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Tong Liu

Publications and source records attributed to Tong Liu.

At least 37 records · Page 2Linked to original sources
PubMed2006

The binding of BmK IT2 on mammal and insect sodium channels by surface plasmon resonance assay.

The binding of BmK IT2 to insect and mammal sodium channels was investigated by surface plasmon resonance technique. The results showed that BmK IT2 could bind not only to cockroach neuronal membranes but also to rat cerebrocortical and hippocampal synaptosomes with distinct affinity. The binding of BmK IT2 could be competed significantly by BmK AS and BmK abT, but not by AaH II, BmK I and veratridine. Furthermore, BmK alphaIV could partially inhibit the binding of BmK IT2 to rat cerebrocortical synaptosomes and cockroach neuronal membranes, but not to rat hippocampal synaptosomes. These results suggested that BmK IT2 had diverse binding properties on the mammal and insect sodium channels.

Animals↗
PubMed2006

Structure-function analysis of Frizzleds.

Frizzleds, cell surface receptors that mediate the actions of Wnt ligands on early development, are heptahelical (based upon hydropathy analysis) and couple to heterotrimeric G proteins. The primary structure of all ten mammalian Frizzleds display many landmarks observed in virtually all G protein-coupled receptors, including an exofacial N-terminus that is N-glycosylated, the presence of seven hydrophobic transmembrane segments predicted to form alpha-helixes, and three intracellular loops as well as a cytoplasmic, C-terminal tail that harbor suspected sites for protein phosphorylation. Prediction of the G proteins to which Frizzleds mediate signaling based upon a bioinformatic analysis of the primary sequence of the intracellular domains are in good agreement with functional screens in Drosophila, zebrafish, and mouse models of development, e.g., predicting Frizzled-1 to interact with members of the Gi/Go protein family. Likewise various Wnt signaling pathways are sensitive to treatment with pertussis toxin and knock-down of specific G protein alpha-subunits. Homology among the sequences encoding the cytoplasmic domains of human Frizzleds is high and the various Frizzleds can be segregated into subsets predicted to share some common downstream signaling elements. Among different species, homologies can reveal conservation of signaling to cognate G protein partners. Additionally, cytoplasmic domains of the prototypic beta2-adrenergic receptor can be substituted with those from either Frizzled-1 or Frizzled-2 to create chimeric receptors that are activated by beta-adrenergic agonists, yet signal with high fidelity to the Wnt/beta-catenin and Wnt/Ca2+, cyclic GMP pathways, respectively, regulating key aspects of early development. The nature of Frizzled-based signaling complexes, their temporal assembly, and spatial distribution via scaffold protein remains to be elucidated, as does whether or not these Wnt receptors display agonist-induced desensitization, internalization, and re-cycling to the cell membrane.

Amino Acid Sequence↗
PubMed2006

Structure and stability of apolipoprotein a-I in solution and in discoidal high-density lipoprotein probed by double charge ablation and deletion mutation.

To identify residues and segments in the central region of apolipoprotein A-I (apoA-I) that are important for the protein structure and stability, we studied the effects of four double charge ablations, D102A/D103A, E110A/E111A, R116V/K118A, and R160V/H162A, and two deletion mutations, Delta(61-78) and Delta(121-142), on the conformation and stability of apoA-I in the lipid-free state and in reconstituted discoidal phospholipid-cholesterol-apoA-I particles (rHDL). The findings suggest that D102/D103 and E110/E111 located in helix 4 and segment(s) between residues 61 and 78 are involved in maintenance of the conformation and stability of apoA-I in both the lipid-free state and in rHDL. R116/K118 located in helix 4 are essential for the conformation and stabilization of apoA-I in rHDL but not vital for the lipid-free state of the protein. The R160V/H162A substitutions in helix 6 lead to a less compact tertiary structure of lipid-free apoA-I without notable effects on the lipid-free or lipid-bound secondary conformation, suggesting involvement of R160/H162 in important interhelical interactions. The results on the Delta(121-142) mutant, together with our earlier findings, suggest disordered structure of a major segment between residues 121 and 143, likely including residues 131-143, in lipid-free apoA-I. Our findings provide the first experimental evidence for stabilization of rHDL by specific electrostatic interhelical interactions, in agreement with the double belt model. The effects of alterations in the conformation and stability of the apoA-I mutants on in vitro and in vivo functions of apoA-I and lipid homeostasis are discussed.

