Relevant bibliographies by topics / Gp100

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Gp100'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Gp100"

1

Bakker, A. B., M. W. Schreurs, A. J. de Boer, Y. Kawakami, S. A. Rosenberg, G. J. Adema, and C. G. Figdor. "Melanocyte lineage-specific antigen gp100 is recognized by melanoma-derived tumor-infiltrating lymphocytes." Journal of Experimental Medicine 179, no. 3 (March 1, 1994): 1005–9. http://dx.doi.org/10.1084/jem.179.3.1005.

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We recently isolated a cDNA clone that encodes the melanocyte lineage-specific antigen glycoprotein (gp)100. Antibodies directed against gp100 are an important tool in the diagnosis of human melanoma. Since the gp100 antigen is highly expressed in melanocytic cells, we investigated whether this antigen might serve as a target for antimelanoma cytotoxic T lymphocytes (CTL). Here, we demonstrate that cytotoxic tumor-infiltrating lymphocytes (TIL) derived from a melanoma patient (TIL 1200) are directed against gp100. HLA-A2.1+ melanoma cells are lysed by TIL from this patient. In addition, murine double transfectants, expressing both HLA-A2.1 and gp100, are lysed by TIL 1200, whereas transfectants expressing only HLA-A2.1 are not susceptible to lysis. Furthermore, the HLA-A2.1+ melanoma cell line BLM, which lacks gp100 expression and is resistant to lysis, becomes susceptible after transfection of gp100 cDNA. Finally, HLA-A2.1+ normal melanocytes are lysed by TIL 1200. These data demonstrate that the melanocyte differentiation antigen gp100 can be recognized in the context of HLA-A2.1 by CTL from a melanoma patient. Gp100 may therefore constitute a useful target for specific immunotherapy against melanoma, provided that no unacceptable cytotoxicity towards normal tissue is observed.
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O'Day, S., F. S. Hodi, D. F. McDermott, R. W. Weber, J. A. Sosman, J. B. Haanen, X. Zhu, M. J. Yellin, A. Hoos, and W. J. Urba. "A phase III, randomized, double-blind, multicenter study comparing monotherapy with ipilimumab or gp100 peptide vaccine and the combination in patients with previously treated, unresectable stage III or IV melanoma." Journal of Clinical Oncology 28, no. 18_suppl (June 20, 2010): 4. http://dx.doi.org/10.1200/jco.2010.28.18_suppl.4.

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4 Background: Ipilimumab, a fully human monoclonal antibody against cytotoxic T-lymphocyte antigen-4, demonstrated activity in advanced melanoma. Gp100 vaccine showed immunological and clinical responses, and enhanced clinical activity when combined with other immunotherapy. This phase III study compared efficacy and safety of ipilimumab or gp100 monotherapy and combination. Methods: Eligible patients (HLA-A*0201+ previously treated adults with unresectable stage III/IV melanoma) were randomized 1:3:1 to ipilimumab (3 mg/kg q3w x 4 doses) + placebo (n=137), ipilimumab + gp100 (peptides 209-217[210M] and 280-288 [288V]; 1mg q3w x 4 doses; n=403), or gp100 + placebo (n=136). There was no maintenance phase. Primary endpoint was comparison of overall survival (OS) between patients who received combination versus gp100 alone; secondary endpoints were all other OS comparisons, best overall response rate (BORR), disease control rate (DCR) to W24, progression-free survival (PFS), and safety. Results: The study demonstrated statistically significant results for all efficacy endpoints (below). Ipilimumab alone or combined with gp100 resulted in a significant improvement in OS with risk reduction of 32-34% compared to gp100. Significant differences in DCR, BORR, and PFS were observed. Adverse events with ipilimumab were consistent with prior studies: generally mild, immune-related, and medically manageable. Conclusions: Ipilimumab is the first agent to improve median and long-term OS in a phase III study of previously treated patients with advanced melanoma. Addition of gp100 vaccine to ipilimumab did not improve outcome. [Table: see text] [Table: see text]
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Harvey, Becca, Dawn Lee, Anne-Francoise Gaudin, Beatrice Gueron, Bruno Bregman, Céleste Lebbé, and Isabelle Borget. "Changes in the quality of life of advanced melanoma patients after 12 weeks of treatment with ipilimumab compared to gp100 in a phase III clinical trial." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 9084. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9084.

