bluuebunny/crossref_metadata_2025_split huggingface dataset:
Binding and functional characteristics of two E‐box motifs within the S100A6 (calcyclin) gene promoter
Authors: Leśniak Wiesława , Kuźnicki Jacek 
Published: November 2005

AbstractS100A6 (calcyclin) is a small calcium‐binding protein of the S100 family often associated with cancer and metastasis. We have previously shown that the E‐box sequence at position −283/−278 of the S100A6 gene promoter interacts with USF transcription factor and contributes to promoter transcriptional activity. We now present evidence that a second E‐box motif at position −593/−588 of the promoter also binds USF and that the USF1/USF2 heterodimer is the prevailing dimeric form of the transcription factor bound. Using the chromatin immunoprecipitation assay (ChIP), we show that USF is bound in vivo to the E‐box regulatory element(s). Depletion of the endogenous USF pool by means of a decoy oligonucleotide evokes a severe inhibition of S100A6 gene promoter activity. Furthermore, we show that S100A6 gene promoter activity can be stimulated by palmitate and that mutation of the −283/−278 E‐box sequence completely blocks this stimulation. J. Cell. Biochem. 97: 1017–1024, 2006. © 2005 Wiley‐Liss, Inc.
Effect of chlorpromazine on bone sialoprotein (BSP) gene transcription
Authors: Nakajima Yu , Kato Naoko , Nakayama Youhei , Kim Dong‐Soon , Takai Hideki , Arai Masato , Saito Ryoichiro , Samoto Hiroshi , Shimizu Emi , Ogata Yorimasa 
Published: November 2005

AbstractBone sialoprotein (BSP), an early marker of osteoblast differentiation. Whereas physical forces may play an important role in the regulation of bone cell function, little is known about how cells are able to sense mechanical loads. Chlorpromazine, a tranquilizing agent for treatments of psychiatric disorders, mimics hypotonic stress and causes membrane deformation. Application of 10 µg/ml of chlorpromazine suppressed BSP mRNA levels after 12 and 24 h in osteoblast‐like ROS17/2.8 cells and rat stromal bone marrow cells (SBMC‐D8). Chlorpromazine (10 µg/ml) decreased luciferase activity of the construct (pLUC3; −116 to +60 of the rat BSP gene promoter) after 12 h, the effect was inhibited by the tyrosine kinase inhibitor herbimycin A (HA) and MAP kinase kinase inhibitor U0126. Introduction of 2‐bp mutation in the pLUC3 construct showed that the chlorpromazine effects were mediated by cAMP response element (CRE) and FGF2 response element (FRE). In gel shift assays, using radiolabeled double‐stranded CRE and FRE oligonucleotides, which revealed decreased binding of nuclear proteins from chlorpromazine‐stimulated cells. These studies, therefore, show that chlorpromazine suppresses BSP gene transcription through tyrosine and MAP kinases‐dependent pathways and that the chlorpromazine effects are mediated by CRE and FRE elements in the proximal promoter of the BSP gene. J. Cell. Biochem. 97: 1198–1206, 2006. © 2005 Wiley‐Liss, Inc.
Microarray and phosphokinase screenings leading to studies on ERK and JNK regulation of connective tissue growth factor expression by angiotensin II 1a and bradykinin B2 receptors in Rat1 fibroblasts
Authors: Liu B. , Yu J. , Taylor L. , Zhou X. , Polgar P. 
Published: November 2005

AbstractRat1 fibroblasts stably transfected with the rat angiotensin II (AngII) AT1a and bradykinin (BK) B2 receptor cDNAs gained the ability to bind Ang II and BK. Wild‐type Rat1 cells bound neither ligand. Exposure to either effector led to characteristic Gαi and Gαq signal cascades, the release of arachidonic acid (ARA), and the intracellular accumulation of inositol phosphates (IP). Microarray analyses in response to BK or AngII showed that both receptors markedly induce the CCN family genes, CTGF (CCN2) and Cyr61 (CCN1), as well as the vasculature‐related genes, Cnn1 and Egr1. Real time PCR confirmed the increased expression of connective tissue growth factor (CTGF) mRNA. Combined sequence‐based analysis of gene promoter regions with statistical prevalence analyses identified CREB, SRF, and ATF‐1, downstream targets of ERK, and JNK, as prominent products of genes that are regulated by ligand binding to the BK or AngII receptors. The binding of AngII or BK markedly stimulated the phosphorylation and thus the activation of ERK2, JNK, and p38MAPK. A BKB2R and an AT1aR chimera which displayed only negligible G‐protein‐related signaling were constructed. Both mutant receptors continued to activate these kinases and stimulate CTGF expression. Inhibitors of ERK1/2 and JNK but not p38MAPK inhibited the BK‐ and AngII‐stimulated expression of CTGF in cells expressing either the WT or mutant receptors, illustrating that ERK and JNK participate in the control of CTGF expression in a manner that appears to be independent of G‐protein. Conversely, addition of BK or AngII to the cell line expressing WT AT1aR and BKB2R downregulated the expression of collagen α1(I) (COL1A1) mRNA. However, these effectors did not have this effect in cells expressing the mutant receptors. Thus, a robust G‐protein related response is necessary for BK or AngII to affect COL1A1 expression. J. Cell. Biochem. 97: 1104–1120, 2006. © 2005 Wiley‐Liss, Inc.
Heparanase mechanisms of melanoma metastasis to the brain: Development and use of a brain slice model
Authors: Murry Brian P. , Blust Bryan E. , Singh Amandip , Foster Timothy P. , Marchetti Dario 
Published: November 2005

