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Human Trafficking

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3361. Sequence Analysis of LRPPRC and Its SEC1 Domain Interaction Partners Suggests Roles in Cytoskeletal Organization, Vesicular Trafficking, Nucleocytosolic Shuttling and Chromosome Activity Full Text available with Trip Pro

Sequence Analysis of LRPPRC and Its SEC1 Domain Interaction Partners Suggests Roles in Cytoskeletal Organization, Vesicular Trafficking, Nucleocytosolic Shuttling and Chromosome Activity LRPPRC (originally called LRP130) is an intracellular, 130-kD, leucine-rich protein that copurifies with the fibroblast growth factor receptor from liver cell extracts and has been detected in diverse multiprotein complexes from the cell membrane, cytoskeleton, and nucleus. Here we report results of a sequence (...) homology analysis of LRPPRC and its SEC1 domain interactive partners. We found that 23 copies of tandem repeats that are similar to pentatricopeptide, tetratricopeptide, and huntingtin-elongation A subunit-TOR repeats characterize the LRPPRC sequence. The amino terminus exhibits multiple copies of leucine-rich nuclear transport signals followed by ENTH, DUF28, and SEC1 homology domains. We used the SEC1 domain to trap interactive partners expressed from a human liver cDNA library. Interactive C19ORF5

2002 Genomics

3362. Kidney trafficking is "big business," says Council of Europe Full Text available with Trip Pro

Kidney trafficking is "big business," says Council of Europe 12896927 2003 08 22 2012 03 06 1756-1833 327 7409 2003 Aug 02 BMJ (Clinical research ed.) BMJ Kidney trafficking is "big business," says Council of Europe. 249 Kovac Carl C eng News England BMJ 8900488 0959-8138 AIM IM Europe Humans Kidney Transplantation economics Tissue and Organ Procurement economics 2003 8 5 5 0 2003 8 23 5 0 2003 8 5 5 0 ppublish 12896927 10.1136/bmj.327.7409.249-a 327/7409/249-a PMC1323242

2003 BMJ : British Medical Journal

3363. Correction of an enzyme trafficking defect in hereditary kidney stone disease in vitro. Full Text available with Trip Pro

Correction of an enzyme trafficking defect in hereditary kidney stone disease in vitro. In normal human hepatocytes, the intermediary-metabolic enzyme alanine:glyoxylate aminotransferase (AGT) is located within the peroxisomes. However, in approx. one-third of patients suffering from the hereditary kidney stone disease primary hyperoxaluria type 1, AGT is mistargeted to the mitochondria. AGT mistargeting results from the synergistic interaction between a common P11L (Pro11-->Leu) polymorphism (...) requirements of the two protein trafficking pathways and the formulation of possible treatment strategies for primary hyperoxaluria type 1.

2003 Biochemical Journal

3364. Police uncover large scale organ trafficking in Punjab Full Text available with Trip Pro

Police uncover large scale organ trafficking in Punjab 12543823 2003 02 20 2012 03 06 1756-1833 326 7382 2003 Jan 25 BMJ (Clinical research ed.) BMJ Police uncover large scale organ trafficking in Punjab. 180 Kumar Sanjay S eng News England BMJ 8900488 0959-8138 AIM E IM Commerce Crime Humans India Physician's Role Tissue and Organ Procurement economics statistics & numerical data 107645 Health Care and Public Health KIE Bib: fraud and misconduct; organ and tissue donation 2003 1 25 4 0 2003 2

2003 BMJ : British Medical Journal

3365. A copper treatable Menkes disease mutation associated with defective trafficking of a functional Menkes copper ATPase Full Text available with Trip Pro