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9084 Background: This study analyses health-related quality of life (HRQL) outcomes for ipilimumab (ipi) with and without gp100 and gp100 alone during the 12 week treatment (T) induction period compared to baseline. The aim of this study was to express the HRQL as proportions of patients experiencing changes during the induction period, when most of the immune-related adverse events (ir-AE) on ipi occur. Methods: Data from the MDX010-20 trial, including 676 previously treated patients (pts) with unresectable stage III or IV melanoma, was analysed. Differences between ipi with/without gp100 and gp100 alone in terms of HRQL 12 weeks after randomisation according to the EORTC QLQ-C30 were searched for. The sample consisted of 388 pts (ipi: 83; ipi + gp100: 227; gp100: 78) completing both baseline and week (W)12 questionnaires. Ordinal regression was performed for these pts to determine a T effect on W12 scores (in ordered categories) whilst adjusting for key covariates. Fisher’s Exact Test was used to detect differences between Ts for each EORTC domain when considering mean change in scores, categorised as “clinically worse” (≤-10 on functional domains, ≥10 on symptoms), “stable” (>-10 to <10) and “clinically improved” (≥10 on functional domains, ≤-10 on symptoms). Results: There were no significant differences for any domain score between the 3 T arms at W12. The odds of attaining high HRQL scores at W12 were heavily dependent on the baseline scores; baseline scores explained most of the variability as per regression analysis. There was no significant difference between the 3 T arms in terms of pts showing a clinically significant reduction or improvement in HRQL. HRQL remained globally stable from baseline to W12, in > 50% of pts for most domains. Conclusions: Ipi with/without gp100 does not have a significant negative HRQL impact in stage III-IV melanoma during the T induction phase relative to gp100 alone after adjustment for differences in baseline scores. The lower rate of pts showing HQRL reduction and the absence of difference with gp100 suggest that ir-AE have little impact on HRQL. Further HRQL studies are needed, as efficacy benefits of ipi continue after W12.
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Lundqvist, Andreas, Sheila Rao, Maria Berg, Aleah Smith, Su Su, Hisayuki Yokoyama, Shivani Srivastava, and Richard Childs. "The Proteasome Inhibitor Bortezomib Simultaneously Enhances NK Cell Tumor Cytotoxicity While Paradoxically Reducing Antigen Specific T-Cell Tumor Cytotoxicity." Blood 110, no. 11 (November 16, 2007): 1789. http://dx.doi.org/10.1182/blood.v110.11.1789.1789.

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Abstract The proteasome inhibitor bortezomib was recently found to render tumor cells susceptible to natural killer (NK) cell-mediated apoptosis in vitro and in vivo. This sensitization appears to occur as a consequence of this agent up-regulating surface expression of tumor necrosis factor-related apoptosis-inducing ligand receptor 2 (TRAIL-R2) on human malignant cells rendering them susceptible to TRAIL-mediated NK cell cytotoxicity. We hypothesized that bortezomib would likewise sensitize tumors to the cytotoxic effects of antigen specific T-cells through similar apoptotic pathways, thereby providing an incentive to use bortezomib as a universal immune-sensitizing agent. The HLA-A2+, gp100+, MART-1+ melanoma cell lines 526 and 624 were treated with 10nM bortezomib for 18 hrs then were analyzed by FACS for expression the cell surface markers (HLA-ABC, MIC-A/B, TRAIL-R1/2 and Fas) and Cr51 cytotoxicity assay for susceptibility to CD8+/HLA-A2+ restricted gp100 and MART-1 specific CTL-mediated lysis. As observed previously, NK cell-mediated apoptosis was significantly higher in tumor cells treated with bortezomib compared to untreated tumor cells. In contrast, an unanticipated and significant reduction in CTL-mediated cytotoxicity was observed in tumors treated with bortezomib compared to untreated tumors; at an effector:target ratio of 3:1, NK cell cytotoxicity increased from 43±2% to 70±2% (p&lt;0.01) while gp100 CTL cytotoxicity decreased from 34±4% to 18±2% (p&lt;0.01) in 624 melanoma cells after exposure to bortezomib (figure). This inhibition in T-cell killing was not due to changes in tumor surface expression of MHC class I, MIC-A/B, TRAIL receptors or Fas. Remarkably, CTL-mediated cytotoxicity was restored to baseline in tumor cells that were pulsed with gp100 antigen following bortezomib treatment, suggesting proteasome inhibition by bortezomib altered or impaired the processing and presentation of the gp100 tumor antigen. Conclusions: Exposure of malignant cells to bortezomib results in simultaneous divergent effects on innate NK cell and adaptive T-cell anti-tumor immunity. While tumors exposed to bortezomib have enhanced susceptibility to NK-cell cytotoxicity, proteasome inhibition appears to disrupt antigen presentation potentially reducing tumor specific CTL effector responses. These findings suggest antigen specific T-cell responses such as graft-vs-host disease, and T-cell mediated graft-vs-tumor effects might be altered when bortezomib is administered following allogeneic hematopoietic cell transplantation. Figure. Melanoma cell line (624) was treated with bortezomib [10 nM] and analyzed for susceptibility to NK cell (left) and gp100-specific CD8+ CTL (middle) - mediated cytotoxicity in a 5h Cr51 cytotoxicity assay. Right - bortezomib-treated and untreated gp100:209 peptide pulsed 624 melanoma cells analyzed for susceptibility to gp100-specific CD8+ CTL-mediated cytotoxicity at a E:T ratio of 4:1 Figure. Melanoma cell line (624) was treated with bortezomib [10 nM] and analyzed for susceptibility to NK cell (left) and gp100-specific CD8+ CTL (middle) - mediated cytotoxicity in a 5h Cr51 cytotoxicity assay. Right - bortezomib-treated and untreated gp100:209 peptide pulsed 624 melanoma cells analyzed for susceptibility to gp100-specific CD8+ CTL-mediated cytotoxicity at a E:T ratio of 4:1
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Dowlath, Sasheen, Katrin Campbell, Farah Al-Barwani, Vivienne L. Young, Sarah L. Young, Greg F. Walker, and Vernon K. Ward. "Dry Formulation of Virus-Like Particles in Electrospun Nanofibers." Vaccines 9, no. 3 (March 3, 2021): 213. http://dx.doi.org/10.3390/vaccines9030213.

