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T Zhou

Publications and source records attributed to T Zhou.

At least 37 records · Page 2Linked to original sources

Structural basis for the catalysis and substrate specificity of homoserine kinase.

Homoserine kinase (HSK), the fourth enzyme in the aspartate pathway of amino acid biosynthesis, catalyzes the phosphorylation of L-homoserine (Hse) to L-homoserine phosphate, an intermediate in the production of L-threonine, L-isoleucine, and in higher plants, L-methionine. The high-resolution structures of Methanococcus jannaschii HSK ternary complexes with its amino acid substrate and ATP analogues have been determined by X-ray crystallography. These structures reveal the structural determinants of the tight and highly specific binding of Hse, which is coupled with local conformational changes that enforce the sequestration of the substrate. The delta-hydroxyl group of bound Hse is only 3.4 A away from the gamma-phosphate of the bound nucleotide, poised for the in-line attack at the gamma-phosphorus. The bound nucleotides are flexible at the triphosphate tail. Nevertheless, a Mg(2+) was located in one of the complexes that binds between the beta- and gamma-phosphates of the nucleotide with good ligand geometry and is coordinated by the side chain of Glu130. No strong nucleophile (base) can be located near the phosphoryl acceptor hydroxyl group. Therefore, we propose that the catalytic mechanism of HSK does not involve a catalytic base for activating the phosphoryl acceptor hydroxyl but instead is mediated via a transition state stabilization mechanism.

Adenosine Triphosphate↗

Conformational changes in four regions of the Escherichia coli ArsA ATPase link ATP hydrolysis to ion translocation.

Structures of ArsA with ATP, AMP-PNP, or ADP.AlF(3) bound at the A2 nucleotide binding site were determined. Binding of different nucleotides modifies the coordination sphere of Mg(2+). In particular, the changes elicited by ADP.AlF(3) provide insights into the mechanism of ATP hydrolysis. In-line attack by water onto the gamma-phosphate of ATP would be followed first by formation of a trigonal intermediate and then by breaking of the scissile bond between the beta- and gamma-phosphates. Motions of amino acid side chains at the A2 nucleotide binding site during ATP binding and hydrolysis propagate at a distance, producing conformational changes in four different regions of the protein corresponding to helices H4-H5, helices H9-H10, helices H13-H15, and to the S1-H2-S2 region. These elements are extensions of, respectively, the Switch I and Switch II regions, the A-loop (a small loop near the nucleotide adenine moiety), and the P-loop. Based on the observed conformational changes, it is proposed that ArsA functions as a reciprocating engine that hydrolyzes 2 mol of ATP per each cycle of ion translocation across the membrane.

Adenine↗

[A survey on blood lipid levels among newborns and healthy inhabitants in urban Shanghai from 1997 to 1999].

OBJECTIVE: To analyze the blood lipid levels among inhabitants of different ages in urban Shanghai by the end of 1990 and compare the results with those in 1970 s and 1980 s. METHODS: Venous blood samples were collected from 3647 persons undergoing annual health examination, including workers and staff members, employees, functionaries, and students of factories, governmental organizations, institutions, enterprises, and schools. Umbilical blood samples were collected from 88 newborns. Serum TC, TG, LDL-C, and HDL-C were determined. RESULTS: 3647 blood samples were collected in total. It is found that: (1) The levels of blood lipids increased along with the age. The levels of TC and LDL-C among females over their fifty were higher that those among the males in the same age groups. The level of TG among females over fifty was similar to that among the males in the same age groups. The levels of LDL-C were higher in families in all of the age groups than those in the males of the same ages. (2) In comparison to those in 1970 s the levels of TC and TG in 1990 s were significantly higher by 6.79% - 17.69% and 21.95% - 45.53% respectively, and the level of HDL-C decreased by 8.02% - 29.19%. (3) The percentage of persons over forty with their TC levels over the upper normal limit was much larger in 1990 s than in 1970 s (for TC 11.57% vs. 4.40% among males and 16.02% vs. 5.40% among females, for TG 21.83% vs. 5.20% among males and 13.32% vs. 5.70% among females). and (4) The percentage of persons with their TC/HDL-C >or= 4 and TG >or= 1.70 mmol/L was much larger among persons over forty than among persons under forty (20.74% vs. 10.99% among males and 13.32% vs. 2.05% among females). CONCLUSION: The mean serum TC, TG, and LDL-C levels increased and the HDL-C level decreased significantly among healthy inhabitants in urban Shanghai in 1990 s. Along with the rise of living standards of people, their mean lipid level increases too. Nutrition education is necessary.

