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PubMed2002

[Calculation of spectroscopic properties of Tm:YVO4 crystals].

Sigma and pi polarized absorption spectra of Tm:YVO4 crystal have been measured at room temperature. Considering the difference of the sigma and pi polarized absorption spectra and the changing of the refractive index with different wavelengths, we calculate the intensity parameters of Tm3+ in crystal YVO4 which are omega 2 = 1.9416 x 10(-20) (cm2), omega 4 = 0.1568 x 10(-20) (cm2), omega 6 = 0.3963 x 10(-20) (cm2) by Judd-Ofelt theory. The spectra characteristic parameters, such as radiative transition rates, luminescence branching ratio, total radiative lifetime and integral cross-section are also calculated. The results show that the spontaneous rate of the transition 1D2-->3F4 is much higher than that of the transition 1D2 to other levels.

Chemical Phenomena↗
PubMed2004

[Mutation of Indy(p115) increases the life expectancy of imago of Drosophila melanogaster depending on sex and genetic background].

The Indyp115 allele in heterozygous state almost doubles the life span of adult Drosophila melanogaster, and this effect largely depends on the strain used for obtaining heterozygotes. Male and female life span depends on Indyp115 to a different degree. Apart from Indyp115 heterozygotes, sexual dimorphism for life span was also observed in strain Hikone-AW, but not in OregonR and TM3 balancer. In heterozygotes Indyp115/OR, both the average life span and female reproductive period increased as compared to OR control. No substantial increase in female reproductive period in Indyp115/Hk heterozygotes was found. In homozygotes for allele Indyp115, we have previously revealed two phases of embryotic lethality and lethality at the larval and pupa stages. Thus, allele Indyp115 has a double and opposite effect on Drosophila viability. On the one hand, it extends the life span of adult flies, on the other, decreases survival at preimaginal stages.

Alleles↗
PubMed1992

Splicing of two alternative exon pairs in beta-tropomyosin pre-mRNA is independently controlled during myogenesis.

Two known tissue-specific tropomyosin (TM) isoforms are produced from the rodent beta-TM gene. Skeletal muscle beta-TM uses the alternative exons 6b and 9a and the exon 9a-associated poly(A) site. Fibroblast and smooth muscle TM-1 use exons 6a and 9b and the exon-9b associated poly(A) site. We have identified a new skeletal muscle beta-TM isoform, beta-TM2. beta-TM2 contains exon 6b (muscle) and exon 9b (nonmuscle). Full-length beta-TM2 cDNA clones were isolated from a cDNA library of mouse muscle BC3H1 cells. Its mRNA was also found in mouse skeletal muscle tissue but not in other tissues. beta-TM2 mRNA level and protein synthesis are differentiation-dependent, with a transient high level in the early stages of myogenesis both in BC3H1 cells and in mouse embryo limbs. Trace amounts of beta-TM3 mRNA, the other hybrid form (exons 6a + 9a), were found in less differentiated BC3H1 cells, mouse uterus, heart, and 3T3 fibroblasts but not skeletal muscle tissue. Thus, the selection of the two alternative exons appears to be controlled independently. Furthermore, during myogenesis, there is a sequential switch in the internal alternative exon, the terminal exon, and the poly(A) site from the nonmuscle to the muscle type.

Amino Acid Sequence↗
PubMed2005

[Upconversion luminescence properties of YLiF4:Er, Tm, Yb synthesized by hydrothermal method].

YLiF4 codoped with Er3+, Tm3+ and Yb3+ ions was synthesized by hydrothermal method. The absorption spectra and upconversion spectra excited at 980 nm were investigated. Under the excitation of infrared photons, strong white emission can be obtained. According to the value of n obtained from the power law, the 484 nm blue emission, 524 and 552 nm green emission, and 665 nm red emission are all due to two photon process, while the UV emission is attributed to three photon process. The authors also analyzed the upconversion mechanism and process.

English Abstract↗
PubMed2007

Genetic and epigenetic changes induced by chronic low dose exposure to arsenic of mouse testicular Leydig cells.

