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A V Gudkov

Publications and source records attributed to A V Gudkov.

At least 91 records · Page 5Linked to original sources
PubMed1983

[Hyperproduction of a specific protein in cells resistant to colchicine and adriablastin].

Resistance of Djungarian hamster cells to colchicine and adriablastin is connected with gene amplification and decreased plasma membrane permeability for cytostatic drugs. Overproduction of protein (mol. weight about 22 Kd and pI about 5.7) was identified in colchicine- and adriablastin-resistant cell lines by means of two-dimensional gel electrophoresis. Obviously, the amplification of this protein genes leads to the changes in plasma membrane permeability and to the development of drug resistance.

Animals↗
PubMed1983

[Amplification of portions of the genome in the somatic cells of mammals resistant to colchicine. IV. Genetic transformation using amplified genes from Djungarian hamster cells highly resistant to colchicine].

DNA-mediated transfer of colchicine-resistance from Djungarian hamster DM5/7 cell line, 750-fold resistant to the drug, was studied. The resistance to colchicine of DM5/7 cells is due to amplification of the genes, possibly coding for the polypeptide p22. Both high-molecular weight DNA (presumably, chromosomal DNA) and low-molecular weight DNA (presumably, extrachromosomal DNA) effectively transferred the colchicine-resistance to Djungarian hamster and mouse cells. DNA of sensitive to colchicine but resistant to ouabain mouse cells CAK-143OuaR was not capable to transfer colchicine-resistance, but effectively transferred ouabain-resistance connected with a mutation in Na+/K+-dependent ATP-ase locus. The differences in genetic transformation with amplified p22 genes and mutant Na+/K+-dependent ATP-ase genes were revealed. All cells of 3 colchicine-resistant transformants of DM-15 cells and all 10 spontaneously derived resistant clones contain the additional chromosome 4. The role of trisomy 4 in the development of colchicine-resistance in DM-15 cells is discussed.

Animals↗
PubMed1983

[Amplification of portions of the genome in the somatic cells of mammals resistant to colchicine. V. The induction of gene amplification in the cells of the Djungarian hamster and the mouse].

The influence of some agents on gene amplification in Djungarian hamster and mouse cells was studied. The tumor promotor 12-O-tetradecanoylphorbol-13-acetate (TPA), the epidermal growth factor (EGF), insulin, and 5-bromodeoxyuridine (BUdR) increase the incidence of colchicine-resistance, connected with amplification of the genes, which probably encode the polypeptide p22. The highest frequency of gene amplification was observed after the pretreatment of cells with TPA, which enhanced the number of colchicine-resistant colonies 44-200-fold. Mitostatic agents colchicine and colcemid increased the number of methotrexate-resistant cells, 2.0-6.5 times. These cells usually arise as the result of amplification of dihydrofolate reductase genes. Dexamethasone and ethidium bromide did not change the portion of cells resistant to colchicine. Ethylmethane sulfonate (EMS) decreased the number of colchicine-resistant cells. The cells of two Djungarian hamster colchicine-resistant clones obtained after treatment with TPA did not differ from those of spontaneously derived colchicine-resistant clones. Both have similar survival patterns in the medium with different colchicine concentrations, unstable inheritance of the drug resistance, the additional chromosome 4 and small chromatin bodies-the structures containing the amplified genes. Possible mechanisms of the induction of gene amplification by the agents used are discussed.

Animals↗
PubMed1983

[Characteristics of the karyotype changes in Djungarian hamster cells resistant to methotrexate].

The chromosomes stained by trypsin G-banding technique were studied in five Djungarian hamster cell sublines, resistant to different concentrations of methotrexate. In all cells of two independent sublines, approximately 13 times more resistant to the drug, an additional material on the distal part of the short arm of chromosome 3 was revealed. The size and banding pattern of this new material were different in two sublines and in individual cells of each subline. In cells, which were 25-fold resistant to methotrexate, the additional material was found both in the short arm of chromosome 3 and in the long arm of chromosome 4. In some cells the additional material in chromosome 4 contained the long homogeneously staining regions (HSRs). In a subline which was 100-fold resistant to methotrexate, all cells had the chromosome 4 bearing the long HSR. The further increase in the level of drug resistance (300-fold) was accompanied by the increase in the size of HSRs in chromosome 4, the appearance of the second HSR in the short arm of chromosome 3 and emergence of small chromatin bodies. In cells with trisomy 4 and a low level of colchicine-resistance, methotrexate-resistance arises more frequently than in colchicine-sensitive cells bearing two chromosomes 4, or in cells possessing the high level of colchicine-resistance and trisomy of the short arm of chromosome 4 only. The similarities and differences of karyotypic alterations accompanying the development of colchicine- and methotrexate-resistance in Djungarian hamster cells, are discussed.

