bluuebunny/crossref_metadata_2025_split huggingface dataset:
BCL6 represses NFκB activity in diffuse large B‐cell lymphomas
Authors: Perez‐Rosado A , Artiga MJ , Vargiu P , Sanchez‐Aguilera A , Alvarez‐Barrientos A , Piris MA 
Published: January 2008

AbstractBCL6 is a transcriptional repressor whose deregulated expression plays a key role in diffuse large B‐cell lymphomas (DLBCLs). BCL6 expression characterizes one of the two main subtypes (GC type) of DLBCL, while the other (ABC type) is recognized by increased NFκB activation. The mechanistic basis of this distinction remains unclear and the BCL6 targets have been only partially explored. Here we describe how NFκB activity is increased after BCL6 silencing by shRNA in DLBCL cells, leading us to propose that BCL6 represses NFκB activity. We also demonstrate that this repression is brought about by a mechanism involving protein–protein interaction between BCL6 and NFκB members, both in vitro and in vivo. Analysis of a series of DLBCLs shows a negative correlation between the expression of NFκB target genes and BCL6. This combined approach using silenced cells and a series of human DLBCL samples leads us to a better understanding of the role of BCL6 as an NFκB regulator in B‐cells. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Expression of coronin‐3 (coronin‐1C) in diffuse gliomas is related to malignancy
Authors: Thal DR , Xavier C‐P , Rosentreter A , Linder S , Friedrichs B , Waha A , Pietsch T , Stumpf M , Noegel AA , Clemen CS 
Published: January 2008

AbstractCoronin‐3 (coronin‐1C), a homotrimeric F‐actin binding protein, has been shown to be important for cell migration and brain morphogenesis. Here, we present for the first time a detailed analysis of the expression pattern of coronin‐3 in human brain tumours and demonstrate that coronin‐3 expression correlates with malignant phenotype in diffuse gliomas. In general, the expression of coronin‐3 varies in different brain tumour entities. However, in diffuse gliomas, the number of coronin‐3 expressing tumour cells correlates with the degree of malignancy. High‐grade gliomas, such as anaplastic astrocytomas, anaplastic oligodendrogliomas, anaplastic oligoastrocytomas and glioblastomas, show high numbers of tumour cells positive for coronin‐3, while diffuse low‐grade gliomas, such as diffuse astrocytomas, oligodendrogliomas and oligoastrocytomas, exhibit low numbers of coronin‐3‐positive tumour cells. In order to explore and verify a contribution of coronin‐3 to the malignant phenotype of diffuse gliomas, we employed an efficient shRNA‐mediated coronin‐3 knockdown in U373 and A172 human glioblastoma cells. Coronin‐3 knockdown glioblastoma cells exhibited reduced levels of cell proliferation, cell motility and invasion into extracellular matrix compared to control cells. Together, our findings demonstrate evidence for a contribution of coronin‐3 expression in the malignant progression of diffuse gliomas. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Endothelial cells and normal breast epithelial cells enhance invasion of breast carcinoma cells by CXCR‐4‐dependent up‐regulation of urokinase‐type plasminogen activator receptor (uPAR, CD87) expression
Authors: Serratì S , Margheri F , Fibbi G , Di Cara G , Minafra L , Pucci‐Minafra I , Liotta F , Annunziato F , Pucci M , Del Rosso M 
Published: January 2008

AbstractHere we show the increase of invasion of three breast cancer cell lines (8701‐BC, MDA‐MB‐231 and SKBR3) upon long‐term co‐incubation with culture medium of normal microvascular endothelial cells (MVEC) and normal breast epithelial cells (HB2). The enhancement of invasion relied on the interaction of microvascular endothelial cell and normal breast epithelial cell CXCL12 (SDF1) chemokine, whose expression by breast cancer cells was very low, with the cognate CXCR4 receptor of malignant cells, which resulted in over‐expression of the urokinase‐type plasminogen activator receptor (uPAR) on their surfaces. uPAR over‐expression, showed by RT–PCR and Western blotting, was paralleled by increased urokinase‐type plasminogen activator (uPA) partitioning on the cell surface with respect to the fluid phase, as demonstrated by zymography. Long‐term interaction of SDF1 with CXCR4 stimulated sustained activation of JNK phosphorylation. Blocking antibodies to CXCR4 were able to block the endothelial/epithelial cell‐dependent enhancement of invasion, as well as to inhibit SDF1‐CXCR4‐dependent JNK phosphorylation and uPAR over‐expression of malignant cells. We suggest that acquisition of the angiogenic phenotype by breast cancer cells triggers an amplification loop, in which endothelial cells and normal breast epithelial cells of the tumour cooperate to provide facilitated routes to cell invasion and metastasis and to enhance the aggressive phenotype of cancer cells. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Acid catalyzed 1, 2 Michael addition reaction: a viable synthetic route in designing fullerene core starlike macromolecule
Authors: Singh Rachana , Goswami Thakohari 
Published: January 2008

