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Biomedical subjects

I L Karnushina

Publications and source records attributed to I L Karnushina.

6 recordsLinked to original sources
PubMed1994

Properties and engineering of a mutant STA promoter of Saccharomyces diastaticus.

A new allelic variant of the STA2 gene of S. diastaticus, designated as STA2K, was cloned and characterized (1; accompanying paper). An application-oriented analysis of the promoter region of STA2K is described, with an emphasis on its peculiar structural feature: A 1.1-kb natural deletion located 189 nucleotides upstream of the translation start codon. The strength of the STA2K promoter was found comparable to that of known strong constitutive yeast promoters (ADH1, GAPDH). Regulated glucoamylase expression was demonstrated by chimeric promoters, which were constructed by placing the STA2K promoter under the control of either the PHO5 or CYC1 upstream regulatory sequences. On high-copy-number vectors, induction of the UASPHO5-STA2K chimeric promoter by phosphate depletion resulted in a destructive overexpression of the secreted glucoamylase, which completely halted cell growth, and promoted cell decay. In contrast, UASCYC1 was shown to mediate a fine-tuned regulation both by glucose concentration and, indirectly, by starch, the substrate for the glucoamylase to produce glucose.

Base Sequence↗
PubMed1983

Cerebral endothelial cell culture. II. Adenylate cyclase response to prostaglandins and their interaction with the adrenergic system.

The response of endothelial adenylate cyclase (AC) to prostaglandins (PGE1, PGE2, PGF1 alpha, PGF2 alpha, PGD2 and PGI2) and the relationship of PGE2 to adrenergic systems were investigated in cerebrovascular endothelial cultures. E-type prostaglandins and PGI2 were more effective in stimulating endothelial AC (EC50 = 3 x 10(-7)M, and 3 x 10(-6)M, respectively) than prostaglandins of the F-series and PGD2 which activated AC at high doses only. A modulation of endothelial AC response to either PGE2 or norepinephrine (NE) was observed in the presence of both agents in the system. It was manifested by a dose-dependent NE inhibition of the PGE2-stimulated formation of cAMP, which was partially restored by phentolamine. Alpha and beta-adrenergic agonists (alpha, clonidine and 6-fluoronorepinephrine; beta, isoproterenol) also partly blocked while forskolin and PGE2 synergistically stimulated the production of cAMP in the endothelial cultures. These findings strongly suggest that the interaction of prostaglandins and alpha- and beta-adrenergic agonists with the AC system in cerebrovascular endothelium may play a role in the regulation of the cerebral microcirculation and/or blood pressure.

Adenylyl Cyclases↗
PubMed1982

Cerebral endothelial cell culture. I. The presence of beta 2 and alpha 2-adrenergic receptors linked to adenylate cyclase activity.

Cultured endothelial cells derived from cerebral microvessels separated from 2-day-old rat brain contain a specific beta 2 and alpha 2-adrenergic sensitive adenylate cyclase (AC). Among the various tested hormones, PGE1 and PGE2 were found to be the most potent activators, while adenosine, angiotensin I and II, gamma-aminobutyric acid and vasoactive intestinal peptide inhibited the enzyme activity. However, acetylcholine, histamine, serotonin, glycine, glutamine, bradykinin, neurotensin and vasopressin (Lysine and Arginine) had no effect on the adenylate cyclase activity in this model. The susceptibility of the cerebrovascular endothelial AC system to the vasoactive substances as well as presence of beta 2 and alpha 2-type adrenergic receptors in the cultured endothelium provides additional support for the proposed endothelial involvement in the regulation of cerebrovascular permeability and blood flow.

Adenylyl Cyclases↗
PubMed1981

Histamine in brain capillaries.

A high amount of histamine was found in capillaries isolated by subcellular fractionation from the brain. In view of the important effects of histamine on vascular permeability in peripheral vessels, it was thought that histamine had a similar function in the cerebral vasculature. Intracarotic histamine infusion resulted in an enhanced pinocytosis of endothelial cells and te oedematous swelling of the astrocytic end-feet system. [3H]-Histamine, injected in the cerebral ventricles, accumulated in the capillary wall. Histamine and cimetidine activated hydroxyfatty acid and prostaglandin D2 synthesis in isolated brain capillaries. The possible function of the capillary histamine in the regulation of permeability of microvessels is discussed.

Animals↗