Anilino Naphthalenesulfonates↗
PubMed2006

Optimized proteomic analysis of a mouse model of cerebellar dysfunction using amine-specific isobaric tags.

Recent proteomic applications have demonstrated their potential for revealing the molecular mechanisms underlying neurodegeneration. The present study quantifies cerebellar protein changes in mice that are deficient in plasma membrane calcium ATPase 2 (PMCA2), an essential neuronal pump that extrudes calcium from cells and is abundantly expressed in Purkinje neurons. PMCA2-null mice display motor dyscoordination and unsteady gait deficits observed in neurological diseases such as multiple sclerosis and ataxia. We optimized an amine-specific isobaric tags (iTRAQ)-based shotgun proteomics workflow for this study. This workflow took consideration of analytical variance as a function of ion signal intensity and employed biological repeats to aid noise reduction. Even with stringent protein identification criteria, we could reliably quantify nearly 1000 proteins, including many neuronal proteins that are important for synaptic function. We identified 21 proteins that were differentially expressed in PMCA2-null mice. These proteins are involved in calcium homeostasis, cell structure and chromosome organization. Our findings shed light on the molecular changes that underlie the neurological deficits observed in PMCA2-null mice. The optimized workflow presented here will be valuable for others who plan to implement the iTRAQ method.

Amines↗
PubMed2006

Room temperature formation of ammonia by oxidizing hydrogenated cerium nanoparticles in the air.

Ammonia formation was observed when hydrogenated cerium nanoparticles prepared by hydrogen plasma-metal reaction (HPMR) were exposed to the air at room temperature. This novel phenomenon represents a successful example of room temperature cleavage of dinitrogen and may find application in low temperature synthesis of ammonia under thermodynamically favorable conditions. A possible mechanism is also proposed. We suggest that the oxidation of cerium hydride offers chemical force to drive the hydrogen atoms out of the lattice. The monoatomic H released to the surface is highly active and readily reacts with N2 to yield ammonia. Some surface processes, which we know little about at the moment, are likely to be involved so as to lower the energy barrier of nitrogen dissociation. Further investigation is required to elucidate the detailed mechanism.

Air↗
PubMed2006

Synthesis and characterization of Fe/Nd2O3 core-shell nanoparticles by hydrogen plasma-metal reaction.

Fe/Nd2O3 core-shell nanoparticles (CSNs) with a mean diameter of 35 nm were produced successfully by using hydrogen plasma-metal reaction (HPMR) method. This core-shell structure was confirmed by high resolution transmission electron microscopy (HRTEM), energy dispersion X-ray spectroscopy (EDS), X-ray photoelectron spectral (XPS), and induction-coupled plasma (ICP) spectroscopy. The magnetic properties were measured by vibrating sample magnetometer (VSM). It was found that the mole ratio of Nd to Fe on the nanoparticle surface is 1.2:1, about 7 times of that of the whole nanoparticle. The saturation magnetization Ms and remanence Mr of Fe/Nd2O3 nanoparticles decrease prominently from Fe nanoparticles, whereas the coercivity Hc drops only less than 5% of Fe nanoparticle. These CSNs have potential applications in magnetic and catalytic fields.

Gases↗
PubMed2005

Diamide stress induces a metallothionein BmtA through a repressor BxmR and is modulated by Zn-inducible BmtA in the cyanobacterium Oscillatoria brevis.

A cysteine-rich metal binding protein MT (metallothionein) (named BmtA) is induced upon exposure to multiple heavy metal ions in the freshwater cyanobacterium Oscillatoria brevis. The SmtB/ArsR family repressor BxmR from O. brevis represses the expression of an operon encoding bmtA and bxmR. In the present study, the expression of bmtA was induced in vivo by diamide, a specific thiol oxidant, in O. brevis cells. In vitro electrophoretic gel mobility shift experiments revealed that the incubation with diamide induces disassembly of the BxmR-bxmR/bmtA operator (O)/promoter (P) complex [multiple resolvable complexes of BxmR with oligonucleotide (named P5) containing a single 12-2-12 inverted repeat derived from the O/P region of bxmR/bmtA]. Thus, the exposure to diamide induces MT mRNA in O. brevis, and this induction is associated with diamide-mediated inhibition of BxmR-P5 complex. BxmR is more sensitive to diamide than to H(2)O(2). Furthermore, pretreatment of O. brevis with Zn decreased intracellular peroxidation products caused by diamide. Thus, these results imply that MT induced by Zn-pretreatment functions to protect O. brevis cells against diamide stress.