AbstractThe paper describes a comprehensive investigation to establish the heterophase acid‐catalyzed 1, 2 Michael addition reaction between fullerenol (nucleophile) and substituted acrylates (R = H, CH3, Ph)/vinyl acrylates (electron deficient olefins). The main emphasis is to evaluate structure–property relationship and establish a mechanism for tuning the structure in different operating conditions, which could be useful while adapting this reaction in designing of fullerene core starlike macromolecules. The effect of substituents on the rate of formation of the product is another important aspect covered in the present paper. The most significant outcome of the present investigation are (i) the nature of the product formed has direct bearing with operating process, whereas, (ii) rate of reaction and the properties of the end‐products depends on the nature and position of substituents attached to olefins. Adopting heterogeneous phase reaction scheme, the reaction can be easily controlled at 1, 2 Michael addition stage which otherwise proceeds further to provide cyclic product in single‐phase reaction. The nature of the substituent at β‐carbon of the olefins have the inverse effect on the rate of the reaction. The steric rather than electronic effect of substituents governs the rate of reaction. However, the significant influence of β‐substituents on the properties of the Michael addition products are observed in a more classical manner. The phenyl substituent at the β‐position measured the slowest rate of reaction but imparts highest thermal stability. In such systems, the vinyl substitution on esteric carbon further reduces both the reaction rate and the thermal stability. Copyright © 2008 John Wiley & Sons, Ltd.
Updated Atom/Functional Group and Atom_Code Volume Additivity Parameters for the Calculation of Crystal Densities of Single Molecules, Organic Salts, and Multi‐Fragment Materials Containing H, C, B, N, O, F, S, P, Cl, Br, and I
Authors: Ammon Herman L. 
Published: January 2008

AbstractData for crystal structures with ≤10 fragments per asymmetric unit from the Cambridge Structural Database were used to update and extend our previously described databases. Atom and functional group volumes and densities were determined for organic compounds with the elements H, C, B, N, O, F, P, S, Cl, Br, I, and halide anions. The datasets included organic ions and multi‐fragment structures. Linear and nonlinear volumes and linear densities were determined for 109 predefined atoms/functional groups from ∼41000 crystal structure data. An updated volume database for atom_codes, which are automatically defined by the atoms and their connections in a dataset, was determined in separate calculations with 2805 atom_codes defined for ∼48000 structures. The atom_code extension to 6‐coordinate C and B allowed carboranes to be modeled. The average percent difference between the observed and calculated densities is about 2%.
A novel transcript from the KLKP1 gene is androgen regulated, down‐regulated during prostate cancer progression and encodes the first non‐serine protease identified from the human kallikrein gene locus
Authors: Kaushal Aneel , Myers Stephen A. , Dong Ying , Lai John , Tan Olivia L. , Bui Loan T. , Hunt Melanie L. , Digby Matthew R. , Samaratunga Hemamali , Gardiner Robert A. , Clements Judith A. , Hooper John D. 
Published: January 2008

AbstractBACKGROUNDThe kallikrein‐related (KLK) serine protease, prostate specific antigen is the current marker for prostate cancer (PCa). Other members of the KLK family are also emerging as potential adjunct biomarkers for this disease. Our aim was to identify and characterize novel KLK‐related genes with potential as PCa bio‐markers.METHODSLow stringency DNA screening was coupled with amplification techniques to identify novel sequences. Transcripts were examined by Northern blot, RT‐PCR, and in situ hybridization analysis and in silico bioinformatics approaches. Protein characterization was performed by Western blot and confocal microscopy analysis. Gene regulation studies were performed by quantitative PCR and promoter reporter assays.RESULTSWe identified a novel kallikrein‐related mRNA designated KRIP1 (kallikrein‐related, expressed in prostate 1) which, together with the recently reported ΨKLK1 and KLK31P transcripts, is transcribed from KLKP1; a gene evolved from, and located within, the KLK locus. Significantly, in contrast to these other non‐coding KLKP1 transcripts, the KRIP1 mRNA generates an ∼18 kDa intracellular protein—the first non‐serine protease identified from the KLK locus. KRIP1 mRNA is abundant only in normal prostate and is restricted to cells of epithelial origin in normal and diseased glands. Ligand binding of the androgen receptor increases transcription from the KLKP1 gene. Consistently, KRIP1 mRNA levels are lower in PCa samples compared to benign prostatic hyperplasia.CONCLUSIONSTranscription from KLKP1 is reduced as cells de‐differentiate on the pathway to malignancy. KLKP1/KRIP1 has potential as a marker of both PCa progression and recent evolutionary events within the KLK locus. Prostate 68: 381–399, 2008. © 2008 Wiley‐Liss, Inc.
Differential localization of MT1‐MMP in human prostate cancer tissue: Role of IGF‐1R in MT1‐MMP expression
Authors: Sroka Isis C. , McDaniel Kathy , Nagle Raymond B. , Bowden G. Tim 
Published: January 2008