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Biologics can be combined with liquid polymer materials and electrospun to produce a dry nanofibrous scaffold. Unlike spray-drying and freeze-drying, electrospinning minimizes the physiological stress on sensitive materials, and nanofiber mat properties such as hydrophobicity, solubility, and melting temperature can be tuned based on the polymer composition. In this study, we explored the dry formulation of a virus-like particle (VLP) vaccine by electrospinning VLP derived from rabbit hemorrhagic disease virus modified to carry the MHC-I gp100 tumor-associated antigen epitope. VLP were added to a polyvinylpyrrolidone (PVP) solution (15% w/v) followed by electrospinning at 24 kV. Formation of a nanofibrous mat was confirmed by scanning electron microscopy, and the presence of VLP was confirmed by transmission electron microscopy and Western blot. VLP from the nanofibers induced T-cell activation and interferon- (IFN-) γ production in vitro. To confirm in vivo cytotoxicity, Pmel mice treated by injection with gp100 VLP from nanofibers induced a gp100 specific immune response, lysing approximately 65% of gp100-pulsed target cells, comparable to mice vaccinated with gp100 VLP in PBS. VLP from nanofibers also induced an antibody response. This work shows that electrospinning can be used to dry-formulate VLP, preserving both humoral and cell-mediated immunity.
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Cassaday, R., P. Sondel, D. King, T. Warner, A. Bridges, J. Gan, H. Schalch, J. Hank, D. Mahvi, and M. Albertini. "Clinical and immunological analysis of melanoma patients receiving immunization using particle-mediated gene transfer of genes for gp100 and GM-CSF into uninvolved skin." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 13033. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.13033.

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13033 Background: To investigate a new method of activating melanoma-specific immune responses, we examined in vivo particle-mediated gene transfer (PMGT) of cDNAs for gp100 and GM-CSF into uninvolved skin of melanoma patients (pts). We now report the analysis of a completed Phase I clinical study. Methods: Two treatment groups of 6 pts each were evaluated. Group I received PMGT with cDNA for gp100 during each 3 week cycle; Group II received PMGT with cDNA for GM-CSF followed 3 days later by PMGT for gp100 at the same site. PMGT used 0.25 ug DNA and 250 ug gold/treatment. Endpoints included vaccine toxicity, transgene expression, immunological activation, and antitumor effects. Results: No systemic toxicity could be attributed to the vaccines, while local toxicity in both groups included mild erythema and induration which resolved within 2 weeks. Monitoring for autoimmunity showed no induction of pathologic autoantibodies. Biopsies of vaccine sites obtained 2 days after the gp100 PMGT showed 16% of gold beads to be in the dermis in Group I vs 3% in Group II, suggesting the prior GM-CSF PMGT inhibited bead penetration (p < 0.001 by chi-square; each bead penetration was analyzed as an independent event). Biopsies in Group I obtained 2 days after vaccination showed 16% of beads in the dermis vs 22% after 4 days (p < 0.001 by chi-square; each bead penetration was analyzed as an independent event). Transgene expression in vaccinated skin sites was detected by ELISA (GM-CSF) and IHC (gp100). One of 4 HLA-A2+ subjects showed a 5 × 5-mm DTH response to gp100 peptide 210M after Cycle 1. Preliminary in vitro studies suggest minimal immunological activation. Of 4 pts who enrolled with no evidence of disease, 2 remain disease-free after 61–73 months of follow-up. Conclusions: PMGT with cDNA for gp100 and GM-CSF yields transgene expression in normal human skin with minimal local or systemic toxicity. Pathologic autoimmunity was not demonstrated. Bead concentration in the dermis increases over time, suggesting persistence of beads in this skin level. Conclusions related to melanoma-specific immune induction await T-cell and antibody studies. Supported in part by the UW General Clinical Research Center (M01 RR03186). No significant financial relationships to disclose.
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Voelkl, Simon, Tamson Moore, Michael Rehli, Michael Nishimura, Karin Fischer, and Andreas Mackensen. "Characterization of MHC Class-I Restricted TCRαβ+CD4−CD8− Double-Negative T Cells Recognizing the gp100 Antigen from a Melanoma Patient after gp100 Vaccination." Blood 112, no. 11 (November 16, 2008): 4905. http://dx.doi.org/10.1182/blood.v112.11.4905.4905.

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Abstract The immune attack against malignant tumors requires the concerted action of CD8+ cytotoxic T lymphocytes (CTL) as well as CD4+ T helper cells. The contribution of T cell receptor (TCR)αβ+ CD4− CD8− double-negative (DN) T cells to anti-tumor immune responses is widely unknown. In previous studies, we have demonstrated that DN T cells with a broad TCR repertoire are present in humans in the peripheral blood and the lymph nodes of healthy individuals. Here we characterize a human DN T cell clone (T4H2) recognizing an HLA-A2-restricted melanoma-associated antigenic gp100-peptide isolated from the peripheral blood of a melanoma patient. Antigen recognition by the T4H2 DN clone resulted in specific secretion of IFN-γ and TNF. Although lacking the CD8 molecule the gp100-specifc DN T cell clone was able to confer antigen-specific cytotoxicity against gp100-loaded target cells as well as HLA-A2+ gp100 expressing melanoma cells. The cytotoxic capacity was found to be perforin/granzymeB-dependent. Together, these data indicate that functionally active antigen-specific DN T cells recognizing MHC class I-restricted tumor-associated antigen (TAA) may contribute to anti-tumor immunity in vivo.
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McKenna, Philip M., Roger J. Pomerantz, Bernhard Dietzschold, James P. McGettigan, and Matthias J. Schnell. "Covalently Linked Human Immunodeficiency Virus Type 1 gp120/gp41 Is Stably Anchored in Rhabdovirus Particles and Exposes Critical Neutralizing Epitopes." Journal of Virology 77, no. 23 (December 1, 2003): 12782–94. http://dx.doi.org/10.1128/jvi.77.23.12782-12794.2003.