AbstractHeparanase (HPSE‐1) is an endo‐β‐D‐glucuronidase that cleaves heparan sulfate (HS) chains of proteoglycans (HSPG), and its expression has been associated with increased cell growth, invasion, and angiogenesis of tumors as well as with embryogenesis and tissue development. Since metastatic cancer cells express HPSE‐1, we have developed an orthotopic brain slice model to study HPSE‐1 involvement in brain‐metastatic melanoma. This model allows for the characterization of tumor cell invasion at both quantitative and qualitative levels. Brain‐metastatic melanoma cells (B16B15b) showed augmenting levels of HPSE‐1 protein expression in a time‐dependent manner. Secondly, B16B15b cells pre‐treated with HPSE‐1 showed a significant increase in the number of cells that invaded into the brain tissue. Finally, HPSE‐1 exposure‐augmented invasion depth in brain sections by brain‐metastatic melanoma cells. We concluded that applying this brain slice model can be beneficial to investigate HPSE‐1‐ related in vivo modalities in brain‐metastatic melanoma and brain invasion in general. These results also further emphasize the potential relevance of using this model to design therapies for controlling this type of cancer by blocking HPSE‐1 functionality. © 2005 Wiley‐Liss, Inc.
Computation of vertical excitation energies of retinal and analogs: Scope and limitations
Authors: López Carlos Silva , Faza Olalla Nieto , Estévez Susana López , de Lera Angel R. 
Published: November 2005

AbstractA comprehensive survey of computational methods: semiempirical (ZINDO/S), Time‐Dependent Hartree–Fock (TD‐HF), Configuration Interaction Singles (CIS), and several approximate functionals within the Time‐Dependent Density Functional Theory (TD‐DFT) has been carried out for the description of vertical excitation energies and oscillator strengths of retinal and related polyenals. ZINDO and TD‐DFT computations showed the best agreement with the experimental data. In particular, hybrid functionals including approximately 25% of exact exchange (B3LYP, B3P86, and PBE0) were found to perform best with these highly conjugated polyenes. A systematic average error of 0.18–0.22 eV has been found after a simple one‐parameter correction. Thus, 0.18 eV might be considered the upper limit of accuracy for current one‐determinant methods in the computation of vertical excitation energies. The consideration of adiabatic excitations, conformational sampling, solvation, and nondynamic correlation should describe this processes more accurately, but this leads to highly demanding methods beyond feasibility for these large polyenes. The trends observed, particularly the good performance of the ZINDO/S method, should pave the way for the prediction of excited states properties in natural and artificial photoreceptor proteins, thus advancing towards the description of their light‐transducing biological role in Nature. © 2005 Wiley Periodicals, Inc. J Comput Chem 27: 116–123, 2006
Optimal holey packings OHP4(2, 4, n ,3)'s
Authors: Wang Jianmin , Yan J. 
Published: November 2005

AbstractAn optimal holey packing OHPd(2, k, n, g) is equivalent to a maximal (g + 1)‐ary (n, k, d) constant weight code. In this paper, we provide some recursive constructions for OHPd(2, k, n, g)'s and use them to investigate the existence of an OHP4(2, 4, n, 3) for n ≡ 2, 3 (mod 4). Combining this with Wu's result (18), we prove that the necessary condition for the existence of an OHP4(2, 4, n, 3), namely, n ≥ 5 is also sufficient, except for n ∈ {6, 7} and except possibly for n = 26. © 2005 Wiley Periodicals, Inc. J Combin Designs 14: 111–123, 2006
Mechanical forces alter zyxin unbinding kinetics within focal adhesions of living cells
Authors: Lele Tanmay P. , Pendse Jay , Kumar Sanjay , Salanga Matthew , Karavitis John , Ingber Donald E. 
Published: November 2005