Arsenic is an important environmental carcinogen that affects millions of people worldwide through contaminated water supplies. Genotoxicity of arsenic has been a topic of controversy. Both genetic alterations (mutations) and epigenetic changes (methylation) have been shown to play a crucial role in environmental carcinogenesis. Chronic exposure to arsenic has been shown to induce malignant transformation of mammalian cells. However, the genetic aberrations induced by arsenic in this process are unclear. The purpose of this study was to determine if both lower (1 pg/ml) and higher concentrations (100 ng/ml) of arsenic induces either mutations or methylation changes that could lead to the development of genomic instability in TM3 cells, immortalized Leydig cells derived from normal mouse testis. Two independent exposure times were used in this study which resulted in cells of 33 and 100 generations in age. Arsenic-induced genetic and epigenetic changes were screened at a genome-wide level by random amplified polymorphic DNA (RAPD), also known as AP-PCR method with undigested DNA as well as DNA digested by the methylation sensitive isosizomeric restriction enzymes MSPI and HpaII and untreated controls. Changes in the DNA fingerprint of both, the restriction enzyme digested DNA (indicating methylation changes) as well as undigested DNA (indicating mutations) from arsenic-treated (low as well as high dose) samples were observed as compared to their controls. Thus, this study provides the first evidence at DNA sequence level for mutagenic potential of arsenic. Further characterization of these altered genomic regions is underway. The understanding of these genetic and epigenetic changes in arsenic-induced carcinogenesis will provide a basis for better interventional approaches in both the treatment and prevention of arsenic-induced cancer.

Animals↗
PubMed1988

Human T lymphotropic virus I infection deregulates surface expression of the transferrin receptor.

Human T-lymphotropic virus I (HTLV-I) is an etiologic agent in adult T cell leukemia. In an effort to understand the relationship between HTLV-I infection and malignant transformation, we have examined transferrin receptor expression in HTLV-I-infected cells. Transferrin receptor expression in normal T cells is tightly regulated and essential for cell proliferation. We have used matched T cell sets originating from a normal donor, consisting of tetanus toxoid-specific normal T cell clones (TM3 and TM5) and their in vitro HTLV-I-infected counterparts (TM3H and TM5H). Using these matched sets of virus-infected and normal T cells, we have determined that HTLV-I infection leads to hyperexpression of surface transferrin receptors (five- to six-fold higher than normal counterparts). Although the growth rates of the virus-infected cells did not differ significantly from their normal controls, HTLV-I-infected cells constitutively hyperexpressed surface transferrin receptors, whereas the level of surface receptor expression of normal counterpart cells varied during the cycle of antigenic stimulation. Immunoprecipitation of total (surface plus cytoplasmic) transferrin expression showed that the HTLV-I-infected cells did not possess a greater total number of transferrin receptors than their normal counterparts. This data was supported by Northern blot analysis, which showed equivalent transferrin receptor mRNA expression in HTLV-I-infected and uninfected cells. Functional analysis revealed a marked defect in 59Fe-transferrin internalization in the HTLV-I-infected cells. Furthermore, the HTLV-I-infected cells showed markedly decreased transferrin receptor phosphorylation and internalization in response to active phorbol ester. Thus the data demonstrate that in peripheral blood T cells, HTLV-I infection is accompanied by surface transferrin receptor overexpression secondary to subcellular redistribution and defective internalization.

Cell Membrane↗
PubMed1984

Suppression of the anti-trimellityl (TM) IgE response in mice by conjugates of TM with polyvinyl alcohol.