Animals↗
PubMed1982

[Amplification of genome regions in the somatic cells of mammals resistant to colchicine. III. Localization of the amplified genes in minute chromatin bodies].

Small chromatin bodies (SCB) were revealed in Djungarian hamster cells resistant to colchicine. They looked like single bodies or like clusters of small particles. SCB were localized both in nucleus and cytoplasm. Similar formations were earlier observed in oocytes of insects with amplified extrachromosomal rDNA genes. DNA in the SCB was able to replicate not only during the S phase but also during other phases of the cell cycle. The restriction analysis showed that in cells with SCB DNA amplified sequences were replicated autonomously too. These data indicate that SCB in colchicine-resistant cells contain amplified genes. Besides, SCB double-minute chromosomes (DMs) were observed in some resistant sublines. In one of them, DMs were the only karyotypic alteration. The relationship between SCB, chromosomal homogeneously staining regions (HSRs) and DMs was studied. Single SCB and DMs appeared at the early stage of the development of colchicine-resistance (the level of drug resistance is 16-22). Selection of variants 170-220-fold resistant to colchicine was usually accompanied by the decrease in the cell number with SCB and DMs and by the increase in the amount of cells containing the chromosomes with HSRs. During the further enhancement of drug resistance (700-750), some decrease in the number of cells with HSRs and the appearance of the great number of cells containing large groups of SCB were found. The loss of colchicine-resistance observed during cultivation in colchicine free medium was accompanied by the disappearance of HSRs, emergence of SCB and DMs and further elimination of SCB and DMs from cells. The quantity of autonomously replicating amplified DNA fragments after digestive by HindIII was increased with the enhancement of SCB number in cultures.

Animals↗
PubMed1981

Variety of endogenous proviruses in the genomes of chickens of different breeds.

We have compared endogenous proviruses in DNA of chickens of 11 breeds by means of Southern's technique. Many of the endogenous virus loci found were missing from the genomes of the extensively studied white leghorn chickens, although some of the proviruses and especially ev-1 appeared to be widely spread among different chickens. Most of the proviruses were similar to Rous-associated virus (RAV-O) as judged by the EcoRI digestion patterns. Several genetically different proviruses were found in the DNA of 28 brown leghorns. They contain neither ev-1 provirus in their genome, nor any other one common for all individuals. All four Italian partridge-coloured chickens examined appeared to be free from ALV-related sequences in their DNA showing the possibility of normal life without known endogenous proviruses. Possible causes of inter-breed differences of chicken endogenous proviruses are discussed.

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PubMedDate not supplied

[Influence of products of thermophilous methane fermentation on the mixed lactic acid bacterial culture].

The effect of products resulting from thermophilous methane fermentation on the accumulation and ratio of different lactic acid bacteria (Str. lactis, Str. cremoris, Str. diacetilactis, Str. diacetil. var. acetoinicus, Leuc. citrovorum8 L. plantarum) was investigated upon their combined cultivation in milk and serum. In combined cultivation of the streptococcal culture the rate of growth of a single strain differed from that in separate cultivation. Str. cremoris was accumulated with the highest rate during its separate cultivation and with the lowest rate during its combined cultivation. An addition of products of thermophilous methane fermentation to the combined culture of streptococci of different strains increased the growth rate and accumulation of each strain. At the same time the products influenced differently the quantitative ratios of various strains in the resulting biomass. For instance, the relative content of Str. cremoris and Leuc. citrovorum decreased insignificantly and that of Str. lactis and Str. diacetil. var. acetoin.increased. The combined cultivation of the five streptococcal strains with L. plantarum in the medium containing no additions of thermophilous methane fermentation products increased the relative content of L. plantarum from the beginning of fermentation. In the medium containing the additions of this parameter varied sinusoidally with a minimum of 6 to 9 hours. Possible mechanisms of these changes are discussed.

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PubMedDate not supplied

[Fractionated low-intensity thermotherapy of benign prostatic hyperplasia].