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ABSTRACT Rabies virus (RV) vaccine strain-based vectors show significant promise as potential live-attenuated vaccines against human immunodeficiency virus type 1 (HIV-1). Here we describe a new RV construct that will also likely have applications as a live-attenuated or killed-particle immunogen. We have created a RV containing a chimeric HIV-1 Env protein, which contains introduced cysteine residues that give rise to an intermolecular disulfide bridge between gp120 and the ectodomain of gp41. This covalently linked gp140 (gp140 SOS) is fused in frame to the cytoplasmic domain of RV G glycoprotein and is efficiently incorporated into the RV virion. On the HIV-1 virion, the gp120 and gp41 moieties are noncovalently associated, which leads to extensive shedding of gp120 from virions and virus-infected cells. The ability to use HIV-1 particles as purified, inactivated immunogens has been confounded by the loss of gp120 during preparation. Additionally, monomeric gp120 and uncleaved gp160 molecules have been shown to be poor antigenic representations of virion-associated gp160. Because the gp120 and gp41 portions are covalently attached in the gp140 SOS molecule, the protein is maintained on the surface of the RV virion throughout purification. Surface immunostaining and fluorescence-activated cell sorting analysis with anti-envelope antibodies show that the gp140 SOS protein is stably expressed on the surface of infected cells and maintains CD4 binding capabilities. Furthermore, Western blot and immunoprecipitation experiments with infected-cell lysates and purified virions show that a panel of neutralizing anti-envelope antibodies efficiently recognize the gp140 SOS protein. The antigenic properties of this recombinant RV particle containing covalently attached Env, as well as the ability to present Env in a membrane-bound form, suggest that this approach could be a useful component of a HIV-1 vaccine strategy.
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Overwijk, Willem W., Allan Tsung, Kari R. Irvine, Maria R. Parkhurst, Theresa J. Goletz, Kangla Tsung, Miles W. Carroll, et al. "gp100/pmel 17 Is a Murine Tumor Rejection Antigen: Induction of “Self”-reactive, Tumoricidal T Cells Using High-affinity, Altered Peptide Ligand." Journal of Experimental Medicine 188, no. 2 (July 20, 1998): 277–86. http://dx.doi.org/10.1084/jem.188.2.277.

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Many tumor-associated antigens are nonmutated, poorly immunogenic tissue differentiation antigens. Their weak immunogenicity may be due to “self”-tolerance. To induce autoreactive T cells, we studied immune responses to gp100/pmel 17, an antigen naturally expressed by both normal melanocytes and melanoma cells. Although a recombinant vaccinia virus (rVV) encoding the mouse homologue of gp100 was nonimmunogenic, immunization of normal C57BL/6 mice with the rVV encoding the human gp100 elicited a specific CD8+ T cell response. These lymphocytes were cross-reactive with mgp100 in vitro and treated established B16 melanoma upon adoptive transfer. To understand the mechanism of the greater immunogenicity of the human version of gp100, we characterized a 9-amino acid (AA) epitope, restricted by H-2Db, that was recognized by the T cells. The ability to induce specific T cells with human but not mouse gp100 resulted from differences within the major histocompatibility complex (MHC) class I–restricted epitope and not from differences elsewhere in the molecule, as was evidenced by experiments in which mice were immunized with rVV containing minigenes encoding these epitopes. Although the human (hgp10025–33) and mouse (mgp10025–33) epitopes were homologous, differences in the three NH2-terminal AAs resulted in a 2-log increase in the ability of the human peptide to stabilize “empty” Db on RMA-S cells and a 3-log increase in its ability to trigger interferon γ release by T cells. Thus, the fortuitous existence of a peptide homologue with significantly greater avidity for MHC class I resulted in the generation of self-reactive T cells. High-affinity, altered peptide ligands might be useful in the rational design of recombinant and synthetic vaccines that target tissue differentiation antigens expressed by tumors.
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Kaufman, Howard, Jose Lutzky, Joseph Clark, Kim Allyson Margolin, David H. Lawson, Asim Amin, Frances A. Collichio, et al. "Safety and efficacy of ipilimumab in melanoma patients who received prior immunotherapy on phase III study MDX010-020." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 9050. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9050.

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9050 Background: MDX010-020 was a phase III comparison of ipilimumab (Ipi), gp100 vaccine or the combination for advanced melanoma. A subset of patients (pts) received other immunotherapy (IM) for advanced disease prior to receiving Ipi, providing the opportunity to evaluate safety and efficacy of Ipi following IM. A prior analysis has shown that pts receiving prior IL-2 had a similar overall survival (OS) to pts who had not received prior IL-2 [Hodi et al NEJM2010]; we now report expanded results for pts receiving any prior IM (interferons and/or interleukin). Methods: Eligible pts (n=676) had unresectable stage III/IV melanoma and were randomized 3:1:1 to q3 wks x 4 doses of Ipi + gp100 or Ipi + placebo or gp100 + placebo. All Ipi doses were 3 mg/kg i.v. OS was retrospectively analyzed for pts receiving any prior IM; immune-related adverse events (irAEs) during induction were evaluated for pts who received any prior IM (322 pts, 48%) and for pts who received prior IL-2 (154 pts, 23%). Results: Demography and OS are summarized below. irAEs of any grade were reported for 60% (Ipi) and 54% (Ipi + gp100) of pts receiving any prior IM. Those receiving prior IL-2 specifically had 73% (Ipi) and 58% (Ipi + gp100) incidence of any grade irAEs. Incidence was similar for those not receiving prior IM or prior IL-2. Diarrhea, rash, and pruritus were the most common events in all groups. Conclusions: Results for OS in this subgroup analysis were similar for both those receiving any prior IM and those who did not receive prior IM and to the overall 020 population. In addition, safety profiles were similar irrespective of prior immunotherapy. Clinical trial information: NCT00094653. [Table: see text]
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Dissertations / Theses on the topic "Gp100"