Adolescent↗

[Effects of aspirin on ferritin expression and resistance to oxidative damage in endothelial cells].

OBJECTIVE: To explore the mechanism of Aspirin induced ferritin synthesis on resistance to oxidative damage in endothelial cells. METHODS: Using cultured endothelial cells, we measured the effect of aspirin with different incubative time (4 - 24 h) and different concentration (0.1 - 3 mmol/L), salicylic acid and indomethacin induced ferritin expression by ELISA kit, and observed the change of lactate dehydrogenase (LDH) release rate, malondialdehyde (MDA) and cellular viability after preincubating the cell for 8 h with aspirin on resistance to hydrogen peroxide toxicity. Statistical analysis using a one-way analysis of variance. RESULTS: Aspirin at low concentration (0.1 mmol/L) induced significant increase ferritin expression in a concentration-dependent fashion: (5.8 +/- 0.3) ng/10(6) cell (0.1 mmol/L As), (6.4 +/- 0.4) ng/10(6) cell (0.5 mmol/L As), (7.0 +/- 0.7) ng/10(6) cell (1 mmol/L As), (7.4 +/- 0.4) ng/10(6) cell (2 mmol/L As), (7.7 +/- 0.5) ng/10(6) cell (3 mmol/L As), significant for all values: P < 0.05 versus normal control. Induction of ferritin levels by aspirin (1 mmol/L) was also time dependent: (5.8 +/- 1.0) ng/10(6) cell (4 h, but P > 0.05 vs control), (6.5 +/- 1.0) ng/10(6) cell (8 h, P < 0.05 vs control) and (7.8 +/- 0.8) ng/10(6) cell (24 h). Preincubating the cells with aspirin (0.1 mmol/L) reduced LDH release rate by 50%, toxicity reduction by 40%, and significant decrease MDA production. Aspirin induced cytoprotection from H(2)O(2) damage was also in a concentration dependent fashion. The cytoprotection of aspirin was mimicked by exogenous iron-free apo-ferritin but not iron-load ferritin. Salicylic acid and indomethacin failed to increase ferritin expression. CONCLUSION: Aspirin could induce significant increase ferritin synthesis at low concentration (0.1 mmol/L). Ferritin induction by aspirin was specific in nonsteroidal anti-inflammatory drugs.

Antioxidants↗

The intronless and TATA-less human TAF(II)55 gene contains a functional initiator and a downstream promoter element.

Human TAF(II)55 (hTAF(II)55) is a component of the multisubunit general transcription factor TFIID and has been shown to mediate the functions of many transcriptional activators via direct protein-protein interactions. To uncover the regulatory properties of the general transcription machinery, we have isolated the hTAF(II)55 gene and dissected the regulatory elements and the core promoter responsible for hTAF(II)55 gene expression. Surprisingly, the hTAF(II)55 gene has a single uninterrupted open reading frame and is the only intronless general transcription factor identified so far. Its expression is driven by a TATA-less promoter that contains a functional initiator and a downstream promoter element, as illustrated by both transfection assays and mutational analyses. Moreover, this core promoter can mediate the activity of a transcriptional activator that is artificially recruited to the promoter in a heterologous context. Interestingly, in the promoter-proximal region there are multiple Sp1-binding sites juxtaposed to a single AP2-binding site, indicating that Sp1 and AP2 may regulate the core promoter activity of the hTAF(II)55 gene. These findings indicate that a combinatorial regulation of a general transcription factor-encoding gene can be conferred by both ubiquitous and cell type-specific transcriptional regulators.

