamina propria and a slightly atrophic glandular mucosa in the stomach.

scholarly journals Decreased expression of humanized Fat-1 in porcine fetal fibroblasts following deletion of PGK-neomycin resistance

2015 ◽  
Vol 14 (3) ◽  
pp. 11594-11604 ◽  
Author(s):  
X.J. Han ◽  
H. Liang ◽  
T. Yun ◽  
Y.H. Zhao ◽  
M.L. Zhang ◽  
...  
Keyword(s):  
Fetal Fibroblasts ◽  
Neomycin Resistance

A stable bovine papillomavirus hybrid plasmid that expresses a dominant selective trait

1983 ◽  
Vol 3 (11) ◽  
pp. 2110-2115
Author(s):  
M F Law ◽  
J C Byrne ◽  
P M Howley
Keyword(s):  
Resistance Gene ◽  
Mammalian Cell ◽  
Morphological Characteristics ◽  
Hybrid Plasmid ◽  
Transcriptional Unit ◽  
Bovine Papillomavirus ◽  
G418 Resistance ◽  
Extrachromosomal Element ◽  
Mouse Cells ◽  
Neomycin Resistance

We describe a bovine papillomavirus hybrid plasmid containing the neomycin resistance gene from Tn5 inserted into a mammalian cell transcriptional unit. This plasmid is maintained as a stable extrachromosomal element (20 to 100 copies per diploid genome) in mouse cells selected either for the transformed phenotype or for resistance to the aminoglycoside G418. Cells selected for G418 resistance initially display a flat, nontransformed phenotype before exhibiting the gross morphological characteristics of transformation. The delay in the appearance of the transformed phenotype indicated that some intracellular event or series of events subsequent to the establishment of transcriptionally active bovine papillomavirus 1 hybrid plasmid is required for the manifestation of the transformed phenotype.

Regulation of pp60c-src synthesis by inducible RNA complementary to c-src mRNA in polyomavirus-transformed rat cells

1986 ◽  
Vol 6 (7) ◽  
pp. 2305-2316
Author(s):  
S Amini ◽  
V DeSeau ◽  
S Reddy ◽  
D Shalloway ◽  
J B Bolen
Keyword(s):  
Resistance Gene ◽  
Tumor Antigen ◽  
Kinase Activity ◽  
Src Kinase ◽  
Soft Agar ◽  
Transformed Cells ◽  
Neomycin Resistance Gene ◽  
Sense Orientation ◽  
Normal Rat ◽  
Neomycin Resistance

To determine the potential role of pp60c-src in polyomavirus-transformed cells, we constructed a recombinant plasmid with the mouse metallothionein-I promoter upstream of a src gene in an anti-sense orientation. We cotransfected this plasmid into middle tumor antigen-transformed FR3T3 cells with a plasmid containing the neomycin resistance gene, and G418 resistant colonies were selected. Analysis of these cells for pp60c-src expression revealed that 50 of the 200 cellular clones screened were found to have decreased levels of c-src expression when compared with the parental middle tumor antigen-transformed cells. Three independent clones which transcribed the expected 3.6-kilobase src complementary RNA and had levels of pp60c-src kinase activity comparable to that of normal FR3T3 cells were further analyzed. In the presence of Cd2+, these clones grew significantly slower in monolayer cultures than either the parental transformed cells (FR18-1) or FR18-1 cells transfected with the neomycin resistance gene alone. The morphology of these clones in the presence of Cd2+ was distinct from that of either the parental FR18-1 cells or normal FR3T3 cells. The clones expressing the complementary src RNA were found to form fewer colonies in soft agar, form fewer foci on monolayers of normal rat cells, and form tumors more slowly following injection into syngenic rats when compared with parental FR18-1 cells. The results of these studies suggest that the level of pp60c-src kinase activity affects the growth characteristics and transformation properties of polyoma virus-transformed rat cells.

Recombination events after transient infection and stable integration of DNA into mouse cells

1985 ◽  
Vol 5 (4) ◽  
pp. 659-666 ◽  
Author(s):  
S Subramani ◽  
J Rubnitz
Keyword(s):  
Resistance Gene ◽  
Mammalian Cells ◽  
Transcription Unit ◽  
Sister Chromatid Exchanges ◽  
Neomycin Resistance Gene ◽  
Stable Integration ◽  
Mouse Cells ◽  
Chromatid Exchanges ◽  
Neomycin Resistance ◽  
Constructed Plasmids

To investigate the recombinational machinery of mammalian cells, we have constructed plasmids that can be used as substrates for homologous recombination. These plasmids contain two truncated nontandem, but overlapping, segments of the neomycin resistance gene, separated by the transcription unit for the xanthine guanine phosphoribosyl transferase gene. Recombination between the two nonfunctional neomycin gene sequences generates an intact neomycin resistance gene that is functional in both bacteria and mammalian cells. Using these plasmid substrates, we have characterized the frequencies and products of recombination events that occur in mouse 3T6 cells soon after transfection and also after stable integration of these DNAs. Among the chromosomal recombination events, we have characterized apparent deletion events that can be accounted for by intrachromatid recombination or unequal sister chromatid exchanges. Other recombination events like chromosomal inversions and possible gene conversion events in an amplification unit are also described.