Cyanobacteria↗
PubMed2005

Point mutations in apolipoprotein A-I mimic the phenotype observed in patients with classical lecithin:cholesterol acyltransferase deficiency.

We have analyzed the effect of charged to neutral amino acid substitutions around the kinks flanking helices 4 and 6 of apoA-I and of the deletion of helix 6 on the in vivo activity of LCAT and the biogenesis of HDL. The LCAT activation capacity of apoA-I in vitro was nearly abolished by the helix 6 point (helix 6P-apoA-I[R160V/H162A]) and deletion {helix 6Delta-apoA-I[Delta(144-165)]} mutants, but was reduced to 50% in the helix 4 point mutant (helix 4P-apoA-I[D102A/D103A]). Following adenovirus-mediated gene transfer in apoA-I deficient mice, the level of plasma HDL cholesterol was greatly reduced in helix 6P and helix 6Delta mutants. Electron microscopy and two-dimensional gel electrophoresis showed that the helix 6P mutant formed predominantly high levels of apoA-I containing discoidal particles and had an increased prebeta1-HDL/alpha-HDL ratio. The helix 6Delta mutant formed few spherical particles and had an increased prebeta1-HDL/alpha-HDL ratio. Mice infected with adenovirus expressing the helix 4P mutant or wild-type apoA-I had normal HDL cholesterol and formed spherical alpha-HDL particles. Coinfection of mice with adenoviruses expressing human LCAT and the helix 6P mutant dramatically increased plasma HDL and apoA-I levels and converted the discoidal into spherical HDL, indicating that the LCAT activity was rate-limiting for the biogenesis of HDL. The LCAT treatment caused only a small increase in HDL cholesterol and apoA-I levels and in alpha-HDL particle numbers in the helix 6Delta mutant. The findings indicate a critical contribution of residue 160 of apoA-I to the in vivo activity of LCAT and the subsequent maturation of HDL and explain the low HDL levels in heterozygous subjects carrying this mutation.

Animals↗
PubMed2005

The epileptic seizures induced by BmK I, a modulator of sodium channels.

In the present study, the susceptibility to rat epileptic seizures induced by the intrahippocampal administration of BmK I, a modulator of sodium channels purified from the venom of Chinese scorpion, has been investigated. The results showed that the strong epileptic behaviors and discharges in the hippocampus were evoked by BmK I dose-dependently. The hippocampal c-Fos expression displayed two peak waves in a specific spatio-temporal pattern elicited by BmK I. The whole cell patch clamp recordings showed that the inactivation of sodium currents in rat cultured hippocampal neurons was prolonged significantly by BmK I, and restored partially after washing. These results indicated that the rat hippocampus is a susceptible target for the proconvulsant effects of BmK I, and the induction of epileptic seizures may be ascribed to the modulation of BmK I on the inactivation of voltage-gated sodium channels distributing in the rat hippocampal neurons.

Animals↗
PubMed2005

A zinc(II)/lead(II)/cadmium(II)-inducible operon from the Cyanobacterium anabaena is regulated by AztR, an alpha3N ArsR/SmtB metalloregulator.