Base Sequence↗

Accurate in vitro end joining of a DNA double strand break with partially cohesive 3'-overhangs and 3'-phosphoglycolate termini: effect of Ku on repair fidelity.

To examine determinants of fidelity in DNA end joining, a substrate containing a model of a staggered free radical-mediated double-strand break, with cohesive phosphoglycolate-terminated 3'-overhangs and a one-base gap in each strand, was constructed. In extracts of Xenopus eggs, human lymphoblastoid cells, hamster CHO-K1 cells, and a Chinese hamster ovary (CHO) derivative lacking the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs), the predominant end joining product was that corresponding to accurate restoration of the original sequence. In extracts of the Ku-deficient CHO derivative xrs6, a shorter product, consistent with 3' --> 5' resection before ligation, was formed. Similar results were seen for a substrate with 5'-overhangs and recessed 3'-phosphoglycolate ends. Supplementation of the xrs6 extracts with purified Ku restored accurate end joining. In Xenopus and human extracts, but not in hamster extracts, gap filling and ligation were blocked by wortmannin, consistent with a requirement for DNA-PKcs activity. The results suggest a Ku-dependent pathway, regulated by DNA-PKcs, that can accurately restore the original DNA sequence at sites of free radical-mediated double-strand breaks, by protecting DNA termini from degradation and maintaining the alignment of short partial complementarities during gap filling and ligation.

Androstadienes↗

Cutting edge: a role for B lymphocyte stimulator in systemic lupus erythematosus.

Increased levels of B lymphocyte stimulator (BLyS) are associated with systemic autoimmunity in animal models of spontaneous autoimmune disease, and transgenic animals expressing BLyS develop typical autoimmune disease. Here, we demonstrate significant elevations of BLyS in the patients with systemic lupus erythematosus (SLE). The BLyS isolated from the sera of SLE patients had the same m.w. as the natural soluble form and was able to stimulate B cell activation in vitro. Increased BLyS in SLE patients was partially associated with higher levels of anti-dsDNA Ab of the IgG, IgM, and IgA classes, but not associated with the disease activity. Our results suggest that BLyS may be a useful marker for early activation of an autoimmune diathesis and likely plays a critical role in triggering activation of self-Ag-driven autoimmune B cells in human SLE. BLyS may provide an effective therapeutic target in systemic autoimmunity.

Animals↗

Defective Fas ligand-mediated apoptosis predisposes to development of a chronic erosive arthritis subsequent to Mycoplasma pulmonis infection.

OBJECTIVE: To determine whether defective T cell apoptosis is associated with the development of a chronic arthritis subsequent to mycoplasma infection, and to determine whether deletion of T cells can prevent the development of this arthritis. METHODS: B6 wild-type (B6-+/+), B6-lpr/lpr, and B6-gld/gld mice were infected with Mycoplasma pulmonis. The severity of lymphocytic infiltration and joint damage was evaluated, and the degree of recovery of viable mycoplasma from the spleen and joints was determined. Antigen-presenting cells derived from Fas mutant lpr mice (lpr-APC) were transfected ex vivo with an adenovirus (Ad) vector to yield lpr-APC expressing high levels of Fas ligand (lpr-APC-AdFasL), which in turn were transferred intraperitoneally into M pulmonis-infected B6-gld/gld mice. The development of arthritis subsequent to M pulmonis infection and the induction of apoptosis of cells within the synovial tissue and lymph nodes of lpr-APC-AdFasL-treated B6-gld/gld mice were determined. RESULTS: Infection of B6-lpr/lpr and B6-gld/gld mice with M pulmonis resulted in an acute-phase inflammation of the synovium that later developed into a chronic erosive arthritis. Similar infection of B6-+/+ mice resulted only in an acute joint inflammatory response that resolved. Chronic arthritis in B6-gld/gld mice and B6-lpr/lpr was not due to persistent infection, since there were no differences in the rates of clearance of M pulmonis from the joints of B6-gld/gld or B6-lpr/lpr mice compared with B6-+/+ mice. Treatment of infected B6-gld/gld mice with lpr-APC-AdFasL resulted in a significantly decreased incidence of chronic arthritis that was associated with a decrease in lymph node T cells, but not with apoptosis of synovial T cells or fibroblasts. CONCLUSION: Defective Fas/FasL-mediated apoptosis of T cells is an important factor that rendered arthritis-resistant B6 mice susceptible to the development of a chronic erosive arthritis subsequent to mycoplasma infection. In vivo lpr-APC-AdFasL cell-gene therapy is a safe and effective method for inhibiting the development of this arthritis.

