Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The transforming activity and the molecular structure of DNA from cells of Diplococcus pneumoniae during thymidine starvation have been analyzed and the effects of thymidine starvation have been compared with the effects of single-strand breaks produced by deoxyribonucleases in DNA of unstarved cells. The decrease in transforming activity of lysates from starved cells as a function of the size of DNA particles, measured by centrifugation in neutral and alkaline sucrose gradients, does not follow the kinetics observed after enzymatic degradation of DNA of unstarved cells. Moreover, a strain lacking exo- and endonuclease activities is not protected from thymineless death. These results suggest that the basic lethal mechanism of thymidine starvation might have an origin other than the activation of nucleases.
 ...
PMID:Size and transforming activity of deoxyribonucleic acid in Diplococcus pneumoniae during thymidine starvation. 1 Feb 77

Decay of pre-existing ribonucleic acid was studied in Escherichia coli cells subjected to high temperature or to starvation for nitrogen, phosphate, amino acids, or a carbon source. In these studies a series of mutants affected in ribonucleic I(RNase I, EC 3.1.4.22) polynucleotide phosphorylase (EC 2.7.7.8) or ribonuclease II (RNase II, EC 3.1.4.23) were used. Degradation of total RNA and the disappearance of 23 S and 16 S rRNA were followed. The results obtained indicated that, by and large, decay of 23 S and 16 S RNA parallels that of total RNA. Decay of RNA depended on the nuclease content of the cells as well as on the treatment of applied. It was most pronounced during carbon starvation and least in cells deprived of phosphate ions. It was most effective in strains containing all three nucleases and least in the strain defective in all three. The exonucleases polynucleotide phosphorylase and RNase II did not seem to affect the extent of 23 S and 16 S RNA disappearance. Strains with modified exonucleases did accumulate low molecular weight RNA species during treatments which induced considerable degradation of 23 S and 16 S RNA. Based on the above date and previous observations, we suggest that during various starvations a similar mechanism is operative. The 23 S and 16 S RNAs are degraded endonucleolytically, and this is the rate-limiting step during starvation. The exonucleases polynucleotide phosphorylase and RNase II seem to participate primarily in the decay of the low molecular weight RNA species formed by the endonuclease(s), not as yet identified.
 ...
PMID:Decay of ribosomal ribonucleic acid in Escherichia coli cells starved for various nutrients. 109 48

Glucocorticoids can mediate the destruction of thymocytes and T cell-derived leukemia cells through a mechanism known as apoptosis. The characteristic feature of apoptosis is fragmentation of DNA at internucleosomal linkers through the activity of a specific endonuclease. In this study, an attempt was made to compare dexamethasone-induced apoptosis in two T cell-derived human leukemia lines (CEM-C1 and CEM-C7) to the cell killing brought about by selected cytotoxic agents. In the CEM-C7 cell line (dexamethasone-sensitive), apoptosis was induced not only by dexamethasone but by actinomycin D, cycloheximide, and 25-OH cholesterol. In the CEM-C1 cell line (dexamethasone-resistant) cycloheximide, 25-OH cholesterol, or cell starvation could induce apoptosis. It appears that in leukemic cells apoptosis may be induced by a variety of unrelated toxic agents and is not limited to glucocorticoids.
 ...
PMID:Apoptosis: mode of cell death induced in T cell leukemia lines by dexamethasone and other agents. 200 65

The production of Moloney murine leukaemia virus from chronically infected cells was inhibited after starvation of glutamine. While the rate of synthesis of the precursor of the core proteins, Pr65gag, was not affected in the starved cells, its proteolytic processing was blocked. Pulse-chase experiments indicated that glutamine was required during the synthesis of Pr65gag to facilitate its subsequent processing. In addition, the synthesis of Pr200gag-pol, the precursor of the protease, reverse transcriptase and endonuclease, was inhibited in the glutamine-starved cells. Starvation for other essential amino acids such as tyrosine and isoleucine affected neither the synthesis nor the processing of the virus proteins. These results suggest that the readthrough mechanism which enables synthesis of the Pr200gag-pol polyprotein is modulated in the chronically infected cells by glutamine levels. Since the viral protease is part of the pol gene, its synthesis may be inhibited in the glutamine-starved cells and Pr65gag is therefore not processed.
 ...
PMID:Glutamine starvation of murine leukaemia virus-infected cells inhibits the readthrough of the gag-pol genes and proteolytic processing of the gag polyprotein. 348 14