A copper treatable Menkes disease mutation associated with defective trafficking of a functional Menkes copper ATPase 12676902 2003 04 17 2017 11 16 1468-6244 40 4 2003 Apr Journal of medical genetics J. Med. Genet. A copper treatable Menkes disease mutation associated with defective trafficking of a functional Menkes copper ATPase. 290-5 Kim B-E BE Smith K K Petris M J MJ eng DK59893 DK NIDDK NIH HHS United States Letter Research Support, U.S. Gov't, P.H.S. England J Med Genet 2985087R 0022 (...) -2593 0 Cation Transport Proteins 0 Recombinant Fusion Proteins 20350-15-6 Brefeldin A 789U1901C5 Copper EC 3.6.1.- Adenosine Triphosphatases EC 3.6.3.54 ATP7A protein, human EC 3.6.3.54 Copper-transporting ATPases IM Adenosine Triphosphatases genetics metabolism Biological Transport drug effects genetics Brefeldin A pharmacology Cation Transport Proteins genetics metabolism Cell Line Copper metabolism therapeutic use Copper-transporting ATPases Golgi Apparatus metabolism Humans Menkes Kinky Hair

2003 Journal of Medical Genetics

3366. A comparison of the inhibitory activity of PDE4 inhibitors on leukocyte PDE4 activity in vitro and eosinophil trafficking in vivo Full Text available with Trip Pro

the activity of five PDE4 inhibitors in vitro and against trafficking of (111)In-eosinophils in cutaneous inflammation in the guinea-pig. 2. The rank order of potency for inhibition of PDE4 activity in guinea-pig eosinophil, neutrophil and macrophage, and human neutrophil lysates was RP73401 > SB207499 >CDP840 > rolipram > LAS31025. On TNFalpha production by human PBMC, all inhibitors with the exception of rolipram showed potency similar to their effect on neutrophil lysates. 3. In a brain cerebellum (...) A comparison of the inhibitory activity of PDE4 inhibitors on leukocyte PDE4 activity in vitro and eosinophil trafficking in vivo 1. Phosphodiesterase (PDE) 4 inhibitors have been shown to inhibit eosinophil PDE4 activity in vitro and accumulation of eosinophils in experimental airways inflammation. However, direct effects on eosinophil trafficking have not been studied in detail and it is not known if activity in vitro translates into efficacy in vivo. In the present study, we compared

1999 British journal of pharmacology

3367. Impaired trafficking of the desmoplakins in cultured Darier's disease keratinocytes. Full Text available with Trip Pro

reticulum lumen to maintain a low cytosolic Ca2+ concentration. Using indirect immunofluorescence and biochemical analysis, we investigated the distribution of key desmosomal proteins in normal human and Darier's disease keratinocytes under various calcium conditions. We show that inhibition of SERCA by thapsigargin in normal human keratinocytes impairs the trafficking of the desmoplakins, desmoglein, and desmocollin to the cell surface; these proteins show a diffuse cytoplasmic distribution (...) Impaired trafficking of the desmoplakins in cultured Darier's disease keratinocytes. Darier's disease is an autosomal dominantly inherited skin disorder characterized by loss of adhesion between epidermal cells, breakdown of desmosome-keratin filaments, and abnormal keratinization. ATP2A2 has been identified as the causative gene of Darier's disease. This gene encodes the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) isoform 2 pump, which transports Ca2+ from the cytosol into the endoplasmic

2003 Journal of Investigative Dermatology

3368. Leukocyte trafficking in experimental autoimmune uveitis: breakdown of blood-retinal barrier and upregulation of cellular adhesion molecules. (Abstract)

Leukocyte trafficking in experimental autoimmune uveitis: breakdown of blood-retinal barrier and upregulation of cellular adhesion molecules. To clarify the order of events occurring in the breakdown of the blood-retinal barrier (BRB) in experimental autoimmune uveoretinitis (EAU) and in particular to study the relationships between increased vascular permeability, upregulation of endothelial cell adhesion molecules, and leukocyte adhesion and infiltration during EAU.B10.RIII mice were (...) immunized with human interphotoreceptor retinoid binding protein (IRBP) peptide 161-180. Changes in the retinal microvasculature were examined on days 3, 6, 7, 8, 9, 10, 16, and 21 postimmunization (pi). Evans blue dye was administered intravenously to assess vascular permeability. Expression of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, P-selectin, E-selectin, and platelet endothelial cell adhesion molecule (PECAM)-1 was evaluated by in vivo administration

2003 Investigative Ophthalmology & Visual Science

3369. Postendocytotic trafficking of the follicle-stimulating hormone (FSH)-FSH receptor complex. Full Text available with Trip Pro

