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Biomedical subjects

W Kemper

Publications and source records attributed to W Kemper.

7 recordsLinked to original sources
PubMed1979

The use of [14C]eukaryotic initiation factor 2 to measure the endogenous pool size of eukaryotic initiation factor 2 in rabbit reticulocyte lysate.

[14C]Eukaryotic initiation factor 2 (eIF-2), obtained by reductive methylation of the purified initiation factor, was shown to be active in the unfractionated reticulocyte lysate. This allowed a direct measurement of the endogenous pool size of eIF-2 in rabbit reticulocyte lysate according to the principle of isotope dilution. A value of 20 to 30 pmol/ml of lysate was obtained. Although translational inhibition resulting from hemin deficiency appears to be characterized by a change from catalytic to stoichiometric utilization of eIF-2, the pool size of eIF-2 is too small to account for the normal period of protein synthesis before the onset of translation inhibition. This suggests, therefore, that additional events to eIF-2 alpha phosphorylation may be required for translational inhibition.

Animals↗
PubMed1978

Identification of a 48 S preinitiation complex in reticulocyte lysate.

When the polypeptide initiation sequence is interrupted by the peptide antibiotic edeine, the sedimentation coefficient of the native small ribosomal subunit is increased from 43 S to 48 S. Formation of the 48 SN particle is absolutely dependent on the binding of both Met-tRNAf and globin mRNA. These results support the concept that Met-tRNAf binds to the native small ribosomal subunit before mRNA, and that processes involved in mRNA binding to the 43 SN preinitiation complex may be the rate-limiting step of 80 S initiation complex formation.

Animals↗
PubMed1977

Influence of cations on the electrical activity of neuroblastoma X glioma hybrid cells.

Electrical excitability is one of the various neuronal properties of neuroblastoma X glioma hybrid cells. At a Ca2+ concentration of 1.8 mM the action potential is inhibited by tetrodotoxin, suggesting that the inward current is carried by Na+ ions. In contrast, at a Ca2+ concentration of 20-36 mM and even in the absence of Na+, spikes (sometimes repetitive) with strong hyperpolarizing afterpotential occur, which are no longer affected by tetrodotoxin. They are, however, blocked by antagonists of Ca2+ like La3+, Co2+, Mn2+, and the synthetic compounds D-600 and BAY a-1040. This seems to indicate that at high concentrations of Ca2+, the inward current of the action potential is essentially carried by Ca2+. Sr2+, but not Mg2+ can effectively substitute for Ca2+. It slows down the time course of the action potential. Ba2+ depolarizes the membrane gradually. If Ca2+ is also present, Ba2+ causes a reduced depolarization and spontaneous action potentials with no hyperpolarizing after-potential are observed.

Action Potentials↗
PubMed1976

Electrical response of glioma cells to acetylcholine.

A bromodeoxyuridine resistant mutant of rat gliom line C6 grown in the presence of N6,02'-dibutyryl adenosine-3':5'-cyclic monophosphate, although inexcitable by electrical current, responds to iontophoretic application of acetylcholine by slow hyperpolarization. The sensitivity to acetylcholine is strongly reduced by excessive amounts of acetylcholine. The hyperpolarization response is inhibited by atropine or alpha-bungarotoxin, but not by D-tubocurarine. In the absence of acetylcholine some cells display spontaneous hyperpolarizations at regular intervals. The membrane resting potential is decreased if the concentration of external K+ is raised.

Action Potentials↗