A multiple mutant strain of Escherichia coli containing mutations affecting the exoribonucleases, RNase II, RNase D, and RNase BN, and also the endonuclease, RNase I, was constructed by P1-mediated transduction. Extracts of the mutant strain were lacking the aforementioned RNase activities. The multiple mutant displayed normal growth in both rich and minimal media at a variety of temperatures, recovered from starvation essentially as the wild-type parent, and could support the growth of a variety of bacteriophages. In addition, RNA synthesis was normal and no precursor RNA accumulation was observed. The properties of the mutant strain indicate that the three exoribonucleases are not essential for the viability of E. coli. The implications of these findings to our understanding of RNA processing and degradation are discussed.
 ...
PMID:A multiple mutant of Escherichia coli lacking the exoribonucleases RNase II, RNase D, and RNase BN. 620 70

Peroxynitrite is a powerful oxidant formed by the near-diffusion-limited reaction of nitric oxide with superoxide. Large doses of peroxynitrite (> 2 mM) resulted in rapid cell swelling and necrosis of undifferentiated PC12 cells. However, brief exposure to lower concentrations of peroxynitrite (EC50 = 850 microM) intially (3-4 h) caused minimal damage to low-density cultures. By 8 h, cytoplasmic shrinkage with nuclear condensation and fragmentation became increasingly evident. After 24 h, 36% of peroxynitrite-treated cells demonstrated these features associated with apoptosis. In addition, 46% of peroxynitrite-treated cells demonstrated DNA fragmentation (by terminal-deoxynucleotide transferase-mediated dUTP-digoxigenin nick end-labeling) after 7 h, which was inhibited by posttreatment with the endonuclease inhibitor aurintricarboxylic acid. Serum starvation also resulted in apoptosis in control cells (23%), the percentage of which was not altered significantly by peroxynitrite treatment. Although peroxynitrite is known to be toxic to cells, the present study provides a first indication that peroxynitrite induces apoptosis. Furthermore, pretreatment of cells with nerve growth factor or insulin, but not epidermal growth factor, was protective against peroxynitrite-induced apoptosis. However, both acidic and basic fibroblast growth factors greatly increased peroxynitrite-initiated apoptosis, to 63 and 70%, respectively. Thus, specific trophic factors demonstrate differential regulation of peroxynitrite-induced apoptosis in vitro.
 ...
PMID:Peroxynitrite-induced cytotoxicity in PC12 cells: evidence for an apoptotic mechanism differentially modulated by neurotrophic factors. 756 48

Diverse classes of phytochemicals initiate biological responses that effectively lower cancer risk. One class of phytochemicals, broadly defined as pure and mixed isoprenoids, encompasses an estimated 22,000 individual components. A representative mixed isoprenoid, gamma-tocotrienol, suppresses the growth of murine B16(F10) melanoma cells, and with greater potency, the growth of human breast adenocarcinoma (MCF-7) and human leukemic (HL-60) cells. beta-Ionone, a pure isoprenoid, suppresses the growth of B16 cells and with greater potency, the growth of MCF-7, HL-60 and human colon adenocarcinoma (Caco-2) cells. Results obtained with diverse cell lines differing in ras and p53 status showed that the isoprenoid-mediated suppression of growth is independent of mutated ras and p53 functions. beta-Ionone suppressed the growth of human colon fibroblasts (CCD-18Co) but only when present at three-fold the concentration required to suppress the growth of Caco-2 cells. The isoprenoids initiated apoptosis and, concomitantly arrested cells in the G1 phase of the cell cycle. Both suppress 3-hydroxy-3-methylglutaryl CoA reductase activity. beta-Ionone and lovastatin interfered with the posttranslational processing of lamin B, an activity essential to assembly of daughter nuclei. This interference, we postulate, renders neosynthesized DNA available to the endonuclease activities leading to apoptotic cell death. Lovastatin-imposed mevalonate starvation suppressed the glycosylation and translocation of growth factor receptors to the cell surface. As a consequence, cells were arrested in the G1 phase of the cell cycle. This rationale may apply to the isoprenoid-mediated G1-phase arrest of tumor cells. The additive and potentially synergistic actions of these isoprenoids in the suppression of tumor cell proliferation and initiation of apoptosis coupled with the mass action of the diverse isoprenoid constituents of plant products may explain, in part, the impact of fruit, vegetable and grain consumption on cancer risk.
 ...
PMID:Apoptosis and cell-cycle arrest in human and murine tumor cells are initiated by isoprenoids. 1020 54