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Johnson, Kenneth. "The Role of Gilt in the Cross Presentation of the Melanoma Antigen gp100." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/623465.

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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.
In this study we examine the utility of using CD8+ T cell hybridomas to measure the ability of bone marrow dendritic cells (BMDCs) to internalize cancer proteins and display them to cytotoxic T cells, a process termed cross‐presentation. We test the ability of a newly generated T cell hybridoma called BUSA14 to detect cross‐presentation of the melanoma antigen gp100. BUSA14 produces a dose‐dependent response to human and mouse gp100 peptides. However, cross‐presentation of gp100 by BMDCs using SK‐MEL‐28 human melanoma cell lysates or direct MHC class I‐restricted presentation by B16 murine melanoma cells was not detected. Both SKMEL‐28 and B16 cells express gp100 protein by immunoblot, and gp100 as a membrane bound protein may be concentrated by cell fractionation techniques. We validated our crosspresentation assay with another T cell hybridoma B3Z to detect cross‐presentation of the model antigen ovalbumin. Lastly, we determined that although BUSA14 expresses the coreceptor CD8, BUSA14 lacks CD3 expression, which likely impairs the ability of this hybridoma to respond to engagement of the T cell receptor and contributes to the inability to detect presentation of native gp100 protein. To resolve these issues, we plan to use primary gp100‐specific T cells from pmel mice expressing the same T cell receptor as the BUSA14 hybridoma to detect presentation of gp100 protein. Ultimately, we plan to evaluate the requirements for cross‐presentation of gp100, including a role for gamma‐interferon‐inducible lysosomal thiol reductase (GILT), a disulfide bond reducing enzyme.
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Grimaud, Eva. "Implications des systèmes LIF/gp130/gp190 et OPG/RANK/RANK-L dans la physiologie ostéoarticulaire." Nantes, 2002. http://www.theses.fr/2002NANT24VS.

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La physiopathologie ostéoarticulaire est un vaste domaine dans lequel interviennent de nombreux facteurs et molécules dont la nature et les rôles ne sont pas encore entièrement élucidés. Ce travail présente l'implication de deux systèmes moléculaires, LIF (Leukemia inhibitory factor)/gp130/gp190 et OPG (ostéoprotégérine)/RANK (receptor activator of nuclear factor kappa b)/RANK-L (RANK-ligand) dans le cartilage en développement et dans des pathologies ostéoarticulaires. La première partie de cette étude a mis en évidence la présence du LIF par immunohistochimie dans les chondrocytes hypertrophiques et les bourgeons conjonctivo-vasculaires sur des coupes de fémurs de rat lors de l'ossification endochondrale. Ces résultats ont également été confirmés chez l'homme. La présence du LIF et son expression ont aussi été mises en évidence par la même technique, ainsi que par RT-PCR, dans une tumeur cartilagineuse de rat, le chondrosarcome de Swarm. Ces résultats suggèrent que la cytokine LIF pourrait être impliquée dans la différenciation des cellules cartilagineuses. .
Many factors and molecules whose nature and roles are not yet entirely elucidated intervene in osteoarticular physiopathology. This work presents the implication of two molecular systems, LIF (Leukemia inhibitory factor)/gp130/gp190 and OPG (osteoprotegerin)/RANK(receptor activator of nuclear Factor kappa b)/RANK-L (RANK-ligand) in developmental cartilage and ostearticular pathologies. The first part of this study highlighted the presence of LIF by immunohistochemistry in the hypertrophic chondrocytes and the conjonctivo-vascular buds on sections of rat femur during endochondral ossification. These results were also confirmed at human. The presence of LIF and its expression were also highlighted by the same technique, like RT-PCR, in a cartilaginous tumour of rat, the Swarm rat chondrosarcoma. These results suggest that LIF could be implied in the differentiation of the cartilaginous cells. In a second part, the expression of LIF and its receiving chains gp130 and gp190 was studied during various stages of endochondral ossification in vitro with cellular cell line ATDC5. . .
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DUPLOMB, LAURENCE. "Contribution a l'etude des recepteurs de la cytokine lif : complexe gp130/gp190 et man 6-p/igfii-r." Paris 7, 2001. http://www.theses.fr/2001PA077078.