A novel Zn(II)/Pb(II)/Cd(II)-responsive operon that consists of genes encoding a Zn(II)/Pb(II) CPx-ATPase efflux pump (aztA) and a Zn(II)/Cd(II)/Pb(II)-specific SmtB/ArsR family repressor (aztR) has been identified and characterized from the cyanobacterium Anabaena PCC 7120. In vivo real time quantitative RT-PCR assays reveal that both aztR and aztA expression are induced by divalent metal ions Zn(II), Cd(II), and Pb(II) but not by other divalent [Co(II), Ni(II)] or monovalent metal ions [Cu(I) and Ag(I)]. The introduction of a plasmid containing the azt operon into a Zn(II)/Cd(II)-hypersensitive Escherichia coli strain GG48 functionally restores Zn(II) and Pb(II) resistance with a limited effect on Cd(II) resistance. Gel mobility shift assays and aztR O/P-lacZ induction experiments confirm that AztR is the metal-regulated repressor of this operon. In vitro biochemical and mutagenesis studies indicate that AztR contains a sole metal-binding site, designated the alpha3N site, that binds Zn(II), Cd(II), and Pb(II) with a high affinity. Optical absorption spectra of Co(II)- and Cd(II)-substituted AztR and (113)Cd NMR spectroscopy of (113)Cd(II)-substituted AztR reveal that the sole alpha3N site in AztR is a CadC-like distorted tetrahedral S(3)(N,O) metal site. The first metal-coordination shell in the AztR alpha3N site differs from other alpha3N family members that sense Cd(II)/Pb(II) and those alpha5 repressors that sense Zn(II)/Co(II). Our results reveal that the alpha3N site in AztR mediates derepression of the azt operon in the presence of Zn(II), as well as Cd(II) and Pb(II); this might have provided Anabaena with an evolutionary advantage to adapt to heavy-metal-rich environments, while maintaining homeostasis of an essential metal ion, Zn(II).

Amino Acid Sequence↗
PubMed2005

Cleavage site selection within a folded substrate by the ATP-dependent lon protease.

Mechanistic studies of ATP-dependent proteolysis demonstrate that substrate unfolding is a prerequisite for processive peptide bond hydrolysis. We show that mitochondrial Lon also degrades folded proteins and initiates substrate cleavage non-processively. Two mitochondrial substrates with known or homology-derived three-dimensional structures were used: the mitochondrial processing peptidase alpha-subunit (MPPalpha) and the steroidogenic acute regulatory protein (StAR). Peptides generated during a time course of Lon-mediated proteolysis were identified and mapped within the primary, secondary, and tertiary structure of the substrate. Initiating cleavages occurred preferentially between hydrophobic amino acids located within highly charged environments at the surface of the folded protein. Subsequent cleavages proceeded sequentially along the primary polypeptide sequence. We propose that Lon recognizes specific surface determinants or folds, initiates proteolysis at solvent-accessible sites, and generates unfolded polypeptides that are then processively degraded.

Adenosine Triphosphate↗
PubMed2005

Deletions of helices 2 and 3 of human apoA-I are associated with severe dyslipidemia following adenovirus-mediated gene transfer in apoA-I-deficient mice.

The objective of this study was to determine the effect of two amino-terminal apolipoprotein A-I (apoA-I) deletions on high-density lipoprotein (HDL) biosynthesis and lipid homeostasis. Adenovirus-mediated gene transfer showed that the apoA-I[Delta(89-99)] deletion mutant caused hypercholesterolemia, characterized by increased plasma cholesterol and phospholipids, that were distributed in the very low density/intermediate density/low-density lipoprotein (VLDL/IDL/LDL) region, and normal triglycerides. The capacity of the mutant protein to promote ATP-binding cassette transporter A1- (ABCA1-) mediated cholesterol efflux and to activate lecithin:cholesterol acyltranserase (LCAT) was approximately 70-80% of the wild-type (WT) control. The phospholipid transfer protein (PLTP) activity of plasma containing the apoA-I[Delta(89-99)] mutant was decreased to 32% of the WT control. Similar analysis showed that the apoA-I[Delta(62-78)] deletion mutant in apoA-I-deficient mice caused combined hyperlipidemia characterized by increased triglycerides, cholesterol, and phospholipids in the VLDL/IDL region. There was enrichment of the VLDL/IDL with mutant apoA-I that resulted in reduction of in vitro lipolysis. The capacity of this mutant to promote ABCA1-mediated cholesterol efflux was normal, and the capacity to activate LCAT in vitro was reduced by 53%. The WT apoA-I and the apoA-I[Delta(62-78)] mutant formed spherical HDL particles, whereas the apoA-I[Delta(89-99)] mutant formed discoidal HDL particles. We conclude that alterations in apoA-I not only may have adverse effects on HDL biosynthesis but also may promote dyslipidemia due to interference of the apoA-I mutants on the overall cholesterol and triglycerides homeostasis.

Adenoviridae↗