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Biomedical subjects

E Yang

Publications and source records attributed to E Yang.

At least 19 recordsLinked to original sources
PubMed2006

catena-Poly[[[cis-aquabis(4-carboxycyclohexane-1-carboxylato-kappa2O,O')cadmium(II)]-mu-4,4'-bipyridine-kappa2N:N] monohydrate].

The title complex, {[Cd(C8H11O4)2(C10H8N2)(H2O)].H2O}(n), consists of linear chains formed through 4,4'-bipyridine ligands linking seven-coordinated Cd(II) ions. Each Cd(II) ion is in a distorted pentagonal-bipyramidal environment, coordinated by one water ligand, two 4-carboxycyclohexane-1-carboxylate ligands and one bridging 4,4'-bipyridine ligand to generate linear chains. The water molecules and the Cd atom on one side, and the 4,4'-bipyridine unit on the other, are bisected by two sets of twofold axes. The carboxylate group of the 4-carboxycyclohexane-1-carboxyl ligand chelates a Cd(II) ion, while the (protonated) carboxyl group forms hydrogen bonds with adjacent chains, resulting in a layered structure. This is the first reported occurrence of a dicarboxycyclohexane ligand exhibiting a non-bridging coordination mode.

Journal Article↗
PubMed2006

The use of comparative genomic hybridization to characterize genome dynamics and diversity among the serotypes of Shigella.

BACKGROUND: Compelling evidence indicates that Shigella species, the etiologic agents of bacillary dysentery, as well as enteroinvasive Escherichia coli, are derived from multiple origins of Escherichia coli and form a single pathovar. To further understand the genome diversity and virulence evolution of Shigella, comparative genomic hybridization microarray analysis was employed to compare the gene content of E. coli K-12 with those of 43 Shigella strains from all lineages. RESULTS: For the 43 strains subjected to CGH microarray analyses, the common backbone of the Shigella genome was estimated to contain more than 1,900 open reading frames (ORFs), with a mean number of 726 undetectable ORFs. The mosaic distribution of absent regions indicated that insertions and/or deletions have led to the highly diversified genomes of pathogenic strains. CONCLUSION: These results support the hypothesis that by gain and loss of functions, Shigella species became successful human pathogens through convergent evolution from diverse genomic backgrounds. Moreover, we also found many specific differences between different lineages, providing a window into understanding bacterial speciation and taxonomic relationships.

DNA, Bacterial↗
PubMed2006

BCL2 family in DNA damage and cell cycle control.

Individual BCL2 family members couple apoptosis regulation and cell cycle control in unique ways. Antiapoptotic BCL2 and BCL-x(L) are antiproliferative by facilitating G0. BAX is proapoptotic and accelerates S-phase progression. The dual functions in apoptosis and cell cycle are coordinately regulated by the multi-domain BCL2 family members (MCL-1) and suggest that survival is maintained at the expense of proliferation. The role of BH3-only molecules in cell cycle is more variable. BAD antagonizes both the cell cycle and antiapoptotic functions of BCL2 and BCL-x(L) through BH3 binding. BID has biochemically separable functions in apoptosis and S-phase checkpoint, determined by post-translational modification. p53-induced PUMA is known only to have apoptotic function. Inhibition of apoptosis is oncogenic, whereas promotion of cell cycle arrest is tumor suppressive. Paradoxically, selected BCL2 family members can be both oncogenic and tumor suppressive. Which of the dual functions predominates is lineage specific and context dependent.

Animals↗
PubMed2006

Genomic compositions and phylogenetic analysis of Shigella boydii subgroup.

Comparative Genomic Hybridization (CGH) microarray analysis was used to compare the genomic compositions of all eighteen Shigella boydii serotype representative strains. The results indicated the genomic "backbone" of this subgroup contained 2552 ORFs homologous to nonpathogenic E. coli K12. Compared with the genome of K12199 ORFs were found to be absent in all S. boydii serotype representatives, including mainly outer membrane protein genes and O-antigen biosynthesis genes. Yet the specific ORFs of S. boydii subgroup contained basically bacteriophage genes and the function unknown (FUN) genes. Some iron metabolism, transport and type II secretion system related genes were found in most representative strains. According to the CGH phylogenetic analysis, the eighteen S. boydii serotype representatives were divided into four groups, in which serotype C13 strain was remarkably distinguished from the other serotype strains. This grouping result corresponded to the distribution of some metabolism related genes. Furthermore, the analysis of genome backbone genes, specific genes, and the phylogenetic trees allowed us to discover the evolution laws of S. boydii and to find out important clues to pathogenesis research, vaccination and the therapeutic medicine development.

Gene Deletion↗
PubMed2005

Comparative genomics and phylogenetic analysis of S. dysenteriae subgroup.