The i.p. injection of 1 microgram of TM3-OA or TM9-OA with 1 mg of A1(OH)3 into B6D2F1 mice elicited the production of antibodies of the IgE and other classes to the trimellityl (TM) group and ovalbumin (OA). The induction of anti-TM antibodies belonging to the IgE and other immunoglobulin classes was specifically suppressed by the administration of tolerogenic conjugates prepared by coupling trimellitic anhydride (TMA) to the hydrophilic non-immunogenic polymer, polyvinyl alcohol (PVA), prior to immunization with TM-OA conjugates. More importantly, established anti-TM responses were also suppressed by these TM-PVA conjugates. By contrast, however, treatment with TM-PVA conjugates did not affect either the primary or the established anti-OA antibody response. The tolerogenic effects of the PVA conjugates were dose-dependent and appeared also to be dependent on the epitope density. Treatment with these conjugates also prevented immunized mice from showing any symptoms of systemic anaphylaxis on challenge with polyvalent TM-protein conjugates. These findings indicate that these conjugates may have the potential of useful therapeutic agents for the treatment of TMA-induced pulmonary hypersensitivity diseases.

Anaphylaxis↗
PubMed1993

Evidence for an alternate model of human P-glycoprotein structure and biogenesis.

We have studied the transmembrane topology of human P-glycoprotein (MDR1) using protein chimeras in Xenopus oocytes and full-length native protein in a cell-free translation system. We find both in vivo and in vitro, that the peptide region between putative transmembrane helices (TM) 8 and 9 resides in the endoplasmic reticulum lumen not in the cytosol as predicted. The topology of the carboxyl-terminal half of MDR1 therefore appears distinct from the homologous amino-terminal half in which the corresponding region between TM2 and TM3 is cytosolic. Thus, topogenic sequences encoded in the homologous amino and carboxyl domains of MDR1 direct fundamentally different events in biogenesis of the two halves of MDR1. We conclude that the transmembrane topology of MDR1, an important member of the ATP binding cassette (ABC) transporter superfamily, is not as predicted and should be revised.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1993

Membrane topology of the N-terminal half of the hamster P-glycoprotein molecule.

P-glycoprotein (Pgp) is a tandemly duplicated plasma membrane protein containing 12 predicted transmembrane (TM) segments and two cytoplasmic ATP-binding domains. Pgp appears to be responsible for multi-drug resistance in cancer cells. A detailed knowledge of the topological structure of Pgp will be required for understanding its mechanism of action. Previously, we have investigated the membrane orientation of Pgp using a cell free translation/translocation system supplemented with canine pancreatic microsomal membranes. We observed unexpectedly that the C-terminal half of the Pgp molecules was present in two different topological orientations (Zhang, J.-T., and Ling, V. (1991) J. Biol. Chem. 266, 18224-18232). In the present study, using a similar approach, we have investigated in detail the topological structure of the N-terminal half of the Pgp molecule. Again, two orientations were observed. One has all six predicted TM segments in the membrane bilayer, the other has only four TM segments in the bilayer with predicted TM3 and TM5 in a cytoplasmic and extracellular location, respectively. Although the primary sequence of Pgp appears to be a tandem duplication, the new topological structure of N-terminal half is not a simple tandem duplication of that in the C-terminal half. Thus it appears that the insertion and orientation of Pgp TM segments are dictated by specific localized sequences. These results, together with our previous findings, raise the possibility that Pgp in the native membrane may be present in different topological orientations and this feature may be important for its function.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1993

p53 mutations in mouse mammary epithelial cells: instability in culture and discordant selection of mutations in vitro versus in vivo.

The phenotypes of p53 mutations found in human and murine tumors often are analyzed using a variety of transformation assays in vitro, but data have not been available to correlate in vitro effects with in vivo activities. We have assessed the effects of p53 mutations using mouse mammary epithelial cell lines which can be analyzed both in vitro and in vivo. Parental mammary epithelial cell lines (FSK series) injected into cleared mammary fat pads of syngeneic mice frequently give rise to preneoplastic lesions (HAN) which can be reestablished in culture (TM lines) to permit analysis of genetic changes important in the development of preneoplasia. Characterization of the FSK3 cell line revealed a cell population mixed with respect to p53 genotypes. One subpopulation of mutant (Ser233-234) p53-expressing cells was selected in a preneoplastic mammary outgrowth in vivo (TM3), whereas another minor population of mutant (Pro135) p53-expressing cells was selected during culturing of FSK3 cells in vitro. When FSK3 cells were subdivided and passaged in parallel in vitro, p53 genotypes continued to evolve and diverge. These findings reveal that selective pressures exerted on mammary epithelial cell populations in vivo are different from pressures present in vitro. Selective forces may vary from one cell culture environment to another. The growth advantage conferred by a specific p53 mutation appears to differ in vivo versus in vitro. We propose that caution should be exercised when attempting to correlate the effects of p53 mutations assayed in cell culture systems with the in situ phenotypes of mutant p53 in cancer.