Postendocytotic trafficking of the follicle-stimulating hormone (FSH)-FSH receptor complex. Although the fates of the internalized hormone-receptor complexes formed by the lutropin/choriogonadotropin and the TSH receptors have been examined in some detail, much less is known about the fate of the internalized FSH-FSH receptor (FSHR) complex. Using biochemical and imaging approaches we show here that the majority of the internalized FSH-FSHR complex accumulates in endosomes and subsequently (...) recycles back to the cell surface where the bound, intact hormone dissociates back into the medium. Only small amounts of FSH and the FSHR are routed to a lysosomal degradation pathway, and the extent of FSH-induced down-regulation of the cell surface and total FSHR is minimal. This pathway was detected in heterologous (human kidney 293T) cells transfected with the rat (r) or human (h) FSHR as well as in a mouse Sertoli cell line (MSC-1) or a mouse granulosa cell line (KK-1) transfected

2003 Molecular Endocrinology

3370. Defective protein trafficking in hERG-associated hereditary long QT syndrome (LQT2): molecular mechanisms and restoration of intracellular protein processing. (Abstract)

Defective protein trafficking in hERG-associated hereditary long QT syndrome (LQT2): molecular mechanisms and restoration of intracellular protein processing. Human hereditary long QT syndrome is a cardiac disease characterized by prolongation of the QT interval and increased susceptibility to ventricular arrhythmias and sudden cardiac death. Mutations in the human-ether-a-go-go-related gene (hERG), encoding the protein underlying the repolarizing cardiac I(Kr) potassium current, cause (...) chromosome 7-linked long QT syndrome 2. Loss of function of mutant hERG channels may be caused by several mechanisms, including altered current kinetics, altered ion selectivity, or defective intracellular protein trafficking. Especially the latter category has become a focus of particular interest recently, because some of the mutant subunits display wild type current properties when normal trafficking is restored and channels are inserted in the cell membrane in vitro. This review summarizes

2003 Cardiovascular Research

3371. Efficacy of Narrative Exposure Therapy (NET) in Treating Women After Human Trafficking or Forced Prostitution

Efficacy of Narrative Exposure Therapy (NET) in Treating Women After Human Trafficking or Forced Prostitution Efficacy of Narrative Exposure Therapy (NET) in Treating Women After Human Trafficking or Forced Prostitution - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (...) (100). Please remove one or more studies before adding more. Efficacy of Narrative Exposure Therapy (NET) in Treating Women After Human Trafficking or Forced Prostitution The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our for details. ClinicalTrials.gov Identifier: NCT00717548 Recruitment Status : Completed First Posted : July 17, 2008 Last Update

2008 Clinical Trials

3372. The Cytoplasmic Tail of Glycoprotein M (gpUL100) Expresses Trafficking Signals Required for Human Cytomegalovirus Assembly and Replication Full Text available with Trip Pro

The Cytoplasmic Tail of Glycoprotein M (gpUL100) Expresses Trafficking Signals Required for Human Cytomegalovirus Assembly and Replication The virion envelope of human cytomegalovirus (HCMV) is complex and consists of an incompletely defined number of glycoproteins. The gM/gN protein complex is the most abundant protein component of the envelope. Studies have indicated that deletion of the viral gene encoding either gM or gN is a lethal mutation. Analysis of the amino acid sequence of gM (...) disclosed a C-terminal acidic cluster of amino acids and a tyrosine-containing trafficking motif, both of which are well-described trafficking/sorting signals in the cellular secretory pathway. To investigate the roles of these signals in the trafficking of the gM/gN complex during virus assembly, we made a series of gM (UL100 open reading frame) mutants in the AD169 strain of HCMV. Mutant viruses that lacked the entire C-terminal cytoplasmic tail of gM were not viable, suggesting that the cytoplasmic

2007 Journal of virology

3373. An Acidic Cluster of Human Cytomegalovirus UL99 Tegument Protein Is Required for Trafficking and Function Full Text available with Trip Pro

