Article Abstract:
A novel regulation mechanism of Ah, or dioxin, receptor function has been found. Ah receptor (AhR), a ligand-activated transcription factor, mediates pleiotropic effects on host animals of environmental pollutants, among them 2,3,7,8-tetrachlorodibenzo-p-dioxin. Besides induction of drug-metabolizing enzymes, the liganded AhR complex activates gene expression of a factor called AhR repressor (AhRR). AhRR inhibits AhR function, competing with AhR for binding to the XRE sequence and dimerizing with AhR nuclear translocator (Arnt). AhRR and AhR make up a regulation circuit in the xenobiotic signal transduction path and give a novel regulation mecahnism for AhR function. Possibly it determines tissue-specific pollutant sensitivity.
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Article Abstract:
A positive transcription elongation factor b (P-TEFb) may control transition from abortive to productive elongation through phosphorylation of the carboxy-terminal domain (CTD) of the largest subunit of RNA polymerase II. Drosophila P-TEFb has been shown to be a cyclin-dependent kinase (CDK9). Cloning of multiple cyclin subunits of human P-TEFb (T1 and T2) has been carried out. Cyclin T1 and T2 are expressed ubiquitously. Immunoprecipitation and immunodepletion experiments have indicated that cyclin T1 and T2 were associated in a mutually exclusive way with CDK9, almost all of which was associated with one or the other.
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Article Abstract:
Almost complete inhibition of V(D)J recombination at the TCR-beta locus and a block in alpha-beta T cell development result from deletion of the TCR beta transcriptional enhancer (E beta). The idea has been tested that V(D)J recombination is promoted by transcriptional enhancers through regulating accessibility of the locus to the recombinase. Loss of accessibility by itself does not account for the loss of TCR beta recombination when the E beta element is absent. It seems an additional function for E beta exists during the late phase of the recombination reaction in the process of DNA repair at certain TCR beta sites.
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