Biomedical subjects

R Zwart

Publications and source records attributed to R Zwart.

4 recordsLinked to original sources

PubMed1992

Neuronal-type nicotinic receptors in human neuroblastoma and small-cell lung carcinoma cell lines.

A beta subunit of the neuronal nicotinic receptor, sharing 88% homology with the rat beta 4 subunit, has been cloned from a human neuroblastoma cell line. The gene encoding the human beta 4 subunit is expressed in association with the alpha 3 gene in neuroblastoma and small-cell lung carcinoma cell lines. Patch-clamp experiments and radioligand binding assays confirm that these neuroendocrine tumor cell lines express functional neuronal nicotinic receptors. We suggest that these receptors might play a crucial role in the control of neurotransmitter and hormone secretion from neurosecretory human tumors.

Acetylcholine↗

PubMed1992

The nitromethylene heterocycle 1-(pyridin-3-yl-methyl)-2-nitromethylene-imidazolidine distinguishes mammalian from insect nicotinic receptor subtypes.

Effects of the insecticidal compound 1-(pyridin-3-yl-methyl)-2-nitromethylene-imidazolidine (PMNI) on different subtypes of the nicotinic acetylcholine receptor were studied in voltage-clamped locust thoracic ganglion neurons, mouse BC3H1 muscle cells and mouse N1E-115 neuroblastoma cells. In locust neurons 10 microM PMNI induced agonistic effects and subsequent complete block of 1 mM acetylcholine-induced inward currents. The same concentration of PMNI produced no significant agonistic and antagonistic effects on the endplate type nicotinic receptor in BC3H1 cells. Neuronal type nicotinic receptor operated ion currents in N1E-115 cells were blocked by 10 microM PMNI to 50% of the control value, while agonistic effects were not observed. The differential action of PMNI designates this compound as a potential new tool to distinguish between subtypes of the nicotinic acetylcholine receptor.

Animals↗

PubMed1992

Major growth reduction and minor decrease in mitochondrial enzyme activity in cultured human muscle cells after exposure to zidovudine.

Zidovudine-induced mitochondrial myopathy in AIDS patients reported recently might be due to inhibition of mitochondrial DNA polymerase gamma. We investigated the effect of zidovudine on proliferation, differentiation, activity of mitochondrial- and nuclear-encoded enzymes, and mitochondrial DNA (mtDNA), in cultured human muscle cells. Marked inhibition of cell proliferation was found, even in the presence of low (10 mumol/L) zidovudine concentrations. Enzyme activity of the nuclear-encoded mitochondrial citrate synthase was not affected, and the partially mitochondrial-encoded cytochrome c oxidase was not decreased, except only after exposure to high concentrations (5 mmol/L) zidovudine. No decrease of mtDNA content and no mtDNA deletions were found in zidovudine-exposed muscle cells. We propose that the effect of zidovudine on muscle, seen in zidovudine-treated AIDS patients, results mainly from decrease in proliferation of muscle cells rather than inhibition of mtDNA replication.

Acquired Immunodeficiency Syndrome↗

PubMed1990

A novel function of the transforming domain of E1a: repression of AP-1 activity.

Adenovirus E1a represses transcription of the collagenase gene via the phorbol ester-responsive element (collTRE). The mechanism involves inhibition of the trans-activating function of the transcription factor AP-1 without reduction of its synthesis and without any apparent change in DNA binding or composition. The ability of E1a to downmodulate AP-1 is a unique property among dominant oncogenes. This repression depends on conserved region 1, one of the transforming domains of E1a, indicating that it is an integral feature of adenovirus transformation.

Adenovirus Early Proteins↗