120 patients with benign prostatic hyperplasia (BPH) (mean age 65.8 +/- 7.7 years) received fractional low-intensity transurethral microwave thermotherapy (FLITMT). Each patient was exposed to 4 FLITMT procedures with 3-4 day interval (duration--60 min at 48.5-49.9 degrees C, ProsTek 3000 unit, USA). Subjective and objective effects of FLITMT were observed in 87 (82.9%) and 75 (71.4%) patients, respectively. A stable effect on IPSS persisted for 3 years, on acceleration of maximal urination rate--within a year. Moreover, FLITMT was associated with a low frequency of complications. This makes the above thermotherapy usable in all BPH patients without absolute indications for surgical treatment.

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PubMedDate not supplied

[Amoeboid properties of cells during early morphogenesis and the nature of a possible protozoan ancestor of Metazoa].

Data analysis reveals that cells of most of the metazoans (especially from the phyla Spongia, Placozoa and Cnidaria) at the early stages of morphogenesis demonstrateas amoeboid properties i.e. ability to form pseudopodia, to move by means of pseudopodia and to phagocyte. In different degress these properties could be found at the late stages of embryogenesis and even in adult organisms. Moreover, during gastrulation and blastulation blastomeres is able to form flagellas and than loose them and return to amoeboid activity. These and other facts indicate that both amoeboid and flagellate types of cellular organization are programmed in the genome of metazoan cells, as well as their ability for mutual transformation. It leads to suggestion that ancestors of Metazoa were amoeboflagellates. Anarchic cleavage observed in some invertebrates evidences that separated blastomeres is able to aggregate into the unite embryo due to cytotaxis. Aggregation of artificially separated cells of sponges, trichoplax and cnidaria results in complete recovery of the organism by cytotaxis. Thus, there are reasons to suppose that ability of cell aggregation was inherited by the Metazoan genome from the amoeboflagellate ancestors. Thus amoeboflagellates may be considered as forerunners of Metazoa, i.e. Prometazoa.

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PubMedDate not supplied

[Sequences homologous to mouse mammary cancer virus are common in mammalian and avian genomes].

Sequences distantly related to mouse mammary tumor virus (MRS) were found in a wide range of mammalian genomes using blot hybridization. The number of MRS copies and the degree of their relationship with the hybridization probe varied and did not correlate with the evolutionary similarity of the species. Nevertheless, within a genus the set of MRS was species-specific and reflected the degree of relationship between species. MRS were also found in avian genomes and the degree of their relationship also did not correlate with the evolutionary similarity of the species. The origin and distribution of MRS are discussed.

Animals↗
PubMedDate not supplied

[Characteristics of new loci of endogenous proviruses in chickens].

The composition and structure of endogenous proviruses in the genome of Italian partridge chicken was studied by the blot-hybridization method using 32P-DNA of RAV-2 virus as a probe. Among 34 fowls examined, 5-contained no endogenous proviruses related to fowl leukemia viruses. DNA of the other fowls contained various combinations of 4 previously undescribed endogenous proviruses varying in structure and localization. None of them was identical in its structure with DNA of endogenous fowl virus RAV-0, all the four discovered loci have deletions. The origin, modes of genetic variability, and function of endogenous proviruses are discussed.

Animals↗
PubMedDate not supplied

[Isolation of DNA probes for the detection of sequences amplified in colchicine-resistant cells].

Earlier we have found that the development of resistance to colchicine in mammalian cells in vitro is due to gene amplification leading to decreased plasma membrane permeability to the selective agent and some other unrelated drugs. By a stepwise self-renaturation procedure followed by chromatography on hydroxyapatite we isolated the fraction of middle-repeated sequences (DNAc0t = 10-250) enriched in amplified DNA from the DNA of colchicine-resistant Djungarian hamster cell line. Blotting-hybridization with [32P]DNAc0t = 10-250 performed in the presence of the excess of unlabelled DNA from wild type cells reveals amplified sequences in resistant cell lines. The comparison of DNAs from cell lines resistant to colchicine, adriablastin and actinomycin D showed that common but not identical DNA sequences are amplified in these cases. In situ hybridization with [3H]DNAc0t = 10-250 indicates that amplified sequences are located in the long homogeneously staining regions (HSRs) of the marker chromosomes. These results suggest that DNAc0t = 10-250 may be used for screening of recombinant molecules containing amplified sequences.

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