Abstract: The invention relates to a cellular protein which is specific and has high affinity for nucleic acid sequences characteristic of an intact TAR RNA loop sequence of the HIV LTR TAR region. The invention also relates to a protein preparation having a protein of about 185 kD that is isolated from a mammalian cell nuclear extract preparation, most specifically a HeLa cell extract that is purified between 1,000-10,000 fold. The protein of about 185 kD is shown to regulate HIV viral gene expression by binding a TAR RNA region of an HIV LTR template, in the presence of a cofactor fraction (including at least a -100 kD cofactor), and a tat protein. A route for the development of immunodiagnostics for AIDS and related disorders may also be provided given the specific and high affinity of TRP-185 for HIV RNA.

Abstract: The present invention provides for the use of Tripterygium wilfordii Hook F extracts and purified components thereof in the treatment of inflammation or an immune disorder with concomitant lack of steroidal effect. Extracts of this plant (T2) bound to the glucocorticoid receptor and competitively inhibited glucocorticoid mediated cellular processes, such as dexamethasone binding to the glucocorticoid receptor, glucocorticoid mediated activation of target genes, dexamethasone dependent cellular growth, with concomitant inhibition of cyclooxygenase-2 induction and inflammatory processes such as the production of prostaglandin E.sub.2. The T2 extract components triptolide and tripdiolide were effective inhibitors. The particular advantage provided by the methods herein is the treatment or prevention of inflammation and the concomitant lack of steroidal agonist effects and NSAID side effects. Conditions treatable by the present methods include inflammation and immune disorders including autoimmune disease.

Abstract: The invention relates to small RNAs encoded within the nucleus of mammalian cells that specifically import to the mitochondria. The RNAs bind to several nucleolar peptides and thus provide potential carriers for import of biological molecules, including metabolites and proteins, into the mitochondrial compartment. Mitochondrial dysfunction in several maternally inherited human diseases may be correctable employing linkage of mitochondrial import signal to mitochondrial tRNA sequences expressed from nuclear trans-genes without requirement for direct genetic transformation of mitochondria.