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At least 541 records · Page 30Linked to original sources
PubMed1996

Human T lymphocytes specific for the immunodominant 83-99 epitope of myelin basic protein: recognition of golli MBP HOG 7.

Myelin basic protein (MBP) is a candidate autoantigen in the disease multiple sclerosis. Although MBP was thought to be sequestered behind the blood-brain barrier, isoforms of MBPs have recently been demonstrated in lymphoid tissues. These isoforms, termed golli MBPs, contain sequences that are shared with "classic" MBP within the CNS. In the present study, we have determined that epitopes within golli MBP isoforms may be recognized by human T lymphocyte clones specific for classic MBP. Ten of 12 T-cell clones recognized golli MBP. Although 11 clones were specific for the immunodominant 83-99 sequence, the clones differed with respect to human leukocyte antigen (HLA) restriction, T-helper phenotype, cytolytic activity, and T-cell receptor usage. Greater responses to classic MBP than to golli MBP suggested a difference in the ability of the two proteins to be processed and to present epitopes therein. These data advance the hypothesis that golli MBP sequences expressed within lymphoid tissues may be recognized by classic MBP-specific T lymphocytes during central or peripheral tolerance.

Antibody Specificity↗
PubMed1989

[The effect of microbial protein from a hydrocarbon base (fermosin) with a defined fatty acid composition on fat metabolism and fat composition in slaughter animals. 2. The effect of "fermosin" on the composition of back fat in hogs].

Two tests have been undertaken to investigate the influence of feeding microbial biomasses to pigs. No alterations of the fat parameters characterizing the fat stability were observed. All the values obtained are in a normal range. Increases in heptadecenic acid were detected dependent on the content of microbial biomasses in the feed and its fat content. The alterations are mainly in a normal range or slightly beyond it. In nature odd-numbered fatty acids are ubiquitous. Uptake and storage suggest that the organism reacts to an increased offer of C17-fatty acids with an accelerated decomposition of these fatty acids or/and with inhibition of their endogenous synthesis. The results are discussed in comparison with those of literature.

Adipose Tissue↗
PubMed2001

Expression of the yeast glycogen phosphorylase gene is regulated by stress-response elements and by the HOG MAP kinase pathway.

Yeast glycogen metabolism responds to environmental stressors such as nutrient limitation and heat shock. This response is mediated, in part, by the regulation of the glycogen metabolic genes. Environmental stressors induce a number of glycogen metabolic genes, including GPH1, which encodes glycogen phosphorylase. Primer extension analysis detected two start sites for GPH1, one of which predominated. Sequences upstream of these sites included a possible TATA element. Mutation of this sequence reduced GPH1 expression by a factor of 10 but did not affect start site selection. This mutation also did not affect the relative induction of GPH1 upon entry into stationary phase. Three candidates for stress response elements (STREs) were found upstream of the TATA sequence. Mutation of the STREs showed that they were required for regulation of GPH1 expression in early stationary phase, and in response to osmotic shock and heat shock. These elements appeared to act synergistically, since the intact promoter exhibited 30-fold more expression in stationary phase than the sum of that observed for each element acting independently. HOG1, which encodes a MAP kinase, has been implicated in control mediated by STREs. For GPH1, induction by osmotic shock depended on a functional HOG1 allele. In contrast, induction upon entry into stationary phase was only partially dependent on HOG1. Furthermore, the heat shock response, which can also be mediated by STREs, was independent of HOG1. These observations suggest that the GPH1 STREs respond to more than one pathway, only one of which requires HOG1.

Base Sequence↗
PubMed1993

Formation and reduction of ascorbate radicals by hog thyroid microsomes.

The formation of ascorbate radicals, identified by ESR experiments, was observed in the ascorbate peroxidase reaction by thyroid microsomes. The steady-state concentration of ascorbate radicals decreased in the presence of NADH. The oxidation of NADH was followed optically. Using the ascorbic acid oxidase system, NADH-dependent electron transport in thyroid microsomes was examined. Ascorbate radicals competed with bound cytochrome b5 for the reaction with reduced NADH-cytochrome b5 reductase. The NADH-ascorbate radical reductase activity of thyroid microsomes was calculated to be 0.17 mumol/mg.s at 3.3 microM ascorbate radicals. Kinetic results show that the properties of NADH-cytochrome b5 reductase in thyroid microsomes were similar to those of the enzyme in liver microsomes. The formation of ascorbate radicals by thyroid microsomes was stimulated by the addition of thyroxine, and the stimulation was decreased also by NADH. The thyroxine-mediated oxidation of ascorbate is explained in terms of consecutive one-electron transfers initiated by bound thyroid peroxidase. These results, along with those described in our previous paper (M. Nakamura, I. Yamazaki, and S. Ohtaki, 1990, J. Biochem. 108, 804-810), support the idea that ascorbate protects thyroid hormones from oxidative degradation through the NADH-cytochrome b5 reductase system.

Animals↗
PubMed2004

Anatomical studies of the fibroblast growth factor-10 mutant, Sonic Hedge Hog mutant and androgen receptor mutant mouse genital tubercle.

OBJECTIVES: Congenital genital abnormalities have a diverse spectrum from hypospadias to cloacal anomalies. The molecular events in the normal and abnormal development of the genital tubercle (GT) are still obscure. Genetically engineered mice with specific gene deletions that affect genital anatomy are a useful tool to better understand the etiology of genital abnormalities. In this study, we compared the genital tubercle anatomy of the androgen receptor (AR) deficient, fibroblastic growth factor (FGF)-10 deficient and Sonic HedgeHog (Shh) deficient mutant male mice to that of the wild type male and female mouse. MATERIALS AND METHODS: The lower pelvis of the androgen receptor deficient, FGF-10 deficient, Shh deficient mutant male and wild type male and female mouse at different gestational days (E13-21) and post natal ages (1 day-1 week) were studied. GTs were imaged, serially sectioned and stained immunohistochemically with antibodies raised against E-Cadherin, Cytokeratin 7, 10 and 14. Serial sections of the GTs were selected and three-dimensional computerized images were created to better elucidate the anatomy. RESULTS: AR deficient mutant male mouse revealed a distinctive GT anatomy, different from both sexes. The corporal bodies and glans remained hypoplastic whereas the urethral spongiosa was more developed than the wild type female counterpart. This finding is consistent with the AR mutant mouse being a unique morphologic phenotype distinct from the normal male and female. FGF-10 deficient mutant male mouse revealed normal corporal bodies with failure of the urethral plate to fuse ventrally consistent with hypospadias. The Shh deficient mutant mouse demonstrated complete agenesis of GT outgrowth and a persistent cloaca. CONCLUSION: Animal models bred by gene knockout technology or natural occurring mutants contribute to the basic understanding of normal and abnormal GT development. The anatomy of the these three mutant mice confirms the importance of the androgen receptor, FGF-10 and Shh in genital development.

Aging↗