Acute Disease↗

Effects of methylmercury on ontogeny of prey capture ability and growth in three populations of larval Fundulus heteroclitus.

We used three populations of mummichogs (Fundulus heteroclitus), one from a polluted site (Piles Creek [PC], New Jersey) and two from cleaner sites (Tuckerton [TK], New Jersey, and East Hampton [EH], New York), to study (1) whether embryonic, embryonic plus larval, or larval exposure to methylmercury (MeHg) altered larval prey capture ability and growth; and (2) whether there were differences in tolerance to MeHg-induced behavioral changes among the three populations. Eggs and sperm were obtained from mummichogs captured in the field, and their embryos and larvae were kept in clean sea water or MeHg solution (5, 10 microg/L). Larvae were then tested regularly for prey capture rates and prey capture efficiencies, and their lengths were measured. Embryonic exposure to MeHg induced transitory and recoverable impairments in larval prey capture ability, whereas larval exposure alone was relatively ineffective. When both embryos and larvae were treated, larval prey capture ability was affected at a lower concentration and a wider range of larval ages. In terms of growth and prey capture ability, response of larvae to embryonic or larval or exposure to both stages to MeHg varied with populations. TK fish were the most tolerant with respect to behavioral changes but were the most sensitive to MeHg in reduction of growth. EH fish were the most sensitive whenever embryos were treated, and PC fish were the most vulnerable after larval exposure. The population differences in response to MeHg intoxication may be due to pollution related factors or differences in behavioral-related genetic factors.

Animals↗

Aged mice exhibit in vivo defective peripheral clonal deletion of D(b)/H-Y reactive CD8(+) T cells.

We previously reported that T cells from aged mice were resistant to activation-induced cell death (AICD) in vitro. To determine whether the presence of AICD-resistant T cells is associated with defects in age-related peripheral clonal deletion in vivo, congenic male SCID mice were reconstituted with T cells from aged or young female D(b)/H-Y TCR (Tg71) transgenic mice. Compared with recipients of young cells, the recipients of T cells from aged mice exhibited a 3-fold increase in the percentage of autoreactive CD8(+) H-Y antigen-reactive T cells as defined by the clonotypic antibody, M33. There were significantly increased sera levels of interferon-gamma, a significantly decreased expression of FasL by M33(+)CD8(+) T cells, and significantly decreased apoptosis by DNA fragmentation staining of the spleen of mice reconstituted with T cells from aged mice compared to those from young mice. By day 21, the recipients of T cells from aged mice but not young mice, exhibited infiltration of CD3(+) cells into the non-lymphoid organs. These results indicate that there is defective peripheral deletion of the self-reactive T cells derived from aged female Tg71 mice, and that failure to delete these cells is associated with the defective T-cell clonal deletion in the recipient mice.

Adoptive Transfer↗

A quartz crystal microbalance cell biosensor: detection of microtubule alterations in living cells at nM nocodazole concentrations.