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Le leukemia inhibitory factor (lif), cytokine de la famille de l'interleukine-6, est une proteine dotee de nombreuses activites biologiques, agissant sur des types cellulaires varies, sains ou tumoraux. Le lif se fixe avec une basse affinite sur la chaine glycoproteique gp190, dont l'heterodimerisation avec la gp130, chaine commune des recepteurs de la famille de l'il-6, forme un recepteur de haute affinite capable de transduire un signal. Dans un premier temps, notre travail decrit la fixation du lif sur un nouveau recepteur membranaire que nous avons identifie et caracterise comme etant le recepteur au mannose 6-phosphate et a l'insulin-like growth factor ii (man 6-p/igfii-r). Nous avons montre que ce recepteur internalise et degrade le lif, mais est incapable de transduire un signal apres fixation de cette cytokine. La seconde partie du travail met en evidence une interaction, via des residus man 6-p, entre la gp130 et le man 6-p/igfii-r, interaction qui peut entrainer une inhibition des effets biologiques des cytokines de la famille il-6. Cette inhibition ne se faisant ni par modulation des taux membranaires de gp130, ni par induction de proteines regulant de facon negative le signal engendre par la cytokine, nous suggerons qu'il s'agisse d'un encombrement sterique aboutissant a un recepteur non fonctionnel : les sites d'interaction entre la cytokine et son recepteur etant masques par le man 6-p/igfii-r soluble, ou le recrutement de la gp130, par la chaine receptrice specifique de la cytokine, impossible. Cette modulation des effets biologiques du lif par le man 6-p/igfii-r nous a permis de reconsiderer l'action de cette cytokine dans le processus cancereux, au cours duquel on peut observer une perte d'expression membranaire ou une secretion de ce recepteur.
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Spiro, Simon George. "The mechanism of action of iminosugars as antiretrovirals." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:7fc4ae01-bdec-49d0-afec-e0f3e9e8f41d.

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Kong, Leopold. "HIV-1 gp120 : flexibility and glycosylation." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.533859.

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Bodemer, Lucia. "Reinigung des nierenspezifischen Glykoproteins gp400 mittels Immunaffinitätschromatographie." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=960425152.

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Chen, Yuxin. "Characterization of Envelope-Specific Antibody Response Elicited by HIV-1 Vaccines: A Dissertation." eScholarship@UMMS, 2001. http://escholarship.umassmed.edu/gsbs_diss/760.

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Despite 30 years of intensive research，an effective human immunodeficiency virus (HIV) vaccine still remains elusive. The desirable immune response capable of providing protection against HIV acquisition is still not clear. The accumulating evidence learned from a recent vaccine efficacy correlate study not only confirmed the importance of antibody responses, but also highlighted potential protective functions of antibodies with a broad repertoire of HIV-1 epitope specificities and a wide range of different antiviral mechanisms. This necessitates a deep understanding of the complexity and diversity of antibody responses elicited by HIV-1 vaccines. My dissertation characterizes antibody response profiles of HIV-1 Env antibodies elicited by several novel immunogens or different immunization regimens, in terms of magnitude, persistence, epitope specificity, binding affinity, and biological function. First, to overcome the challenge of studying polyclonal sera without established assays, we expanded a novel platform to isolate Env-specific Rabbit mAbs (RmAb) elicited by DNA prime-protein boost immunization. These RmAbs revealed diverse epitope specificity and cross-reactivity against multiple gp120 antigens from more than one subtype, and several had potent and broad neutralizing activities against sensitive Tier 1 viruses. Further, structural analysis of two V3 mAbs demonstrated that a slight shift of the V3 epitope might have a dramatic impact on their neutralization activity. All of these observations provide a useful tool to study the induction of a desired type of antibody by different immunogens or different immunization regimens. Since heavily glycosylated HIV Env protein is a critical component of an HIV vaccine, we wanted to determine the impact of the HIV Env-associated glycan shield on antibody responses. We were able to produce Env proteins with a selective and homogeneous pattern of N-glycosylation using a glycoengineered yeast cell line. Antigenicity of these novel Env proteins was examined by well-characterized human mAbs. Immunogenicity studies showed that they were immunogenic and elicited gp120- specific antibody responses. More significantly, sera elicited by glycan-modified gp120 protein immunogens revealed better neutralizing activities and increased diversity of epitopes compared to sera elicited by traditional gp120 produced in Chinese Hamster Ovary (CHO) cells. Further, we examined the impact of the delivery order of DNA and protein immunization on antibody responses. We found that DNA prime-protein boost induced a comparable level of Env-specific binding Abs at the peak immunogenicity point to codelivery of DNA. However, antibody responses from DNA prime-protein boost had high avidity and diverse specificities, which improved potency and breadth of neutralizing Abs against Tier 1 viruses. Our data indicate that DNA vaccine priming of the immune system is essential for generation of high-quality antibodies. Additionally, we determined the relative immunogenicity of gp120 and gp160 Env in the context of DNA prime-protein boost vaccination to induce high-quality antibody responses. Immunized sera from gp120 DNA primed animals, but not those primed with gp160 DNA, presented with distinct antibody repertoire specificities, a high magnitude of CD4 binding site-directed binding capabilities as well as neutralizing activities. We confirmed the importance of using the gp120 Env form at the DNA priming phase, which directly determined the quality of antibody response.
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Chen, Yuxin. "Characterization of Envelope-Specific Antibody Response Elicited by HIV-1 Vaccines: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/760.