Genomic compositions of representatives of thirteen S. dysenteriae serotypes were investigated by performing comparative genomic hybridization (CGH) with microarray containing the whole genomic ORFs (open reading frames, ORFs) of E. coli K12 strain MG1655 and specific ORFs of S. dysenteriae A1 strain Sd51197. The CGH results indicated the genomes of the serotypes contain 2654 conserved ORFs originating from E. coli. However, 219 intrinsic genes of E. coli including those prophage genes, molecular chaperones, synthesis of specific O antigen and so on were absent. Moreover, some specific genes such as type II secretion system associated components, iron transport related genes and some others as well were acquired through horizontal transfer. According to phylogenic trees based on genetic composition, it was demonstrated that A1, A2, A8, A10 were distinct from the other S. dysenteriae serotypes. Our results in this report may provide new insights into the physiological process, pathogenicity and evolution of S. dysenteriae.

Genes, Bacterial↗
PubMed2004

Interweaving 3D network with double helical tubes filled by 1D coordination polymer chains.

The hydrothermal reaction of mellitic acid, 4,4'-bipydine, and Cu(CH(3)COO)(2).H(2)O gave rise to a novel 3D supramolecular architecture interpenetrated by three types of coordination polymer motifs. Two independent [[Cu(2)(mellitate)(4,4'-bpy)(H(2)O)(2)](2)(-)] 3D polymers incorporating helical substructures were interwoven into a 3D network with double-stranded helical tubes that host 1D linear polymers [Cu(4,4'-bpy)(H(2)O)(4)](2+)](n).

Journal Article↗
PubMed2004

Bis(micro-ethyl pyridine-2,6-dicarboxylato)bis[diaquachlorocadmium(II)] dihydrate.

The reaction of cadmium chloride with pyridine-2,6-dicarboxylic acid (PDA) and 98% H2SO4 in ethanol led to the formation of the title compound, bis[mu-6-(ethoxycarbonyl)pyridine-2-carboxylato]-1:2kappa4O6,N,O2:O2;1:2kappa4O2:O2,N,O6-bis[diaquachlorocadmium(II)] dihydrate, [Cd2(C9H8NO4)2Cl2(H2O)4].2H2O. PDA is esterified to monoethyl pyridine-2,6-dicarboxylate (MEPD) by the catalysis of H2SO4 during the reaction. The dinuclear Cd(II) complex lies about an inversion centre and the unique Cd atom has a pentagonal-bipyramidal geometry. The two Cd atoms are bridged by two carboxylate O atoms, forming a planar Cd2O2 unit. Stair-like chains are formed via O-H.Cl hydrogen bonds and these are further arranged into two-dimensional layers via hydrogen bonds involving solvate water molecules.

Journal Article↗
PubMed2004

Poly[[diaquatris(mu6-benzene-1,2,4,5-tetracarboxylato)tris(mu2-4,4'-bipyridine)hexacopper(II)] dihydrate].

The hydrothermal reaction of an aqueous solution of Cu(CH(3)COO)(2).H(2)O, 1,2,4,5-benzenetetracarboxylic acid and 4,4'-bipyridine gave rise to the interesting title three-dimensional polymer [[Cu(6)(btec)(3)(4,4'-bpy)(3)(H(2)O)(2)].2H(2)O](n) (btec is 1,2,4,5-benzenetetracarboxylate, C(10)H(2)O(8)(4-), and 4,4'-bpy is 4,4'-bipyridine, C(10)H(8)N(2)), in which each btec ligand links six copper(II) cations into a lamellar [Cu(6)(btec)(3)(H(2)O)(2)](n) subpolymer framework. There are two distinct diamine units and two distinct carboxylate units, with one of each lying across an inversion centre.

Journal Article↗
PubMed2004

Overexpression of LIM kinase 1 renders resistance to apoptosis in PC12 cells by inhibition of caspase activation.

LIM kinases (LIMKs) regulate actin polymerization by phosphorylating cofilin and are predominantly expressed in neural tissue. In this study, the effect of LIMK1 overexpression in PC12 cell apoptosis was investigated. PC12 cells overexpressing the wild-type LIMK1 were more resistant to serum-withdrawal-induced cell death and the level of caspase 3 activation in these cells was lower than in the control PC12 cells or than in the PC12 cells expressing a mutant LIMK1 lacking the kinase domain. The inhibition of JNK activation was observed in the PC12 cells overexpressing the wild-type LIMK1 after serum withdrawal. These results suggest that the LIMK1 might allow resistance to apoptosis in PC12 cells by inhibiting JNK activation.

Actin Cytoskeleton↗
PubMed2004

Temporal lobe encephalocoele presenting with seizures and hearing loss.

A case of a bilateral temporal lobe encephalocoele that presented as seizures and hearing loss for many years. Diagnosis was confirmed on CT and MR imaging, which showed deficiencies in the temporal bone. The patient subsequently underwent surgical repair and recovered from his presenting symptoms.