Amino Acid Sequence↗
PubMed1996

The molecular mechanism of T-cell control of Chlamydia in mice: role of nitric oxide.

T-cell mediated immunity (CMI) is crucial for protection against genital chlamydial infection in mice. To define the underlying molecular mechanism for this protection, several T-cell clones generated against the Chlamydia trachomatis agent of mouse pneumonitis (MoPn) were analysed in an in vitro model of the mucosal epithelium, the polarized epithelial-lymphocyte co-culture (PELC) system, for immunobiological functions that correlated with chlamydial inhibition. The six clones analysed were classified as protective or non-protective on the basis of their ability to cure genital chlamydial infection in syngeneic mice. The results revealed a direct relationship between the ability of a clone to protect in vivo and to inhibit the multiplication of MoPn in vitro. Also, the protective ability of a clone correlated with its capacity to elaborate relatively high levels of interferon-gamma (IFN-gamma) and to induce nitric oxide (NO) production. Moreover, neutralizing anti-IFN-gamma antibodies used alone at 50 micrograms/ml or in combination with anti-tumour necrosis-factor (TNF-alpha), and the L-arginine analogue and NO synthase inhibitor, NG-monomethyl-L-arginine monoacetate (MLA), could significantly suppress the ability of protective clones to inhibit MoPn in epithelial cells. The results suggested that the IFN-gamma-inducible NO synthease pathway is important for chlamydial control in mice. Furthermore, IFN-gamma could stimulate infected murine epithelial cells (line TM3) to secrete NO, resulting in inhibition of MoPn growth. However, the degree of MoPn inhibition obtained with IFN-gamma alone was less than that observed when T cells were co-cultured with infected epithelial cells. T-cell-derived NO could partly explain the enhanced chlamydial inhibition when T cells were co-cultured with infected epithelial cells. These results are consistent with the hypothesis that, besides T-cell-derived IFN-gamma, other factors associated with lymphoepithelial interactions are likely to contribute an important role in chlamydial control by T cells in mice.

Animals↗
PubMed1996

Molecular modeling of interactions between tetrahydroprotoberberines and dopamine receptors.

AIM: To build up the structure models of dopamine receptors, then combined with the receptor models, to investigate the action mechanism of tetrahydroprotoberberines (THPB) on dopamine receptors at the molecular level. METHODS: Using the three-dimensional structure of bacteriorhodopsin as a template, we have constructed dopamine D1 and D2 receptor models on computer. l-Stepholidine was selected as the leading compound of THPB and docked into D1 and D2 receptor active sites. RESULTS: After manual adjustment and energy minimization, the ligand-receptor interaction models were achieved. Based on these models, the possible action mechanism of THPB on dopamine receptors was suggested that the protonated N atom of THPB form electrostatic interaction and hydrogen-bonding interaction with residue Asp in TM3 of the receptor, the two substituents in D ring of THPB form hydrogen-bonding interactions with two Ser residues in TM5 of the receptor, and the aryl groups form pi-pi interactions with some aryl residues of the receptor around ligand. CONCLUSION: Our ligand-receptor interaction models should be helpful for rational design of more potent drugs.

Amino Acid Sequence↗
PubMed1996

Site-directed mutagenesis of the human A1 adenosine receptor: influences of acidic and hydroxy residues in the first four transmembrane domains on ligand binding.