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Despite 30 years of intensive research，an effective human immunodeficiency virus (HIV) vaccine still remains elusive. The desirable immune response capable of providing protection against HIV acquisition is still not clear. The accumulating evidence learned from a recent vaccine efficacy correlate study not only confirmed the importance of antibody responses, but also highlighted potential protective functions of antibodies with a broad repertoire of HIV-1 epitope specificities and a wide range of different antiviral mechanisms. This necessitates a deep understanding of the complexity and diversity of antibody responses elicited by HIV-1 vaccines. My dissertation characterizes antibody response profiles of HIV-1 Env antibodies elicited by several novel immunogens or different immunization regimens, in terms of magnitude, persistence, epitope specificity, binding affinity, and biological function. First, to overcome the challenge of studying polyclonal sera without established assays, we expanded a novel platform to isolate Env-specific Rabbit mAbs (RmAb) elicited by DNA prime-protein boost immunization. These RmAbs revealed diverse epitope specificity and cross-reactivity against multiple gp120 antigens from more than one subtype, and several had potent and broad neutralizing activities against sensitive Tier 1 viruses. Further, structural analysis of two V3 mAbs demonstrated that a slight shift of the V3 epitope might have a dramatic impact on their neutralization activity. All of these observations provide a useful tool to study the induction of a desired type of antibody by different immunogens or different immunization regimens. Since heavily glycosylated HIV Env protein is a critical component of an HIV vaccine, we wanted to determine the impact of the HIV Env-associated glycan shield on antibody responses. We were able to produce Env proteins with a selective and homogeneous pattern of N-glycosylation using a glycoengineered yeast cell line. Antigenicity of these novel Env proteins was examined by well-characterized human mAbs. Immunogenicity studies showed that they were immunogenic and elicited gp120- specific antibody responses. More significantly, sera elicited by glycan-modified gp120 protein immunogens revealed better neutralizing activities and increased diversity of epitopes compared to sera elicited by traditional gp120 produced in Chinese Hamster Ovary (CHO) cells. Further, we examined the impact of the delivery order of DNA and protein immunization on antibody responses. We found that DNA prime-protein boost induced a comparable level of Env-specific binding Abs at the peak immunogenicity point to codelivery of DNA. However, antibody responses from DNA prime-protein boost had high avidity and diverse specificities, which improved potency and breadth of neutralizing Abs against Tier 1 viruses. Our data indicate that DNA vaccine priming of the immune system is essential for generation of high-quality antibodies. Additionally, we determined the relative immunogenicity of gp120 and gp160 Env in the context of DNA prime-protein boost vaccination to induce high-quality antibody responses. Immunized sera from gp120 DNA primed animals, but not those primed with gp160 DNA, presented with distinct antibody repertoire specificities, a high magnitude of CD4 binding site-directed binding capabilities as well as neutralizing activities. We confirmed the importance of using the gp120 Env form at the DNA priming phase, which directly determined the quality of antibody response.
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9

Farfan, Arribas Diego Jose. "DNA Vaccines Against HIV-1: Augmenting Immunogenicity of gp120." Link to electronic thesis, 2002. http://www.wpi.edu/Pubs/ETD/Available/etd-0107102-160706/.

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Li, Yan. "Processing and secretion of human immunodeficiency virus glycoprotein,gp120." Thesis, University of Ottawa (Canada), 1992. http://hdl.handle.net/10393/10962.

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The natural signal sequence of HIV-1 gp120 contains an unusually long hydrophobic domain and five positively charged amino acids. When the gp120 gene was cloned into a baculovirus expression vector under the control of the baculovirus polyhedrin gene promoter, it exhibited an extremely low level of secretion. However, deletion of the signal sequence resulted in the production of large quantities of a nonglycosylated form of gp120 and fusion of honeybee melittin or murine interleukin 3 signal sequences, which contain only one or no positively charged residues, respectively, resulted in a high level of expression as well as glycosylation and secretion. Four charge-altered signal mutants were generated by oligonucleotide-directed mutagenesis. Positively charged amino acids in the natural signal sequence were substituted with neutral amino acids. The results of these experiments showed that the expression and secretion of gp120 was progressively increased by decreasing the positive charge in a stepwise fashion from + 5 to + 3, + 2, and + 1. However, elimination of all five positive charges (leaving a net negative charge of -1 at the NH 2 terminus) caused accumulation of large amounts of a nonglycosylated form of gp120 but decreased the amounts of glycosylated forms of gp120. These signal peptide mutants clearly demonstrate that the positively charged amino acids in the natural signal sequence of HIV-1 gp120 are key factors determining its poor expression and secretion in insect cells. Analysis of intracellular transport and folding of gp120 further indicates that the highly charged uncleaved signal peptide rather than disulfide bond formation is an important factor limiting transport of gp120 from the rough endoplasmic reticulum (RER) to the Golgi apparatus; its presence affects gp120 folding and slows its rate of transport to the cell surface. The requirement for carbohydrate on HIV gp120 in CD4 binding has been the subject of much debate. There have been conflicting reports regarding the role of gp120 glycans in binding to CD4. An important question is whether the carbohydrate itself plays an important role in this interaction. Nonglycosylated and glycosylated forms of gp120 from HIV-1 and HIV-2 were produced using the baculovirus expression system and their CD4 binding properties were determined. The nonglycosylated forms of gp120 generated by either deletion of the signal sequence or synthesized in the presence of tunicamycin failed to bind to CD4. In contrast, highly mannosylated recombinant gp120 bound well to soluble CD4. Enzymatic removal of carbohydrate chains from glycosylated gp120 by endoglycosidase H (endo H) or by a mixture of endoglycosidase F and N-glycanase (endo FNG) in the presence or absence of SDS had little or no effect on the ability of gp120 to bind CD4. The data indicate that carbohydrate chains per se do not play a significant role in interaction between gp120 and CD4 molecules but that N-linked glycosylation is required for correct protein folding that provides the proper conformation for CD4 binding. Analysis of intracellular folding of gp120, using its ability to bind CD4 as a functional assay for overall conformation, further supports the hypothesis that N-linked glycosylation of HIV gp120 plays an essential role in promoting either the correct folding of the protein or in its stabilization.
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Books on the topic "Gp100"

1

Rogers, Chris. Suzuki GP100 & 125 owners workshop manual. Sparkford: Haynes, 1992.