AbstractBackgroundMT1‐MMP is a metalloproteinase involved in prostate cancer metastasis. The IGF‐1R is a tyrosine kinase receptor involved with tumor progression and metastasis. The purpose of this investigation was to examine MT1‐MMP and IGF‐1R expression and localization in prostate cancer tissues and explore the role of IGF‐1R in regulating MT1‐MMP in prostate cancer cell lines.MethodsImmunohistochemistry was utilized to study MT1‐MMP and IGF‐1R expression in human prostate tissues. IGF‐1R regulation of MT1‐MMP expression was determined by gene promoter analysis, quantitative RT‐PCR and Western blot analysis following pharmacological inhibition of the receptor in PC‐3N cells and treatment of LNCaP cells with androgen and IGF‐1.ResultsMT1‐MMP expression was high in the apical regions of the luminal cells in PIN and prostate cancer and less intense in the basalateral regions of benign tissues. IGF‐1R was expressed primarily in the basal cells of normal glands and highly expressed in prostate cancer. Inhibition of IGF‐1R in PC‐3N cells decreased MT1‐MMP expression and treatment of LNCaP cells with a synthetic androgen and IGF‐1 increased MT1‐MMP expression.ConclusionsThese data demonstrate that MT1‐MMP is highly expressed in the apical cytoplasmic regions of the luminal cells in PIN and prostate cancer when compared to basalateral cytoplasmic membrane staining in benign glands. Additionally, we demonstrate that IGF‐1R is highly expressed in human prostate carcinoma. These findings suggest that MT1‐MMP localization and IGF‐1R expression in prostate carcinoma could be predictive biomarkers for aggressive disease and support IGF‐1R as a promising therapeutic target to decrease processes of prostate cancer metastasis. Prostate 68: 463–476, 2008. © 2008 Wiley‐Liss, Inc.
Androgen receptor‐dependent regulation of Bcl‐xL expression: Implication in prostate cancer progression
Authors: Sun Aijing , Tang Jianxi , Hong Yan , Song Jiawu , Terranova Paul F. , Thrasher J. Brantley , Svojanovsky Stan , Wang Hong‐gang , Li Benyi 
Published: January 2008

AbstractBackgroundRecently we reported that silencing the androgen receptor (AR) gene reduced Bcl‐xL expression that was associated with a profound apoptotic cell death in prostate cancer cells. In this study we further investigated AR‐regulated Bcl‐xL expression.MethodsProstate cancer cell line LNCaP and its sublines, LNCaP/PURO and LNCaP/Bclxl, were used for cell proliferation assay and xenograft experiments in nude mice. Luciferase gene reporters driven by mouse or human bcl‐x gene promoter were used to determine androgen regulation of Bcl‐xL expression. RT‐PCR and Western blot assays were conducted to assess Bcl‐xL gene expression. Chromatin immunoprecipitation assay was performed to determine AR interaction with Bcl‐xL promoter. Bcl‐xL‐induced alteration of gene expression was examined using cDNA microarray assay.ResultsIn cultured prostate cancer LNCaP cells, androgen treatment significantly increased Bcl‐xL expression at mRNA and protein levels via an AR‐dependent mechanism. Promoter analyses demonstrated that the AR mediated androgen‐stimulated bcl‐x promoter activation and that the AR interacted with bcl‐x promoter. Enforced expression of Bcl‐xL gene dramatically increased cell proliferation in vitro and promoted xenograft tumor growth in vivo. Genome‐wide gene profiling analysis revealed that Bcl‐xL expression was significantly higher in metastatic and castration‐resistant diseases compared to normal prostate tissues or primary cancers. Bcl‐xL overexpression significantly increased the expression of cyclin D2, which might be responsible for Bcl‐xL‐induced cell proliferation and tumor growth.ConclusionsTaken together, our data strongly suggest that androgen stimulates Bcl‐xL expression via the AR and that increased Bcl‐xL expression plays a versatile role in castration‐resistant progression of prostate cancer. Prostate 68: 453–461, 2008. © 2008 Wiley‐Liss, Inc.
Triiodothyronine modulates cell proliferation of human prostatic carcinoma cells by downregulation of the B‐Cell translocation gene 2
Authors: Tsui Ke‐Hung , Hsieh Wen‐Chi , Lin Mei‐Hsien , Chang Phei‐Lang , Juang Horng‐Heng 
Published: January 2008