An Acidic Cluster of Human Cytomegalovirus UL99 Tegument Protein Is Required for Trafficking and Function The human cytomegalovirus (HCMV) virion is comprised of a linear double-stranded DNA genome, proteinaceous capsid and tegument, and a lipid envelope containing virus-encoded glycoproteins. Of these components, the tegument is the least well defined in terms of both protein content and function. Several of the major tegument proteins are phosphoproteins (pp), including pp150, pp71, pp65 (...) , and pp28. pp28, encoded by the UL99 open reading frame (ORF), traffics to vacuole-like cytoplasmic structures and was shown recently to be essential for envelopment. To elucidate the UL99 amino acid sequences necessary for its trafficking and function in the HCMV replication cycle, two types of viral mutants were analyzed. Using a series of recombinant viruses expressing various UL99-green fluorescent protein fusions, we demonstrate that myristoylation at glycine 2 and an acidic cluster (AC; amino

2004 Journal of virology

3374. Monocyte/macrophage trafficking in acquired immunodeficiency syndrome encephalitis: Lessons from human and nonhuman primate studies Full Text available with Trip Pro

Monocyte/macrophage trafficking in acquired immunodeficiency syndrome encephalitis: Lessons from human and nonhuman primate studies Here the authors discuss evidence in human and animal models supporting two opposing views regarding the pathogenesis of human immunodeficiency virus (HIV) in the central nervous system (CNS): (1) HIV infection in the CNS is a compartmentalized infection, with the virus-infected macrophages entering the CNS early, infecting resident microglia and astrocytes (...) is normally expressed by perivascular MPhi s but not resident microglia in normal CNS of humans and rhesus macaques. In agreement with other studies, the authors demonstrate expression of CD163 by brain MPhi s in HIVE and simian immunodeficiency virus encephalitis (SIVE). CNS tissues from HIV-sero positive individuals with HIVE or HIV-associated progressive multifocal leukoencephalopathy (PML) were also examined. In HIVE, the authors further demonstrate colocalization of CD163 and CD16 (Fcgamma III

2008 Journal of neurovirology

3375. Human Immunodeficiency Virus Type 1 Nef: Adapting to Intracellular Trafficking Pathways Full Text available with Trip Pro

Human Immunodeficiency Virus Type 1 Nef: Adapting to Intracellular Trafficking Pathways The Nef protein of primate lentiviruses is a unique protein that has evolved in several ways to manipulate the biology of an infected cell to support viral replication, immune evasion, pathogenesis, and viral spread. Nef is a small (25- to 34-kDa), myristoylated protein that binds to a collection of cellular factors and acts as an adaptor to generate novel protein interactions to accomplish specific (...) trafficking of several other host molecules has also been reported, and an emerging theory suggests that Nef generates pleiotrophic effects in the secretory and endocytic pathways that reprogram intracellular protein trafficking and may ultimately provide an efficient platform for viral assembly. This review critically discusses some of the major findings regarding the impact of human immunodeficiency virus type 1 Nef on host protein transport and addresses some emerging directions in this area of human

2006 Microbiology and Molecular Biology Reviews

3376. 14-3-3-affinity purification of over 200 human phosphoproteins reveals new links to regulation of cellular metabolism, proliferation and trafficking. Full Text available with Trip Pro

14-3-3-affinity purification of over 200 human phosphoproteins reveals new links to regulation of cellular metabolism, proliferation and trafficking. 14-3-3-interacting proteins were isolated from extracts of proliferating HeLa cells using 14-3-3 affinity chromatography, eluting with a phosphopeptide that competes with targets for 14-3-3 binding. The isolated proteins did not bind to 14-3-3 proteins (14-3-3s) after dephosphorylation with protein phosphatase 2A (PP2A), indicating that binding (...) to 14-3-3s requires their phosphorylation. The binding proteins identified by tryptic mass fingerprinting and Western blotting include many enzymes involved in generating precursors such as purines (AMP, GMP and ATP), FAD, NADPH, cysteine and S-adenosylmethionine, which are needed for cell growth, regulators of cell proliferation, including enzymes of DNA replication, proteins of anti-oxidative metabolism, regulators of actin dynamics and cellular trafficking, and proteins whose deregulation has