Encephalocele↗
PubMed2001

BAD/BCL-[X(L)] heterodimerization leads to bypass of G0/G1 arrest.

The pro-apoptotic molecule BAD binds BCL-[X(L)] or BCL2 and inactivates their survival function. In addition to their anti-apoptotic function, BCL2 and BCL-[X(L)] also delay cell cycle entry from quiescence. We found that the BH3-only molecule BAD also exerted a cell cycle effect. BAD expression resulted in failure to cell cycle block in growth arrest conditions. In low serum and in confluence, fibroblasts constitutively or inducibly expressing BAD persisted in S phase, continued to incorporate BrdU, and exhibited sustained cyclin E/cdk2 activity. Mutation analysis indicated that the cell cycle effect of BAD was not dependent on its phosphorylation status or subcellular localization, but strictly co-segregated with BCL-[X(L)] binding. bclx(-/-) MEFs expressing BAD and bad(-/-) MEFs both arrested in G0/G1 in low serum similar to wild-type controls, suggesting that the ability to overcome the G0/G1 checkpoint resulted from the presence of BAD/BCL-x(L) heterodimers, rather than the absence of BCL-[X(L)] or BAD. These data provide evidence that in addition to regulating apoptosis, the BAD/BCL-[X(L)] heterodimer has a novel cell cycle function.

Animals↗
PubMed2001

Protein phosphatase 2A activates the proapoptotic function of BAD in interleukin- 3-dependent lymphoid cells by a mechanism requiring 14-3-3 dissociation.

BAD is a proapoptotic member of the BCL-2 family of proteins, which play a major role in regulating apoptosis in cytokine-dependent hematopoietic cells. The function of BAD is regulated by reversible phosphorylation. Deprivation of survival factors induces BAD dephosphorylation, resulting in apoptosis. Serine-threonine phosphatase activity dephosphorylated BAD in interleukin-3-dependent FL5.12 lymphoid cells. Inhibition of PP2A activity by treatment of cells with PP2A-selective inhibitors, okadaic acid and fostriecin, prevented BAD dephosphorylation in these cells. Conversely, BAD dephosphorylation was not inhibited by the PP1-selective inhibitor tautomycin. In cell-free extracts, BAD phosphatase activity was also inhibited by the PP2A-selective inhibitors okadaic acid and fostriecin, but not by the PP1-specific protein inhibitor I-2. Dissociation of 14-3-3 from BAD was a prerequisite for BAD dephosphorylation in vitro, suggesting a mechanism by which 14-3-3 can regulate the activation of the proapoptotic function of BAD in vivo. Significantly, the inhibition of BAD phosphatase activity rescued cell death induced by survival factor withdrawal in FL5.12 cells expressing wild-type BAD but not phosphorylation-defective mutant BAD. These data indicate that PP2A, or a PP2A-like enzyme, dephosphorylates BAD and, in conjunction with 14-3-3, modulates cytokine-mediated survival.

14-3-3 Proteins↗
PubMed2001

Cloning of an immunoglobulin family adhesion molecule selectively expressed by endothelial cells.

To gain fundamental information regarding the molecular basis of endothelial cell adhesive interactions during vascular formation, we have cloned and characterized a unique cell adhesion molecule. This molecule, named endothelial cell-selective adhesion molecule (ESAM), is a new member of the immunoglobulin superfamily. The conceptual protein encoded by cDNA clones consists of V-type and C2-type immunoglobulin domains as well as a hydrophobic signal sequence, a single transmembrane region, and a cytoplasmic domain. Northern blot analysis showed ESAM to be selectively expressed in cultured human and murine vascular endothelial cells and revealed high level expression in lung and heart and low level expression in kidney and skin. In situ hybridization analysis indicated that ESAM is primarily expressed in the developing vasculature of the embryo in an endothelial cell-restricted pattern. Epitope-tagged ESAM was shown to co-localize with cadherins and catenins in cell-cell junctions. In aggregation assays employing ESAM-expressing Chinese hamster ovary cells, this novel molecule was shown to mediate cell-cell adhesion through homophilic interactions. The endothelial cell-selective expression of this immunoglobulin-like adhesion molecule coupled with its in vitro functional profile strongly suggests a role in cell-cell interactions that is critical for vascular development or function.

Amino Acid Sequence↗
PubMed2000

Rapid induction of senescence in human cervical carcinoma cells.

Expression of the bovine papillomavirus E2 regulatory protein in human cervical carcinoma cell lines repressed expression of the resident human papillomavirus E6 and E7 oncogenes and within a few days caused essentially all of the cells to synchronously display numerous phenotypic markers characteristic of cells undergoing replicative senescence. This process was accompanied by marked but in some cases transient alterations in the expression of cell cycle regulatory proteins and by decreased telomerase activity. We propose that the human papillomavirus E6 and E7 proteins actively prevent senescence from occurring in cervical carcinoma cells, and that once viral oncogene expression is extinguished, the senescence program is rapidly executed. Activation of endogenous senescence pathways in cancer cells may represent an alternative approach to treat human cancers.