AbstractThe formation of focal adhesions that mediate alterations of cell shape and movement is controlled by a mechanochemical mechanism in which cytoskeletal tensional forces drive changes in molecular assembly; however, little is known about the molecular biophysical basis of this response. Here, we describe a method to measure the unbinding rate constant kOFF of individual GFP‐labeled focal adhesion molecules in living cells by modifying the fluorescence recovery after photobleaching (FRAP) technique and combining it with mathematical modeling. Using this method, we show that decreasing cellular traction forces on focal adhesions by three different techniques—chemical inhibition of cytoskeletal tension generation, laser incision of an associated actin stress fiber, or use of compliant extracellular matrices—increases the kOFF of the focal adhesion protein zyxin. In contrast, the kOFF of another adhesion protein, vinculin, remains unchanged after tension dissipation. Mathematical models also demonstrate that these force‐dependent increases in zyxin's kOFF that occur over seconds are sufficient to quantitatively predict large‐scale focal adhesion disassembly that occurs physiologically over many minutes. These findings demonstrate that the molecular binding kinetics of some, but not all, focal adhesion proteins are sensitive to mechanical force, and suggest that force‐dependent changes in this biophysical parameter may govern the supramolecular events that underlie focal adhesion remodeling in living cells. J. Cell. Physiol. 207: 187–194, 2006. © 2005 Wiley‐Liss, Inc.
Slow virus disease: Deciphering conflicting data on the transmissible spongiform encephalopathies (TSE) also called prion diseases
Authors: Bastian Frank O. , Fermin Cesar D. 
Published: November 2005

AbstractThe transmissible spongiform encephalopathies (TSE) that manifest as Creutzfeldt‐Jakob disease in humans, as scrapie in sheep and goats, mad cow disease in cattle, or chronic wasting disease in cervids (deer) represent a serious human health crisis and a significant economical problem. Despite much research, the nature of the elusive pathogen directly involved with TSE is currently unresolved. This article reviews current pathogen‐cell plasma membrane properties, showing that the primary biochemical marker of the prion disease is used as a receptor by the intracellular bacterium Brucella abortus. Such observation makes plausible the role for the prion in the pathogenesis of TSE, and supports the concept that Spiroplasma, a wall‐less bacterium, may be a transmissible agent of TSE. Over the past three decades, we have published convincing evidence that Spiroplasma infection is associated with TSE. The bacterial‐prion‐receptor concept by other laboratories support a model for TSE wherein a Spiroplasma bacterium can bind to prion receptors (alone or with anchors) on the cell surface lipid raft, allowing entry of the microbe into the cell to initiate infection. The relevance of this new concept is that it offers a new window for future research involving a bacterium in the pathogenesis of TSE. Data from the bacterial‐prion‐receptor model will aid in the development diagnostic tests and/or treatment protocols for TSE. Microsc. Res. Tech. 68:239–246, 2005. © 2005 Wiley‐Liss, Inc.
Coexpression of major histocompatibility complex class I and LMP1 in Epstein‐Barr virus‐positive Hodgkin's Lymphoma in a pediatric age group
Authors: Aybar Argelia , Krause John R. 
Published: November 2005

AbstractThe Epstein‐Barr virus (EBV)‐encoded latent membrane proteins (LMP1 and LMP2) are consistently expressed by malignant Hodgkin Reed‐Sternberg (HRS) cells of EBV‐associated Hodgkin's disease (HD). The EBV LMP1 has been implicated in tumorogenesis. Cytotoxic T lymphocyte (CTL) responses to both of these proteins have been shown in the blood of EBV‐seropositive individuals, and in HD, the apparent failure of the CTL response to eliminate HRS cells expressing LMP1 in vivo has given rise to the suggestion that HD may be characterized by the presence of defects in antigen CTL‐presentation or in CTL dysfunction. This study examined 28 cases seen at the Regional Children's Hospital Arturo Grullón in Santiago, the Dominican Republic, by immunohistochemistry. High level of expression of major histocompatibility complex (MHC) class I molecules in HRS cells of EBV‐associated HD was recorded. These results suggest that deregulation of MHC class I molecules does not account for the apparent ability of EBV to infect HRS cells and to evade CTL protection. Therefore, the result from our work and similar studies will help to determine whether, or which, immunotherapy should be used in positive and negative cases of HD related to EBV. Microsc. Res. Tech. 68:247–249, 2005. © 2005 Wiley‐Liss, Inc.
Of mice, cats, and men: Is human breast cancer a Zoonosis?
Authors: Szabo Sara , Haislip Allyson M. , Garry Robert F. 
Published: November 2005

