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

The Tpr protease of Porphyromonas gingivalis W83 is a membrane-associated enzyme capable of hydrolyzing chromogenic substrates for trypsin and bacterial collagenases. A previous study by us indicated that Tpr expression was increased under conditions of nutrient limitation. In the present study, we further characterized expression of the tpr gene using a tpr::lacZ reporter gene construct under a range of nutrient conditions. In P. gingivalis, transcription of tpr was initiated 215 bp upstream of the coding region and regulation of tpr expression was at the level of transcription. Deletion mutations in the tpr upstream region identified the promoter region immediately upstream of the transcription start site, determined by primer extension analysis. Three identical 17-bp direct repeats identified within the 5' end of tpr mRNA were involved in tpr regulation. In an Escherichia coli background, tpr transcription was initiated after an AT-rich region upstream of tpr but not at the P. gingivalis start site. Tpr expression in P. gingivalis was suppressed by the addition of peptide and protein nutrients to a peptide-limited growth medium but was only slightly affected by addition of free amino acids. Low-molecular-weight fractions of brain heart infusion rich in phenylalanine, proline, and alanine had the greatest inhibitory effects on expression of the tpr::lacZ construct. Addition of the dipeptide phenylalanyl-phenylalanine to the growth medium resulted in a 10-fold decrease in tpr expression. This suggests that specific phenylalanine-containing peptides are a major factor controlling Tpr expression. Neither hemin starvation, heat shock, nor pH change had significant effects on Tpr expression.
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PMID:Expression of the tpr protease gene of Porphyromonas gingivalis is regulated by peptide nutrients. 978 16

A yeast mutant was isolated encoding a single amino acid substitution [serine-53 --> proline (S53P)] in transcription factor TFIIB that impairs activation of the PHO5 gene in response to phosphate starvation. This effect is activation-specific because S53P did not affect the uninduced level of PHO5 expression, yet is not specific to PHO5 because Adr1-mediated activation of the ADH2 gene also was impaired by S53P. Pho4, the principal activator of PHO5, directly interacted with TFIIB in vitro, and this interaction was impaired by the S53P replacement. Furthermore, Pho4 induced a conformational change in TFIIB, detected by enhanced sensitivity to V8 protease. The S53P replacement also impaired activation of a lexA(op)-lacZ reporter by a LexA fusion protein to the activation domain of Adr1, thereby indicating that the transcriptional effect on ADH2 expression is specific to the activation function of Adr1. These results define an activation-specific role for TFIIB in vivo and suggest that certain activators induce a conformational change in TFIIB as part of their mechanism of transcriptional stimulation.
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PMID:An activation-specific role for transcription factor TFIIB in vivo. 1007 85

The activity profile of the periplasmic asparaginase of Saccharomyces cerevisiae was determined during cell growth in an ure2 mutant; in an ure2 transformed with a plasmid containing the gene URE2 and, for comparison, in the strain D273-10B. Cells were cultivated in media presenting variable quantitative and qualitative nitrogen availability and the enzyme activity was evaluated in fresh and in nitrogen-starved cells. Nitrogen affected the asparaginase II level in fresh and starved cells of all strains. In the best condition, enzyme was produced by the wild-type cells at the late log-phase in the glucose/ammonium medium with a carbon to nitrogen ratio 4.3:1. Upon starvation, the activity doubled. The overall profile of the transformed strain was similar to that of the wild-type strain. In the ure2 mutant, high-enzyme levels were observed during growth, as expected. However the activity level, upon starvation, in proline grown cells, increased sixfold, suggesting that in addition to the Ure2p-Gln3p system, another system regulates asparaginase II biosynthesis.
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PMID:L-asparaginase II of saccharomyces cerevisiae. Activity profile during growth using an ure2 mutant P40-3C and a P40-3C + URE2p strain. 1039 75