Changes in the outer membrane of apoptotic cells can induce neighboring cells to become phagocytic. Using genetically marked prostate cancer cell lines, we explored the possibility that genetic information might be transferred from an apoptotic cell to a phagocytic neighbor. Neomycin-resistant LNCaP cells that overexpress bcl-2 (LNCaP(bcl-2/neo-r)) were cocultured with hygromycin-resistant LNCaP cells (LNCaP(hygr-r)). The cocultures were then transiently exposed to serum starvation to induce apoptosis of LNCaP(hygr-r) cells. Surviving cells were then coselected in medium containing both antibiotics. Whereas monocultures of LNCaP(bcl-2/neo-r) or LNCaP(hygr-r) treated this way yielded no colonies, cocultures yielded dual-antibiotic-resistant clones at a frequency of approximately 1 in 10(5). Pre-exposure to an apoptotic agent was required; cocultures not exposed to serum starvation yielded no dual-selectable colonies. Analysis of DNA extracted from a dual-resistant clone demonstrated that the restriction endonuclease pattern of the neo-r gene was unaltered when compared with the parental LNCaP(bcl-2/neo-r). However the hygr-r gene demonstrated an altered restriction endonuclease pattern in the dual-resistant derivative compared with the parental LNCaP(hygr-r) cell line. This is evidence that genetic information can be transferred from one prostate cancer cell to another through the process of apoptosis, and we term this form of genetic transfer "apoptotic conversion."
 ...
PMID:Apoptotic conversion: evidence for exchange of genetic information between prostate cancer cells mediated by apoptosis. 1055 18

Cds1, a serine/threonine kinase, enforces the S-M checkpoint in the fission yeast Schizosaccharomyces pombe. Cds1 is required for survival of replicational stress caused by agents that stall replication forks, but how Cds1 performs these functions is largely unknown. Here we report that the forkhead-associated-1 (FHA1) protein-docking domain of Cds1 interacts with Mus81, an evolutionarily conserved damage tolerance protein. Mus81 has an endonuclease homology domain found in the XPF nucleotide excision repair protein. Inactivation of mus81 reveals a unique spectrum of phenotypes. Mus81 enables survival of deoxynucleotide triphosphate starvation, UV radiation, and DNA polymerase impairment. Mus81 is essential in the absence of Bloom's syndrome Rqh1 helicase and is required for productive meiosis. Genetic epistasis studies suggest that Mus81 works with recombination enzymes to properly replicate damaged DNA. Inactivation of Mus81 triggers a checkpoint-dependent delay of mitosis. We propose that Mus81 is involved in the recruitment of Cds1 to aberrant DNA structures where Cds1 modulates the activity of damage tolerance enzymes.
 ...
PMID:Damage tolerance protein Mus81 associates with the FHA1 domain of checkpoint kinase Cds1. 1107 77

During starvation induced encystment, cells of the myxomycete Didymium iridis accumulate a 7.5-kb RNA that is the result of alternative processing of pre-rRNA. The 5' end corresponds to an internal processing site cleaved by the group I-like ribozyme DiGIR1, located within the twin-ribozyme intron Dir.S956-1. The RNA retains the majority of Dir.S956-1 including the homing endonuclease gene and a small spliceosomal intron, the internal transcribed spacers ITS1 and ITS2, and the large subunit rRNA lacking its two group I introns. The formation of this RNA implies cleavage by DiGIR1 in a new RNA context, and presents a new example of the cost to the host of intron load. This is because the formation of the 7.5-kb RNA is incompatible with the formation of functional ribosomal RNA from the same transcript. In the formation of the 7.5-kb RNA, DiGIR1 catalysed cleavage takes place without prior splicing performed by DiGIR2. This contrasts with the processing order leading to mature rRNA and I-DirI mRNA in growing cells, suggesting an interplay between the two ribozymes of a twin-ribozyme intron.
 ...
PMID:The group I-like ribozyme DiGIR1 mediates alternative processing of pre-rRNA transcripts in Didymium iridis. 1244 68


1 2 3 Next >>