AbstractMouse mammary tumor virus (MMTV), a member of the betaretroviridae, is the most common cause of breast cancer (BC) in mice. MMTV is transmitted in mice both in the germline as endogenous proviruses and exogenously as infectious virions. Here, we review a variety of evidence accumulated for six decades that has suggested that a human homologue of MMTV may exist. The findings include recent studies from several independent laboratories that have detected sequences very closely related to MMTV in DNA isolated from human BC tumors. Other laboratories, however, have failed to detect the MMTV‐related sequences in human DNA samples, and conclusive evidence for a human mammary tumor virus has been elusive. We also reviewed additional studies, suggesting that betaretroviruses are present in a much wider range of species than previously known, including rodents, felines, and primates. The observation that a subset of cats may be infected with a close homologue of MMTV may be of epidemiological significance for human BC. Cats may become infected by MMTV from mice, and in turn may transmit the virus to humans, possibly after selection for variants with an expanded host range. Microsc. Res. Tech. 68:197–208, 2005. © 2005 Wiley‐Liss, Inc.
Human, rhesus macaque, and feline sequences highly similar to mouse mammary tumor virus sequences
Authors: Szabo Sara , Haislip Allyson M. , Traina‐Dorge Vicki , Costin Joshua M. , Crawford Byron E. , Wilson Russell B. , Garry Robert F. 
Published: November 2005

AbstractSequences highly similar (>95%) to the mouse mammary tumor virus (MMTV) env gene have been amplified from human DNA samples, including DNA samples from patients with breast cancer (BC) and persons who did not have BC. The sequences from human DNA were distinct from the MMTV sequences used as controls in these PCR reactions, indicating that these results are not simply due to contamination. In addition to both, mouse and human‐related sequences were also amplified from some monkey and cat genomic DNA samples. These products were shown to be distinct from, but highly related to, the MMTV env gene, whereas, testing of other sources (lambda phage, snake, cockroach, sea urchin, chicken, or dog) demonstrated no specific amplification. A sequence ˜90% similar to the MMTV group antigen gene (gag) was amplified from cat DNA. These results indicate that DNA from vertebrate species other than rodents, including some but not all humans, monkeys, and cats, can contain sequences closely related to MMTV. Microsc. Res. Tech. 68:209–221, 2005. © 2005 Wiley‐Liss, Inc.
Human mesenchymal stem cells (hMSCs) expressing truncated soluble vascular endothelial growth factor receptor (tsFlk‐1) following lentiviral‐mediated gene transfer inhibit growth of Burkitt's lymphoma in a murine model
Authors: Kyriakou Chara A. , Yong Kwee L. , Benjamin Reuben , Pizzey Arnold , Dogan Ahmet , Singh Nalini , Davidoff Andrew M. , Nathwani Amit C. 
Published: November 2005

AbstractBackgroundEfficient gene transfer to bone marrow derived mesenchymal stem cells (MSC) would provide an important opportunity to express potent anticancer agents in the tumour microenvironment because of their contribution to the tumour stroma.MethodsHIV‐based lentiviral vectors were pseudotyped with four different envelope proteins; amphotropic murine leukaemia virus (ampho), murine leukaemia virus (10A1), feline endogenous virus (RD114), and the vesicular stomatitis virus glycoprotein (VSVG). These pseudotypes were examined for transduction efficiency in human bone marrow derived MSC. The effect of lentiviral expression of truncated soluble vascular endothelial growth factor decoy receptor (tsFlk‐1) in MSC on growth of Raji cells was determined, both in vitro and in vivo.ResultsAll lentiviral vectors produced significant levels of transduction at an multiplicity of infection (MOI) of 1, those bearing the RD114 envelope glycoprotein consistently produced higher transduction levels (mean 70 ± 6%) compared with the other pseudotyped lentiviral vectors, although there was significant inter‐donor variation. Stable transgene expression was achieved after multiple rounds of transduction with VSVG‐pseudotyped particles, without alteration in the differentiative capacity of transduced cells. Co‐injection of MSC stably expressing tsFlk‐1 with Raji Burkitt's lymphoma cells significantly impaired subcutaneous tumour growth in immunodeficient mice when compared to controls where either unmanipulated MSC or GFP‐expressing MSC were used.ConclusionsHuman MSC are easily transduced by pseudotyped lentiviral particles but there is inter‐donor variation in transduction efficiency. Gene‐modified MSC expressing a gene of therapeutic potential can moderate growth of haematological malignancies. Copyright © 2005 John Wiley & Sons, Ltd.
Polybrene improves transfection efficacy of recombinant replication‐deficient adenovirus in cutaneous cells and burned skin
Authors: Jacobsen F. , Hirsch T. , Mittler D. , Schulte M. , Lehnhardt M. , Druecke D. , Homann H. H. , Steinau H. U. , Steinstraesser L. 
Published: November 2005

