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  • 1
    Electronic Resource
    Electronic Resource
    Human DNA polymerase-β promoter: Phorbol ester activation is mediated through the cAMP response element and cAMP-response-element-binding protein (1997)
    Springer
    Journal of biomedical science 4 (1997), S. 279-288 
    Details
    ISSN: 1423-0127
    Keywords: Promoter ; Transcription factor ; Transactivation ; Signal transduction ; Phorbol ester ; Protein kinase A ; Protein kinase C ; DNA repair enzyme
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract That mammalian DNA polymerase-β (β-pol) gene transcription is upregulated by activatedras and also by phorbol ester (TPA) treatment suggests the involvement of protein kinase C in the gene expression control for this DNA repair enzyme. Yet, the core promoters of the human, bovine and rodent β-pol genes do not have a TPA response element or other binding site for the transcriptional activator AP-1. Instead, these β-pol promoters appear to be regulated mainly by proteins binding to the cAMP response element (CRE) centered within 50 bp 5′ of the transcriptional start site. In this study, the CRE in the human β-pol promoter was found to mediate TPA upregulation of the cloned promoter in HeLa cell transient expression experiments. To further examine the role of this CRE in TPA stimulation, we used several mutated promoters that were either deficient in protein binding to the CRE or contained extra CRE sites arranged as tandem repeats. All constructs with at least one functional CRE were upregulated by TPA, whereas mutants lacking CRE protein-binding function were not TPA upregulated. Analyses of HeLa nuclear extract DNA-binding proteins indicated that the β-pol CRE was bound by CRE-binding protein (CREB) family members CREB-1 and activating transcription factor-1, but not by AP-1 or complexes containg AP-1 subunits. These results suggest that CREB, rather than AP-1 proteins, are required for the CRE-mediated TPA activation of the β-pol promoter.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02258351
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  • 2
    Electronic Resource
    Electronic Resource
    Reversal of defective G-proteins and adenylyl cyclase/cAMP signal transduction in diabetic rats by vanadyl sulphate therapy (1995)
    Springer
    Molecular and cellular biochemistry 153 (1995), S. 113-119 
    Details
    ISSN: 1573-4919
    Keywords: Adenylyl cyclase ; G-proteins ; diabetes ; insulin ; vanadate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Vanadium salts exhibit a wide variety of insulinomimetic effects. In the present studies, we have examined the modulation of G-protein levels and adenylyl cyclase activity in the liver of streptozotocin-induced chronic diabetic rats (STZD) by vanadyl sulfate treatment and compared it with that of insulin. The basal enzyme activity, as well as the stimulatory effects of guanine nucleotides, glucagon, N-Ethylcarboxamideadenosine (NECA), isoproterenol, forskolin and sodium fluoride (NaF) on adenylyl cyclase were significantly increased in STZ-D rat liver as compared to control. In addition, the levels of stimulatory (Gsα) as well as inhibitory (Giα-2 and Giα-3) as determined by immunoblotting techniques were also significantly higher in the STZ-D rat liver, however, the inhibitory effects of oxotremorine and low concentration of GTPγS on adenylyl cyclase were not different in the two groups. Vanadyl sulfate and insulin treatments restored the augmented basal enzyme activity, the stimulations exerted by stimulatory inputs on adenylyl cyclase and the G-protein levels to various degrees, however, vanadyl sulfate was more effective than insulin. In addition, unlike vanadyl sulfate, insulin was unable to improve the stimulation exerted by glucagon and isoproterenol on adenylyl cyclase activity in STZD rats. These results suggest that vanadyl sulfate mimics the effects of insulin to restore the defective levels of G-proteins and adenylyl cyclase activity. From these results it may be suggested that one of the mechanisms by which vanadyl sulfate improves the glucose homeostasis in STZ-D rats may be through its ability to modulate the levels of G-proteins and adenylyl cyclase signal transduction system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01075925
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