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Artificial cell microcapsules containing genetically engineered E. coli DH5 cells for in-vitro lowering of plasma potassium, phosphate, magnesium, sodium, chloride, uric acid, cholesterol, and creatinine: a preliminary report.

Lowering of plasma Mg, P, Na, Cl, uric acid, cholesterol, and creatinine is required in renal failure and other diseases. In this preliminary report, we studied the ability of artificial cells microencapsulated genetically engineered E. coli DH5 cells in lower K, Mg, P, Na, Cl, uric acid, cholestrol, creatinine, and billirubin from plasma in-vitro. Result shows that this novel approach has the ability to significantly lower these metabolites from the plasma in-vitro.

Animals↗

Genetically engineering mammalian cell lines for increased viability and productivity.

The generation of new host cell lines for the production of foreign proteins can be achieved by cell engineering. This approach can be used to enhance the cell's ability to produce proteins that are properly processed and secreted at elevated levels and consequently can increase the overall productivity of an expression system. One potential target for cell engineering is the modification of the cell's protein folding capacity. The appropriate folding, assembly, localization and secretion of newly synthesized proteins is dependent upon the action of a group of proteins known as molecular chaperones. Improving the host cell's chaperoning capacity might increase the yield of properly folded recombinant proteins by preventing the formation of insoluble aggregates. Another potentially beneficial cell engineering goal is the inhibition of physiological cell death. The productivity of genetically engineered cells is dependent upon the maintenance of high levels of cell viability throughout the bioprocess period. Fluctuations in a cell's environment can trigger a deliberate form of cell death known as apoptosis. The proteins that mediate this self-destruction are currently being characterized. Regulating the expression of these death genes by cellular engineering could limit the loss of productivity that results from the physiological death of the recombinant cell line.

Journal Article↗

Genetically engineered multi-component virus-like particles as veterinary vaccines.

Multiprotein structures can be constructed to mimic virus particles. These engineered particles lack genetic material and are not infectious but they can elicit protective immune responses in animals against challenges with infectious viruses. As a prototype, insect cells were co-infected with two recombinant baculoviruses. One recombinant baculovirus contained an insert of L2 and M5 genes, which encode for outer capsid proteins VP2 and VP5, respectively, from bluetongue virus (BTV) downstream of duplicated copies of the baculovirus (Autographa californica nuclear polyhedrosis virus, AcNPV) polyhedrin promoter. Another recombinant baculovirus expressed two major core proteins (VP3 and VP7) from BTV virions. The co-infected cells synthesized non-infectious, double-shelled, virus-like particles (VLP). The VLP resembled the authentic BTV in size, appearance, and biochemical constitution but they lacked the double-stranded-RNA genome and three minor polypeptides normally contained in the icosahedral inner capsid. The VLP consisted of an outer shell of VP2 and VP5 from US BTV-10 attached to an icosahedral framework formed by the two major core proteins VP3 and BTV-17 and VP7 from US BTV-10. Sheep immunized with VLP expressing BTV capsid proteins produced antibodies that neutralized homologous serotypes of BTV. The assembly of VLP from different proteins simultaneously expressed indicates the potential of this novel approach for producing safe and effective vaccines against several viral agents.

Animals↗

Genetically engineered models relevant to neurodegenerative disorders: their value for understanding disease mechanisms and designing/testing experimental therapeutics.

Significant progress in the identification of disease-specific genes for a variety of neurodegenerative diseases have provided opportunities to understand molecular mechanisms and to test experimental therapeutic for these disorders. Recent works on clarifying the selective vulnerability of neurons and pathogenic mechanisms using genetically engineered mouse models of familial forms of Alzheimer's disease and motor neuron disease will be reviewed.

Alzheimer Disease↗