Use of Allogeneic Bone Marrow Labeled with Neomycin Resistance Gene to Examine Bone Marrow-Derived Chimerism in Experimental Organ Transplantation

1997 ◽  
Vol 6 (4) ◽  
pp. 369-376 ◽  
Author(s):  
J. P. Smith ◽  
J. Kasten-Jolly ◽  
L. Rebellato ◽  
Carl E. Haisch ◽  
Judith M. Thomas
Keyword(s):  
Bone Marrow ◽  
Resistance Gene ◽  
Nonhuman Primate ◽  
Antithymocyte Globulin ◽  
Molecular Techniques ◽  
Allogeneic Bone ◽  
Nonhuman Primate Model ◽  
Primate Model ◽  
Neomycin Resistance Gene ◽  
Neomycin Resistance

Posttransplant infusion of viable donor bone marrow cells (DBMC) has been shown in our previous studies to promote acceptance of incompatible kidney allografts in rhesus monkeys after treatment with polyclonal antithymocyte globulin to deplete peripheral T-lymphocytes. In this nonhuman primate model, the infusion of the DBMC is requisite for the induction of functional graft tolerance and specific MLR and CTLp unresponsiveness, although the relevant role and fate of bone marrow-derived chimeric cells is uncertain. Standard immunological and molecular techniques applied to this monkey model are unable to differentiate between chimeric cells derived from the infused DBMC and those derived from allograft-borne passenger leukocyte emigrants. To distinguish chimerism due to infused DBMC, we transduced DBMC with a functional neomycin resistance gene (Neor) using the retroviral vector pHSG-Neo. Neor-Mransduced BMC were infused into recipients approximately 2 wk after kidney transplantation and treatment with rabbit antithymocyte globulin. No maintenance immunosuppressive drugs were given. Genomic DNA isolated from peripheral blood leukocytes was used to monitor the presence of Neor-positive cells. Tissue samples obtained at necropsy also were assessed for Neor-positive chimeric cells. The presence of DBMC-derived chimerism was assessed by polymerase chain reaction using Neor sequence-specific primers (PCR-SSP). Chimerism was detectable in recipient tissues at various times for up to 6 mo after DBMC infusion. These studies using gene transduction methodology indicate that a stable genetic marker can provide capability to examine DBMC-derived chimerism for prolonged periods in a nonhuman primate model. This approach should facilitate future studies in preclinical models to study the role and type of chimeric cell lineages in relation to functional allograft tolerance.

scholarly journals P transposons controlled by the heat shock promoter.

1986 ◽  
Vol 6 (5) ◽  
pp. 1640-1649 ◽  
Author(s):  
H Steller ◽  
V Pirrotta
Keyword(s):  
Heat Shock ◽  
Germ Line ◽  
Fusion Gene ◽  
P Element ◽  
Translational Efficiency ◽  
Heat Shock Promoter ◽  
P Elements ◽  
Heat Shocks ◽  
Neomycin Resistance ◽  
Heat Shock Induction

We have transformed Drosophila melanogaster with modified P-element transposons, which express the transposase function from the heat-inducible hsp70 heat shock promoter. The Icarus transposon, which contains a direct hsp70-P fusion gene, behaved like a very active autonomous P element even before heat shock induction. Although heat shock led to abundant somatic transcription, transposition of the Icarus element was confined to germ line cells. To reduce the constitutive transposase activity observed for the Icarus element, we attenuated the translational efficiency of the transposase RNA by inserting the transposon 5 neomycin resistance gene between the hsp70 promoter and the P-element sequences. The resulting construct, called Icarus-neo, conferred resistance to G418, and its transposition was significantly stimulated by heat shock. Heat shocks applied during the embryonic or third instar larval stage had similar effects, indicating that transposition of P elements is not restricted to a certain developmental stage. Both Icarus and Icarus-neo destabilized snw in a P-cytotype background and thus at least partially overcome the repression of transposition. Our results suggest that the regulation of P-element transposition occurs at both the transcriptional and posttranscriptional levels.

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