The quartz crystal microbalance (QCM) was used to create a piezoelectric biosensor utilizing living endothelial cells (ECs) as the biological signal transduction element. ECs adhere to the hydrophilically treated gold QCM surface under growth media containing serum. At 24 h following cell addition, calibration curves were constructed relating the steady state Deltaf and DeltaR shift values observed to the numbers of electronically counted cells requiring trypsinization to be removed from the surface. We then utilized this EC QCM biosensor for the detection of the effect of [nocodazole] on the steady state Deltaf and DeltaR shift values. Nocodazole, a known microtubule binding drug, alters the cytoskeletal properties of living cells. At the doses used in these studies (0.11-15 microM), nocodazole, in a dose dependent fashion, causes the depolymerization of microtubules in living cells. This leads a monolayer of well spread ECs to gradually occupy a smaller area, lose cell to cell contact, exhibit actin stress fibers at the cell periphery and acquire a rounded cell shape. We observed the negative Deltaf shift values and the positive DeltaR shift values to increase significantly in magnitude over a 4-h incubation period following nocodazole addition, in a dose dependent fashion, with a transition midpoint of 900 nM. Fluorescence microscopy of the ECs, fixed on the gold QCM surface and stained for actin, demonstrated that the shape and cytoskeleton of ECs were affected by as little as 330 nM nocodazole. These results indicate that the EC QCM biosensor can be used for the study of EC attachment and to detect EC cytoskeletal alterations. We suggest the potential of this cellular biosensor for the real time identification or screening of all classes of biologically active drugs or biological macromolecules that affect cellular attachment, regardless of their molecular mechanism of action.

Actins↗

The Fas signaling connection between autoimmunity and embryonic lethality.

The first gene to cause systemic autoimmune disease in mice was identified as the fas gene, which is mutated in lymphoproliferative (lpr) mice. These mice exhibited a defect in activation-inducted cell death of T cells and B cells in vivo, causing a failure of proper clearance of immune cells and defective down-modulation of an immune response. This led to the speculation that apoptosis defects may play a role in defective down-modulation of the hyperimmune response observed in human autoimmune diseases. More recently, scientists have generated different mouse lines with defects in Fas-apoptosis-associated molecules such as FADD and Apaf-1. These mice, however, died during embryonic development and did not develop autoimmune disease. These findings suggest that molecules associated with Fas apoptosis signaling can be important at the most limited levels for development of the immune system but also have more global apoptosis roles in other systems. We propose that the more global role of Fas-associated apoptosis molecules should be considered when evaluating their role in autoimmune disease.

Animals↗

Tumoricidal activity of a novel anti-human DR5 monoclonal antibody without hepatocyte cytotoxicity.

A novel anti-human DR5 monoclonal antibody, TRA-8, induces apoptosis of most tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-sensitive tumor cells both in vitro and in vivo. In contrast to both the membrane-bound form of human TRAIL, which induced severe hepatitis in mice, and the soluble form of human TRAIL, which induced apoptosis of normal human hepatocytes in vitro, TRA-8 did not induce significant cell death of normal human hepatocytes. However, both primary hepatocellular carcinoma cells and an established liver cancer cell line were highly susceptible to the killing mediated by TRA-8. We show here that elevated levels of cell-surface expression of DR5 and increased susceptibility to DR5-mediated apoptosis are characteristics of malignant tumor cells. In contrast, DR5 alone is not sufficient to trigger apoptosis of normal hepatocytes. Therefore, selective, specific targeting of DR5 with an agonistic antibody might be a safe and effective strategy for cancer therapy.

Animals↗

Study of the separation and determination of monosaccharides in soluble coffee by capillary zone electrophoresis with electrochemical detection.