AbstractBackgroundThe hostile environment found in acute and chronic wounds decreases the physiological half‐life of purified synthetic or recombinant peptides dramatically. Gene therapy, on the other hand, may be a viable option since it relies on the cellular machinery of the host to locally manufacture the proteins of interest. The aim of this study was to evaluate and optimize the local administration of transient cutaneous adenoviral gene delivery in wounds.MethodsPrimary human keratinocytes (HKC) and HaCaT cells were transfected with replication‐deficient adenovirus (Ad5) containing the reporter gene for β‐galactosidase (LacZ). The vector was used alone or precoated with either (1) Lipofectamine™ 2000, (2) FuGENE™ 6, or (3) Polybrene. For in vivo testing a rat burn model was used. Animals were randomized into three groups: (1) Ad5‐LacZ alone; (2) Ad5‐LacZ precoated with Polybrene, or (3) carrier control (phosphate‐buffered saline (PBS)). Samples were harvested from burned and unburned tissue sections after either 48 h or 7 days. Transgene expression was quantified by bioluminometric assay and localized using immunohistochemistry. A BrdU assay was performed to determine the influence of the used transfection reagents on cell proliferation.ResultsTransfection efficacy was significantly improved in vitro (p < 0.001) as well as in partial thickness burned (p = 0.015) and unburned skin (p > 0.001) after precoating Ad5 with Polybrene compared to Ad5 alone. Transgene expression was 10‐fold higher in burned skin (9305 pg/mg protein) compared to unburned skin (859 pg/mg protein).ConclusionsIt is feasible to improve transfection efficacy in vitro and in vivo by precoating the adenovirus with Polybrene. Copyright © 2005 John Wiley & Sons, Ltd.
Polyethylenimine‐based antisense oligodeoxynucleotides of IL‐4 suppress the production of IL‐4 in a murine model of airway inflammation
Authors: Seong Ji‐Hye , Lee Kyung‐Mi , Kim Sung Tae , Jin Su‐Eon , Kim Chong‐Kook 
Published: November 2005

AbstractBackgroundInterleukin‐4 (IL‐4) plays a crucial role as an inflammatory mediator in allergic asthma via inducing Th2 inflammation and IgE synthesis. To develop an effective therapeutic agent which specifically inhibits production of IL‐4, antisense oligodeoxynucleotides (AS‐ODNs) against murine IL‐4 mRNA were generated and complexed with polyethylenimine (PEI) to improve intracellular delivery.MethodsAS‐ODNs were generated against the translation initiation region of murine IL‐4 mRNA, and complexed with linear PEI. In vitro efficacy of AS‐ODNs/PEI complexes was tested by measuring IL‐4 production in the D10.G4.1 cell line, and cytotoxicity was tested by XTT assay. Physicochemical properties of polyplexes were examined using atomic force microscopy (AFM) and DNase I protection assay. In vivo effects of IL‐4 AS‐ODNs/PEI complexes were tested in a murine model of airway inflammation. IL‐4 concentrations in the bronchoalveolar lavage (BAL) fluid and circulating IgE levels were measured by ELISA, and histological analysis of lung tissues was performed.ResultsIL‐4 AS‐ODNs/PEI complexes were spheres with an average diameter of 98 nm and resistant to DNase I‐mediated degradation. IL‐4 AS‐ODNs/PEI complexes showed up to 35% inhibition of IL‐4 production in D10.G4.1 cells without causing any toxicity, while naked ODNs gave less than 1% reduction. Furthermore, IL‐4 AS‐ODNs/PEI complexes were effective in suppressing secretion of IL‐4 (up to 30% reduction) in the BAL fluid in an ovalbumin‐sensitized murine model of airway inflammation. Circulating IgE levels were decreased, and airway inflammation was alleviated by treatment with IL‐4 AS‐ODNs polyplexes.ConclusionsThese data demonstrate that complexation of IL‐4 AS‐ODNs with PEI provides a potential therapeutic tool in controlling inflammation associated with allergic asthma, and further presents an opportunity to the development of clinical therapy based on combination of multiple AS‐ODNs of cytokines and/or signaling effectors involved in Th2 inflammation and eosinophilia. Copyright © 2005 John Wiley & Sons, Ltd.