Amino acid starvation markedly stimulates the activity of system A, a widely distributed transport route for neutral amino acids. The involvement of MAPK (mitogen-activated protein kinase) pathways in this adaptive increase of transport activity was studied in cultured human fibroblasts. In these cells, a 3-fold stimulation of system A transport activity required a 6-h amino acid-free incubation. However, a rapid tyrosine phosphorylation of ERK (extracellular regulated kinase) 1 and 2, and JNK (Jun N-terminal kinase) 1, but not of p38, was observed after the substitution of complete medium with amino acid-free saline solution. ERK1/2 activity was 4-fold enhanced after a 15-min amino acid-free incubation and maintained at stimulated values thereafter. A transient, less evident stimulation of JNK1 activity was also detected, while the activity of p38 was not affected by amino acid deprivation. PD98059, an inhibitor of ERK1/2 activation, completely suppressed the adaptive increase of system A transport activity that, conversely, was unaffected by inhibitors of other transduction pathways, such as rapamycin and wortmannin, as well as by chronic treatment with phorbol esters. In the presence of either L-proline or 2-(methylaminoisobutyric) acid, two substrates of system A, the transport increase was prevented and no sustained stimulation of ERK1/2 was observed. To identify the stimulus that maintains MAPK activation, cell volume was monitored during amino acid-free incubation. It was found that amino acid deprivation caused a progressive cell shrinkage (30% after a 6-h starvation). If proline was added to amino acid-starved, shrunken cells, normal values of cell volume were rapidly restored. However, proline-dependent volume rescue was hampered if cells were pretreated with PD98059. It is concluded that (a) the triggering of adaptive increase of system A activity requires a prolonged activation of ERK1 and 2 and that (b) cell volume changes, caused by the depletion of intracellular amino acid pool, may underlie the activation of MAPKs.
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PMID:Adaptive increase of amino acid transport system A requires ERK1/2 activation. 1050 37

Chronic energy restriction (ER) dramatically enhances intestinal absorption of nutrients by aged mice. Do adaptations in nutrient absorption develop only after extended ER or immediately after its initiation? To determine the time course of adaptations, we measured rates of intestinal glucose, fructose and proline transport 1-270 d after initiation of ER (70% of ad libitum) in 3-mo old mice. Mice of the same age that consumed food ad libitum (AL) served as controls; a third group was starved for 1 or 2 d only, to distinguish the effects of acute ER from those of starvation. Acute ER of 1, 2 and 10 d had no effect on nutrient absorption. Starvation significantly decreased intestinal mass per centimeter, thereby reducing transport per centimeter and intestinal absorptive capacity without significantly altering transport per milligram of intestine. ER for 24 d enhanced only fructose uptake, whereas ER for 270 d enhanced uptake of all nutrients by 20-100%. Despite marked differences in body weights, the wet weights of the stomach, small intestine, cecum and large intestine were generally similar in AL and ER mice, suggesting that the gastrointestinal tract was spared during ER. In contrast, the wet weights of the lungs, kidneys, spleen, heart, pancreas and liver each differed by 40-120% between ER and AL mice. Intestinal transport adaptations develop gradually during ER, and the main mechanism underlying these adaptations is a dramatic increase in transport activity per milligram tissue.
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PMID:Chronic but not acute energy restriction increases intestinal nutrient transport in mice. 1123 59

The jlbA (jun-like hZIP) gene of Aspergillus nidulans was isolated. The deduced amino acid motif of the C-terminal region of jlhA encodes a putative DNA-binding site composed of a basic amino acid domain and an adjacent leucine zipper motif. This region shares highest similarities to the C-terminal DNA-binding domain and the basic zipper (bZIP)-motifs of transcription factors like CPCA from A. niger, Gcn4p from Saccharomyces cerevisiae, human JUNB and c-JUN. The putative jlbA protein contains a PEST-rich region (an instability region rich in the amino acids proline, glutamic acid, serine and threonine) described to be implicated in protein stability. The jlbA mRNA formation is elevated up to 40-fold upon amino acid starvation induced by the addition of the false feedback inhibitor 3-amino-1,2,4-triazole. This induction is partially dependent and partially independent on the presence of the transcription factor CPCA. Therefore jlbA is a novel gene of A. nidulans which is transcriptionally activated by amino acid starvation conditions.
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PMID:Induction of jlbA mRNA synthesis for a putative bZIP protein of Aspergillus nidulans by amino acid starvation. 1152 6