AbstractBackgroundStudies suggest that triiodothyronine (T3) and cognate nuclear receptors (hTR) are involved in regulation of prostatic cell growth and differentiation. To probe mechanisms for T3 effects, we studied prostate carcinoma cells, investigating the effect of T3 on expression of the B‐cell translocation gene 2 (BTG2), which regulates the G1/S transition of the cell cycle.MethodsEffects of T3 on cell proliferation were determined by 3H‐thymidine incorporation. T3 modulation of BTG2 expression was investigated using immunoblots, Northern blots, and transient gene expression assays. The putative T3 response element was determined by electrophoretic mobility shift assay.ResultsT3 (0.1–1,000 nM) enhanced threefold the proliferation of prostate carcinoma cells and human androgen‐dependent prostate carcinoma cells (LNCaP), but not PC‐3 cells. T3 also inhibited BTG2 gene expression in LNCaP cells. Reporter assays showed that T3 downregulates by 50% promoter activity of the BTG2 gene in LNCaP cells but not PC‐3 cells or thyroid‐hormone receptor (TRβ1)‐overexpression PC‐3 cells. Deleting the putative thyroid hormone response element (TRE; AGCGATGACCTCAGCG) blocked the inhibitory effect of T3 on BTG2 promoter activity. Electrophoretic mobility shift assays with purified TRβ1 from in vitro translation, or with nuclear extracts from LNCaP cells and PC‐3 cells, demonstrated the presence of T3 receptor binding sites in the TRE region.ConclusionsThese results suggested that the T3 upregulates proliferation of LNCaP cells by downregulating BTG2 gene expression through the consensus TRE pathway. Prostate 68: 610–619, 2008. © 2008 Wiley‐Liss, Inc.
Enfuvirtide effects on human erythrocytes and lymphocytes functional properties
Authors: Vieira Catarina R. , Castanho Miguel , Saldanha Carlota , Santos Nuno C. 
Published: January 2008

AbstractEnfuvirtide (T‐20) is the first inhibitor of human Immunodeficiency Virus type‐1 (HIV‐1) entrance on a target cell approved for clinical use. Recent studies indicated that its action mechanism involves the interaction with the membrane surface, increasing the concentration in the site of action. In the present study, the in vitro interaction between enfuvirtide and blood cells of healthy human donors, namely erythrocytes and lymphocytes, and the peptide effect on plasma and lymphocyte suspensions supernatant ions were evaluated, in order to better characterize the action of this peptide. Enfuvirtide causes a decrease in the concentration of hemoglobin and in the percentages of methemoglobin and carboxyhemoglobin, together with increased values of P50, pCO2, and [HCO3−], and significant decreases of pO2 and pH, in blood plasma. The supernatants of lymphocyte suspensions derived from blood incubated with enfuvirtide presented a decrease in pH and [HCO3−]. Fluorescence anisotropy measurements of 1,6‐diphenyl‐1,3,5‐hexatriene (DPH) and 1‐(4‐(trimethylamino)‐phenyl)‐6‐phenyl‐1,3,5‐hexatriene (TMA‐DPH), used to assess erythrocyte and lymphocyte membrane fluidity, did not yield enfuvirtide‐induced changes (an effect could be expected due to peptide partition to lipid bilayers). Erythrocytes incubated with high enfuvirtide concentrations showed a significant decrease in osmotic fragility. As for erythrocyte deformability, enfuvirtide leads to increased elongation indexes for low shear stress values, whereas for high shear stress values it has the opposite effect. Despite the observed statistically significant variations in several parameters, these enfuvirtide‐induced changes are not expected to lead to any detectable biomedical outcome for enfuvirtide‐treated patients. Copyright © 2008 European Peptide Society and John Wiley & Sons, Ltd.
Temperature and pH effects on biophysical and morphological properties of self‐assembling peptide RADA16‐I
Authors: Ye Zhaoyang , Zhang Hangyu , Luo Hanlin , Wang Shunkang , Zhou Qinghan , DU Xinpeng , Tang Chengkang , Chen Liyan , Liu Jingping , Shi Ying‐Kang , Zhang Er‐Yong , Ellis‐Behnke Rutledge , Zhao Xiaojun 
Published: January 2008