Animals↗
PubMed2000

Structural determinants of aortic regurgitation in type A dissection and the role of valvular resuspension as determined by intraoperative transesophageal echocardiography.

Disruption of the aortic root by dissection often produces significant aortic regurgitation (AR). Resuspension of the native valve usually reestablishes competence. The mechanisms of this complex process are poorly understood. We used intraoperative transesophageal echocardiography to characterize the in vivo aortic root structure of type A aortic dissection and the changes brought about by native valve resuspension. Intraoperative transesophageal echocardiograms were obtained from 34 patients with type A dissection and aortic resuspension between January 1990 and April 1997. The severity of AR, aortic root diameter, circumference of the aortic annulus, percentage of the annulus dissected, and presence of leaflet prolapse were assessed in multiple planes. Preoperatively, AR of varying degree was present in 25 patients (73%). Multivariate analysis revealed that preoperative AR was most related to percentage of the annulus dissected (p<0.0001) and less related to root diameter (p<0.01). Leaflet prolapse was predicted by percent aortic annulus dissected (p <0.0001). After resuspension, annular dissection and leaflet prolapse were no longer present. Postoperative AR was significantly decreased from preoperative AR (p<0.0001) and was considered trace to mild. Although postoperative root diameter and annular circumference decreased (p<0.001), individual reductions in AR did not correlate with individual changes in root diameter or annular circumference. The degree of dissection of the valve annulus is the most significant determinant of leaflet prolapse and AR severity. Overall size of the aortic root also contributes to AR. Surgical resuspension significantly decreases root size, but its primary benefit is restoration of the structural integrity of the aortic annulus.

Aortic Dissection↗
PubMed1999

Structural examination of autoregulation of multifunctional calcium/calmodulin-dependent protein kinase II.

Regulation of Ca(2+)/calmodulin-dependent protein kinase II is likely based on an auto-inhibitory mechanism in which a segment of the kinase occupies the catalytic site in the absence of calmodulin. We analyze potential auto-inhibitory associations by employing charge reversal and hydrophobic-to-charged residue mutagenesis. We identify interacting amino acid pairs by using double mutants to test which modification in the catalytic domain complements a given change in the auto-inhibitory domain. Our studies identify the core pseudosubstrate sequence (residues 297-300) but reveal that distinct sequences centered about the autophosphorylation site at Thr-286 are involved in the critical auto-inhibitory interactions. Individual changes in any of the residues Arg-274, His-282, Arg-283, Lys-291, Arg-297, Phe-293, and Asn-294 in the auto-inhibitory domain or their interacting partners in the catalytic domain produces an enhanced affinity for calmodulin or generates a constitutively active enzyme. A structural model of Ca(2+)/calmodulin-dependent protein kinase II that incorporates these interactions shows that Thr-286 is oriented inwardly into a hydrophobic channel. The model explains why calmodulin must bind to the auto-inhibitory domain in order for Thr-286 in that domain to be phosphorylated and why introduction of phospho-Thr-286 produces the important Ca(2+)-independent state of the enzyme.

Amino Acid Sequence↗
PubMed1999

Resolution of the paradox of red cell shape changes in low and high pH.

The molecular basis of cell shape regulation in acidic pH was investigated in human erythrocytes. Intact erythrocytes maintain normal shape in the cell pH range 6.3-7.9, but invaginate at lower pH values. However, consistent with predicted pH-dependent changes in the erythrocyte membrane skeleton, isolated erythrocyte membranes evaginate in acidic pH. Moreover, intact cells evaginate at pH greater than 7.9, but isolated membranes invaginate in this condition. Labeling with the hydrophobic, photoactivatable probe 5-[125I]iodonaphthyl-1-azide demonstrated pH-dependent hydrophobic insertion of an amphitropic protein into membranes of intact cells but not into isolated membranes. Based on molecular weight and on reconstitution experiments using stripped inside-out vesicles, the most likely candidate for the variably labeled protein is glyceraldehyde-3-phosphate dehydrogenase. Resealing of isolated membranes reconstituted both the shape changes and the hydrophobic labeling profile seen in intact cells. This observation appears to resolve the paradox of the contradictory pH dependence of shape changes of intact cells and isolated membranes. In intact erythrocytes, the demonstrated protein-membrane interaction would oppose pH-dependent shape effects of the spectrin membrane skeleton, stabilizing cell shape in moderately abnormal pH. Stabilization of erythrocyte shape in moderately acidic pH may prevent inappropriate red cell destruction in the spleen.

Azides↗