A simple, fast and reliable method, based on capillary electrophoresis with electrochemical detection, for the separation and determination of six monosaccharides, namely glucose, galactose, arabinose, fructose, xylose and ribose, in soluble coffees was developed. A copper disk electrode was used as the working electrode. The optimum conditions for separation and detection were 50 mmol L-1 sodium hydroxide buffer (pH 12.7), separation voltage 5 kV and detection potential 0.65 V (vs. Ag/AgCl). The linear ranges were from 5.0 x 10(-3) to 0.5 mmol L-1 for all six sugars. All regression coefficients were > 0.99. The detection limits for all the sugars were 1.0 x 10(-3) mmol L-1. The RSD of the peak current was < 4.2% (n = 5). The proposed method was applied directly to the separation and determination of the six sugars without prior derivatization, and the assay results were satisfactory.

Journal Article↗

Effects of short-term in vivo exposure to polybrominated diphenyl ethers on thyroid hormones and hepatic enzyme activities in weanling rats.

Polybrominated diphenyl ethers (PBDEs), used as flame retardants, are ubiquitous environmental contaminants. PBDEs act as endocrine disruptors via alterations in thyroid hormone homeostasis. We examined thyroid hormone concentrations and hepatic enzyme activity in weanling rats exposed to three commercial PBDE mixtures: DE-71, DE-79, and DE-83R. Female Long-Evans rats, 28 days old, were orally administered various doses of DE-71, DE-79, or DE-83R for 4 days. Serum and liver samples were collected 24 h after the last dose and analyzed for serum total thyroxine (T(4)), triiodothyronine (T(3)), thyroid-stimulating hormone (TSH), hepatic microsomal ethoxy- and pentoxy-resorufin-O-deethylase (EROD and PROD), and uridinediphosphate-glucuronosyltransferase (UDPGT) activities. The PBDE-treated groups did not exhibit significant changes in body weight; however, increased liver weights, as well as 10- to 20-fold induction in EROD and 30- to 40-fold induction in PROD were found in the DE-71-- and DE-79--treated animals. DE-71 and DE-79 caused dose-dependent depletion of T(4), accompanied by up to 3- to 4-fold induction in UDPGT activities. Serum total T(4) was decreased a maximum of 80% for DE-71 and 70% for DE-79 in the highest dose, with benchmark doses (BMDs) of approximately 12.74 mg/kg/day for DE-71 and 9.25 mg/kg/day for DE-79. Dose-related effects in serum T(3) levels were less apparent, with maximal reductions of 25-30% at the highest dose for both DE-71 and DE-79. The two mixtures showed no effect on serum TSH levels. Benchmark dose analysis revealed that the two mixtures were comparable in altering thyroid hormone levels and hepatic enzyme activity. DE-83R was not effective in altering any of the measured parameters. The present study suggests that short-term exposure to some commercial PBDE mixtures interferes with the thyroid hormone system via upregulation of UDPGTS:

Animals↗

Fastigial nucleus-mediated respiratory responses depend on the medullary gigantocellular nucleus.

Electrical stimulation of the rostral fastigial nucleus (FNr) alters respiration via activation of local neurons. We hypothesized that this FNr-mediated respiratory response was dependent on the integrity of the nucleus gigantocellularis of the medulla (NGC). Electrical stimulation of the FNr in 15 anesthetized and tracheotomized spontaneously breathing rats significantly altered ventilation by 35.2 +/- 11.0% (P < 0.01) with the major effect being excitatory (78%). This respiratory response did not significantly differ from control after lesions of the NGC via bilateral microinjection of kainic or ibotenic acid (4.5 +/- 1.9%; P > 0.05) but persisted in sham controls. Eight other rats, in which horseradish peroxidase (HRP) solution was previously microinjected into the left NGC, served as nonstimulation controls or were exposed to either 15-min repeated electrical stimulation of the right FNr or hypercapnia for 90 min. Histochemical and immunocytochemical data showed that the right FNr contained clustered HRP-labeled neurons, most of which were double labeled with c-Fos immunoreactivity in both electrically and CO(2)-stimulated rats. We conclude that the NGC receives monosynaptic FNr inputs and is required for fully expressing FNr-mediated respiratory responses.

Animals↗