To provide new insights into ligand/A1 adenosine receptor (A1 AR) interactions, site-directed mutagenesis was used to test the role of several residues in the first four transmembrane (TM) domains of the human A1 AR. Based on multiple sequence analysis of all known ARs, both acidic (glutamic acid and aspartic acid) and polar hydroxy (serine and threonine) amino acids were identified that could potentially play a role in binding adenosine. Glu16 (TM1), Asp55 (TM2), Ser93 and Ser94 (TM3), Ser135 (TM4), and Thr 141 (TM4) were identified in all ARs, and Ser6 and Ser23 (TM1) were identified in all A1 ARs. To test the role of these residues, each was individually mutated to alanine. When Ala6, Ala23, Ala50, Ala93, Ala135, and Ala141 constructs were tested, affinities for [3H]2-chloro-N6-cyclopentyladenosine (CCPA) and [3H]1,3-dipropyl-8-cyclopentylxanthine (DPCPX) were similar to those seen for the wild-type receptor. After conversion of Glu16 to Ala16, the affinity for [3H]CCPA and other agonists fell 10-100-fold, whereas the affinity for [3H]DPCPX and other antagonists was not affected. After conversion of Asp55 to Ala55, the affinity for [3H]CCPA and other agonists increased < or = 100-fold, whereas the affinity for [3H]DPCPX and other antagonists was not affected. Studies of the Ala55 construct also revealed that Asp55 is responsible for allosteric regulation of binding by sodium because the affinity for [3H]CCPA did not change over broad ranges of sodium concentrations. When Ser94 was converted to Ala94, A1 AR immunoreactivity was present on stable cell lines; however, functional binding sites could not be detected. When Ser94 was converted to Thr94, the affinity for some xanthine antagonists fell. These data show that Glu16 in TM1 and Asp55 in TM2 play important roles in agonist/A1 AR interactions and show that Asp55 is responsible for allosteric regulation of ligand/A1 AR binding by sodium. We also identify Ser94 as an important site for ligand binding.

Allosteric Regulation↗
PubMed1998

Molecular modelling of the vasopressin V2 receptor/antagonist interactions.

We predict some essential interactions between the V2 vasopressin renal receptor (V2R) and its selective peptide antagonist desGly9-[Mca1,D-Ile2,Ile4]AVP, and compare these predictions with the earlier ones for the non-peptide OPC-36120 antagonist- and the [Arg8]vasopressin (AVP) agonist-V2 receptor interactions. V2R controls antidiuresis in mammals and belongs to the superfamily of the heptahelical transmembrane (7TM) G protein-coupled receptors (GPCR)s. V2R was built, the ligands docked and the structures relaxed using advanced molecular modeling techniques. Both the agonist and the antagonists (no matter whether of peptide- or non-peptide type) appear to prefer a common V2R compartment for docking. The receptor amino-acid residues, potentially important in ligand binding, are mainly in the TM3-TM7 helices. A few of these residues are invariant for the whole GPCR superfamily while most of them are conserved in the subfamily of neurohypophyseal receptors, to which V2R belongs. Some of the equivalent residues in a related V1a receptor have been earlier reported as critical for the ligand affinity.

Amino Acid Sequence↗
PubMed1998

Influence of genistein (4',5,7-trihydroxyisoflavone) on the growth and proliferation of testicular cell lines.

The effects of genistein on testicular cells, TM3, TM4, and GC-1 spg, were studied in vitro. First, each cell line was cultured with pre-determined concentrations of genistein for a maximum of 72 h to assess the effects of genistein on in vitro growth of the test cells. A second series of experiments were performed to determine the degree of genistein-induced apoptosis in these cells, using Apop-Tag kit reagents, to detect apoptotic cells in situ by specific end labeling, and detection of DNA fragments produced by the apoptotic process. The results obtained indicate that: i) genistein inhibits the growth and proliferation of testicular cells; ii) growth inhibition and proliferation is dose- and exposure-time dependent; iii) there is significant difference in sensitivity of the different testicular cells to genistein; iv) genistein induces apoptosis in testicular cells in a concentration-dependent manner. Genistein-induced apoptosis identifies genistein as a potential diagnostic and therapeutic tool in testicular pathophysiological research.

Animals↗