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Role Of Heat Shock Protein 70 Kda Cognate In Limiting Thermal Inactivation And Refolding Of Heat-Denatured Nuclear Type I Topoisomerase, Kuo-Kuang Wen
Role Of Heat Shock Protein 70 Kda Cognate In Limiting Thermal Inactivation And Refolding Of Heat-Denatured Nuclear Type I Topoisomerase, Kuo-Kuang Wen
Theses and Dissertations in Biomedical Sciences
Previous studies (Ciavarra et al., 1994) demonstrated that the constitutive 70 kDa heat shock protein (hsc70) protected purified topoisomerase I from thermal injury. In addition, hsc70 was capable of regenerating catalytic activity of heat-denatured topoisomerase I. A whole cell lysate was also active in this reaction assay. The present study demonstrates that heat-denatured topoisomerase I is reactivated by a cytosolic fraction and that this activity is dependent on the presence of cytosolic hsc70. The efficacy of hsc70-mediated refolding of heat-denatured topoisomerase I is greatly enhanced by a cytosolic cofactor(s). In all these refolding reactions, exogenous ATP is not required. Size …
Structure-Substrate Binding Relationships Of Hiv-1 Reverse Transcriptase, Steve Chien-Wen Huang
Structure-Substrate Binding Relationships Of Hiv-1 Reverse Transcriptase, Steve Chien-Wen Huang
Theses and Dissertations in Biomedical Sciences
Human Immunodeficiency Virus, type 1 (HIV-1), is the causative agent of the Acquired Immunodeficiency Syndrome (AIDS). HIV-1 reverse transcriptase (RT), a heterodimer p66/p51, has been the major target for treatment of AIDS. The significance of the p51 subunit and the RNase H domain of p66 in terms of their influence on the RNA-dependent DNA synthesis was investigated. Clones of the wildtype HIV-1 RT subunits, p66 and p51, and a recombinant C-terminal deletion mutant, p64, [Barr, P. J. (1987) Bio/Technoloav 5, 486-489] were employed to study the structure-substrate binding relationships of HIV-1 RT. The activity assays of RNA-dependent DNA synthesis on …
Translational Regulation Of The C-Jun Proto-Oncogene, Anil Sehgal
Translational Regulation Of The C-Jun Proto-Oncogene, Anil Sehgal
Theses and Dissertations in Biomedical Sciences
The v-jun oncogene was originally isolated from the ASV17 virus in 1987. Ever since its isolation, extensive work has been done to understand the role of the v-jun oncogene in cell transformation. The c-Jun protein is a transcription factor which binds to the DNA target TGACTCA. The c-Jun protein binds to DNA in the form of dimers. It can form homodimers with itself and heterodimers with Jun family (JunB and JunD), Fos family (FosB, Fra1 and Fra2), or with CREB family members through the leucine zipper motif. Because the c-jun proto-oncogene plays an important role in cell transformation, extensive work …
Subunit Interactions Of Recombinant Hiv-1 Reverse Transcriptase With Mutations At L289, Jacquelyn R. Smith
Subunit Interactions Of Recombinant Hiv-1 Reverse Transcriptase With Mutations At L289, Jacquelyn R. Smith
Theses and Dissertations in Biomedical Sciences
Reverse transcriptase (RT) is a dimeric enzyme required for replication of the human immunodeficiency virus (HIV). If the subunits of the RT dimer are dissociated, the enzyme is no longer active; therefore, identification of subunit binding sites could lead to potential targets for antiviral therapy. In order to identify where subunit binding of RT occurs, mutations were made at leucine (L) 289, a residue believed to be involved in dimerization through hydrophobic interactions with other leucines. L289 is the central leucine of a leucine repeat sequence which resembles a leucine zipper protein-DNA binding motif. Two mutations, leucine to arginine (L289R) …
An Analysis Of Mitochondrial Dna In Rett Syndrome And Other Neurodegenerative Disorders, Catherine Erickson Burgess
An Analysis Of Mitochondrial Dna In Rett Syndrome And Other Neurodegenerative Disorders, Catherine Erickson Burgess
Theses and Dissertations in Biomedical Sciences
Mitochondrial dysfunction resulting from mutations on mitochondrial DNA (mtDNA) is being recognized in a growing spectrum of diseases. These diseases, resulting from single base mutations, large deletions, or insertions, have been largely neuromuscular in origin. However, as an understanding of the effects of mtDNA mutations progresses, attention is now focusing on neurodegenerative diseases. Rett Syndrome (RS), a progressive neurodegenerative disease with predominantly female cases, demonstrates morphologic mitochondrial changes, mitochondrial enzyme deficiencies and maternal inheritance (characteristic of mtDNA diseases). No investigation of mtDNA involvement has been previously conducted and, to date, no biological marker exists for this disorder.
Our preliminary studies …