The amino acid permease Bap2p in Saccharomyces cerevisiae mediates a major part of the uptake of leucine, isoleucine, and valine from media containing a preferred nitrogen source. Although the transcriptional controls of BAP2 have been well studied, the posttranslational down-regulation mechanisms for Bap2p have not been established. Here we show that Bap2p is subject to a starvation-induced degradation upon rapamycin treatment or cultivation with proline as the sole nitrogen source. The starvation-induced degradation of Bap2p was dependent on the cellular functions of ubiquitination and endocytosis. Down-regulation of the permease required the most probable ubiquitination sites, the lysine residues situated in the N-terminal 49 residues, as well as the C-terminal domain. Furthermore, when the N-terminal domain of Bap2p was fused to the general amino acid permease Gap1p, the resultant chimeric permease became susceptible to the starvation-induced degradation, indicating that the Bap2p N-terminus contains a determinant responsive to the starvation signals.
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PMID:The N-terminal domain of the yeast permease Bap2p plays a role in its degradation. 1158 26

This study is based on our previous findings showing that certain amino acids may protect hybridoma cells against starvation-induced apoptosis. In the present work we have screened 44 amino acids and analogs for their capacity of modulating apoptosis in human T-lymphoblastic leukemia cell line MOLT-4 exposed to starvation in a nutrient-poor medium. The panel of tested substances was found to contain not only compounds with antiapoptotic activity (e.g., l-glutamine, l-histidine, glycine, l-proline, and l-2-aminopentanoic acid), but also compounds with proapoptotic activity (e.g., l-phenylalanine, l-tryptophan, l-arginine, and l-2-aminohexanoic acid). The apoptosis-modulating effects were dependent on fine details of the structure of the compounds. A switch from antiapoptotic activity to proapoptotic activity was found between 6-aminohexanoic acid and 7-aminoheptanoic acid, as well as between l-2-aminopentanoic acid and l-2-aminohexanoic acid. D-amino acids tested were without effect.
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PMID:Antiapoptotic and proapoptotic action of various amino acids and analogs in starving MOLT-4 cells. 1181 59

Prolidase [E.C. 3.4.13.9] plays an important role in the recycling of proline for collagen synthesis and cell growth and this enzyme activity determines the rate of collagen turnover. It has been previously suggested that prolidase activity is regulated through signal mediated by the interaction of ECM proteins, with b1 integrin receptor and that this interaction is disturbed in MCF-7 cells. The potential candidates for mediating signal transduction are the nonreceptor tyrosine kinase p125FAK and two mitogen-activated protein (MAP) kinases, ERK-1 and ERK-2, which are activated upon attachment of cells to ECM. We found that serum starvation of MCF-7 cells for 24 hours contributed to a significant decrease (by about 30%) in prolidase activity and collagen biosynthesis. These phenomena were accompanied by suppression of MAP kinases expression without any effect on the expression of FAK. The data suggest that prolidase activity and collagen biosynthesis respond to signal mediated by MAP kinases, independently of FAK expression in MCF-7 cells.
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PMID:FAK-independent regulation of prolidase activity and collagen biosynthesis in MCF-7 cells. 1182 Jun 13

Colletotrichum trifolii is the causative organism of alfalfa anthracnose. We previously cloned and characterized the small prototypical G protein, Ras, of C. trifolii, which is involved in the signaling pathways that mediate interaction between the pathogen and its host. Transformants expressing constitutively active forms of Ras have growth medium-dependent phenotypes. In nutrient-rich media (e.g., yeast extract and peptone), the phenotype of the transformants was indistinguishable from that of the wild type. However, during nutrient starvation, the transformants lose polarity, have distended hyphae, and fail to sporulate and produce appressoria. Since peptone caused the phenotype to revert, amino acids were tested singly and in combination to identify the responsible amino acid(s). We found that 1.6 mM proline in the medium reverses the constitutively active Ras phenotype.
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PMID:Proline reverses the abnormal phenotypes of Colletotrichum trifolii associated with expression of endogenous constitutively active Ras. 1191 80


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