AbstractIt has been found that the self‐assembling peptide RADA 16‐I forms a β‐sheet structure and self‐assembles into nanofibers and scaffolds in favor of cell growth, hemostasis and tissue‐injury repair. But its biophysical and morphological properties, especially for its β‐sheet and self‐assembling properties in heat‐ and pH‐denatured conditions, remain largely unclear. In order to better understand and design nanobiomaterials, we studied the self‐assembly behaviors of RADA16‐I using CD and atomic force microscopy (AFM) measurements in various pH and heat‐denatured conditions. Here, we report that the peptide, when exposed to pH 1.0 and 4.0, was still able to assume a typical β‐sheet structure and self‐assemble into long nanofiber, although its β‐sheet content was dramatically decreased by 10% in a pH 1.0 solution. However, the peptide, when exposed to pH 13.0, drastically lost its β‐sheet structure and assembled into different small‐sized globular aggregates. Similarly, the peptide, when heat‐denatured from 25 to 70 °C, was still able to assume a typical β‐sheet structure with 46% content, but self‐assembled into small‐sized globular aggregates at much higher temperature. Titration experiments showed that the peptide RADA16‐I exists in three types of ionic species: acidic (fully protonated peptide), zwitterionic (electrically neutral peptide carrying partial positive and negative charges) and basic (fully deprotonated peptide) species, called ‘super ions’. The unordered structure and β‐turn of these ‘super ions’ via hydrogen or ionic bonds, and heat Brownian motion under the above denatured conditions would directly affect the stability of the β‐sheet and nanofibers. These results help us in the design of future nanobiomaterials, such as biosensors, based on β‐sheets and environmental changes. These results also help understand the pathogenesis of the β‐sheet‐mediated neuronal diseases such as Alzheimer's disease and the mechanism of hemostasis. Copyright © 2008 European Peptide Society and John Wiley & Sons, Ltd.
Enhancement of luminescence in ZnMgO thin‐film nanophosphors and application for white light generation
Authors: Chawla Santa , Jayanthi K. , Chander Harish 
Published: January 2008

AbstractA series of ZnMgO thin‐film nanophosphors with varied Zn:Mg ratio has been prepared by chemical bath deposition. The structure, photoluminescence, time‐resolved decay and chromaticity of the films are presented. ZnMgO films absorb light efficiently in the near UV (330–400 nm) and the emission covers a large part of the visible spectrum. Luminescence enhancement is maximum for 25% Mg. All ZnMgO films show luminescence lifetimes in the microsecond range while low Mg content (0–10%) films also exhibit fast decay (10–10 s). Measured colorimetric coordinates of (0.28, 0.32) when excited by 350 nm light make them suitable for generation of white light in conjunction with near UV LEDs. (© 2008 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
On the improvement of the electroluminescent signal of organic light‐emitting diodes by the presence of an ultrathin metal layer at the interface organic/ITO
Authors: Bernède J. C. , Martinez F. , Neculqueo G. , Cattin L. 
Published: January 2008

AbstractUnder DOI 10.1002/pssa.200723206 erroneously a paper was published online in January 2008 which already had been published elsewhere. Please find this paper, entitled “On the improvement of the electroluminescent signal of organic light emitting diodes by the presence of an ultra‐thin metal layer at the interface organic/ITO” by J. C. Bernède, F. Martinez, G. Neculqueo, and L. Cattin under DOI 10.1002/pssr.200701217, published in phys. stat. sol. (RRL) 2, No. 1, 10–12 (2008). (© 2008 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Crystallization behavior of Sb70Te30 and Ag3In5Sb60Te32 chalcogenide materials for optical media applications
Authors: Lee M. L. , Shi L. P. , Tian Y. T. , Gan C. L. , Miao X. S. 
Published: January 2008

AbstractAddition of In and Ag into eutectic Sb70Te30 fast‐growth material was studied. We explored the optical transitions and crystallization kinetics of Sb70Te30 and Ag3In5Sb60Te32 recording films. The results showed that Ag3In5Sb60Te32 has a higher crystallization temperature but a similar melting point compared to Sb70Te30. In both the crystalline and amorphous states, addition of Ag and In increased the refractive index and decreased the extinction coefficient of Sb70Te30. Ag3In5Sb60Te32 has better thermal stability and a lower crystallization speed than Sb70Te30 film. (© 2008 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)