2004 Biochemical Journal

3377. Palmitoylation is not required for trafficking of human anion exchanger 1 to the cell surface. Full Text available with Trip Pro

Palmitoylation is not required for trafficking of human anion exchanger 1 to the cell surface. AE1 (anion exchanger 1) is a glycoprotein found in the plasma membrane of erythrocytes, where it mediates the electroneutral exchange of chloride and bicarbonate, a process important in CO2 removal from tissues. It had been previously shown that human AE1 purified from erythrocytes is covalently modified at Cys-843 in the membrane domain with palmitic acid. In this study, the role of Cys-843 in human (...) AE1 trafficking was investigated by expressing various AE1 and Cys-843Ala (C843A) mutant constructs in transiently transfected HEK-293 cells. The AE1 C843A mutant was expressed to a similar level to AE1. The rate of N-glycan conversion from high-mannose into complex form in a glycosylation mutant (N555) of AE1 C843A, and thus the rate of trafficking from the endoplasmic reticulum to the Golgi, were comparable with that of AE1 (N555). Like AE1, AE1 C843A could be biotinylated at the cell surface

2004 Biochemical Journal

3378. Intracellular trafficking of the human Wilson protein: the role of the six N-terminal metal-binding sites. Full Text available with Trip Pro

Intracellular trafficking of the human Wilson protein: the role of the six N-terminal metal-binding sites. The Wilson protein (ATP7B) is a copper-transporting CPx-type ATPase defective in the copper toxicity disorder Wilson disease. In hepatocytes, ATP7B delivers copper to apo-ceruloplasmin and mediates the excretion of excess copper into bile. These distinct functions require the protein to localize at two different subcellular compartments. At the trans-Golgi network, ATP7B transports copper (...) for incorporation into apo-ceruloplasmin. When intracellular copper levels are increased, ATP7B traffics to post-Golgi vesicles in close proximity to the canalicular membrane to facilitate biliary copper excretion. In the present study, we investigated the role of the six N-terminal MBSs (metal-binding sites) in the trafficking process. Using site-directed mutagenesis, we mutated or deleted various combinations of the MBSs and assessed the effect of these changes on the localization and trafficking of ATP7B

2004 Biochemical Journal

3379. Copper binding to the N-terminal metal-binding sites or the CPC motif is not essential for copper-induced trafficking of the human Wilson protein (ATP7B) Full Text available with Trip Pro

Copper binding to the N-terminal metal-binding sites or the CPC motif is not essential for copper-induced trafficking of the human Wilson protein (ATP7B) The Wilson protein (ATP7B) is a copper-translocating P-type ATPase that mediates the excretion of excess copper from hepatocytes into bile. Excess copper causes the protein to traffic from the TGN (trans-Golgi network) to subapical vesicles. Using site-directed mutagenesis, mutations known or predicted to abrogate catalytic activity (copper (...) translocation) were introduced into ATP7B and the effect of these mutations on the intracellular trafficking of the protein was investigated. Mutation of the critical aspartic acid residue in the phosphorylation domain (DKTGTIT) blocked copper-induced redistribution of ATP7B from the TGN, whereas mutation of the phosphatase domain [TGE (Thr-Gly-Glu)] trapped ATP7B at cytosolic vesicular compartments. Our findings demonstrate that ATP7B trafficking is regulated with its copper-translocation cycle

2006 Biochemical Journal

3380. Israel is set to outlaw trafficking in human organs Full Text available with Trip Pro

Israel is set to outlaw trafficking in human organs 18048526 2007 12 17 2012 03 06 1756-1833 335 7630 2007 Dec 01 BMJ (Clinical research ed.) BMJ Israel is set to outlaw trafficking in human organs. 1117 Siegel-Itzkovich Judy J eng News England BMJ 8900488 0959-8138 AIM IM Crime Humans Israel Tissue and Organ Procurement economics legislation & jurisprudence 2007 12 1 9 0 2007 12 18 9 0 2007 12 1 9 0 ppublish 18048526 335/7630/1117-b 10.1136/bmj.39409.472072.DB PMC2099532

2007 BMJ : British Medical Journal

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