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1952-, Shoemark Pete, ed. Suzuki GP100 & 125 owners workshop manual. Sparkford: Haynes, 1988.

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Rogers, Chris. Suzuki GP100 & 125 owners workshop manual. Sparkford: Haynes, 1986.

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Rogers, Chris. Suzuki GP100 and 125 owner's workshop manual: [978 to 1993 - 98cc, 123cc]. Yeovil: Haynes, 1993.

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Papworth, Monika Anna. Expression and analysis of the Epstein-Barr virus glycoprotein gp110. Manchester: University of Manchester, 1995.

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Sjolander, Sigrid. Studies on immune responses to the HIV envelope glycoprotein gp120. Uppsala: Sveriges Lantbruksuniversitet, 1995.

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See, Hilario. Purification of the major stilbene disulfonate- and concanavalin A-binding protein (GP130) of the porcine renal brush border membrane and its identification as aminopeptidase N. Ottawa: National Library of Canada, 1990.

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Rogers, Chris. Suzuki GP100 & 125 Singles (Motorcycle Manuals). Haynes Publishing, 1988.

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Rogers, Chris. Suzuki GP100 & 125 owners workshop manual. Haynes, 1991.

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King James Version Gp101 Black Index Leather. Nelson Bibles, 1987.

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Book chapters on the topic "Gp100"

1

Schwartzentruber, Doug. "gp100." In Cancer Therapeutic Targets, 261–66. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_26.

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Schwartzentruber, Doug. "gp100." In Cancer Therapeutic Targets, 1–7. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6613-0_26-3.

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Kangueane, Pandjassarame. "HIV-1 GP160 (GP120/GP40) Trimer ENV Spike Protein." In Bioinformation Discovery, 173–81. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95327-4_9.

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Meigs, Thomas E., Alex Lyakhovich, Hoon Shim, Ching-Kang Chen, Denis J. Dupré, Terence E. Hébert, Joe B. Blumer, et al. "GPR100." In Encyclopedia of Signaling Molecules, 806. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100563.

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Auernhammer, Christoph J., and Shlomo Melmed. "gp130-Related Cytokines." In Principles of Molecular Regulation, 115–32. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-032-2_7.

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Tani, Y., N. Nishimoto, A. Ogata, Y. Shima, K. Yoshizaki, and T. Kishimoto. "GP130 in Human Myeloma/Plasmacytoma." In Current Topics in Microbiology and Immunology, 229–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79275-5_27.

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Cicala, Claudia, and James Arthos. "Virion Attachment and Entry: HIV gp120 Env Biotinylation, gp120 Env, or Integrin Ligand-Binding Assay." In Methods in Molecular Biology, 3–12. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-670-2_1.

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Kishimoto, Tadamitsu, and Tetsuya Taga. "gp130, common signal transducer for cytokines including IL-6." In Progress in Immunology Vol. VIII, 887–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-51479-1_113.

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Xie, Zhuojun, Song He, and Hongmin Ao. "Development and Application of GP500+ Energy Saving Aluminum Reduction Cell." In Light Metals 2020, 827–34. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36408-3_110.

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Gregory, Timothy, James Hoxie, Colin Watanabe, and Michael Spellman. "Structure and Function in Recombinant HIV-1 gp120 and Speculation about the Disulfide Bonding in the gp120 Homologs of HIV-2 and SIV." In Advances in Experimental Medicine and Biology, 1–14. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-6000-1_1.

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Conference papers on the topic "Gp100"

1

Mullaly, Rachel, Elena Nechita, Mags Clancy, and Dara Gallagher. "GP100 Toddlers, teens and everything in between. should all children be admitted to the same ward?" In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.165.

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Cole, David, Ross Robinson, Velupillai Srikannathasan, Vijay Karuppiah, Stephen Harper, Charlotte Coles, Viren Patel, et al. "Abstract 2271: Tebentafusp recognition of melanoma cells is restricted by HLA-A0201 presentation of a gp100 peptide." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2271.

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Aris, Mariana, Mariana Rodriguez Zubieta, Marina Colombo, Juan Martín Arriaga, Michele Bianchini, Myriam Alperovich, Alicia Inés Bravo, Maria Marcela Barrio, and José Mordoh. "Abstract B43: MART-1 and gp100 expressing and nonexpressing melanoma cells are equally proliferative in tumors and clonogenic in vitro." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-b43.

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Palermo, Belinda, Cosmo Di Donna, Ornella Franzese, Duilia Del Bello, Novella Gualtieri, Luisa Imberti, Carmen Nuzzo, et al. "Abstract 4406: Clinical efficacious combined chemo/immunotherapy differently activates AKT pathway and functionality of gp100 and Melan-A specific T cell clones." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4406.

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Gordy, James, and Richard B. Markham. "Abstract 2511: Therapeutic dendritic cell targeting MIP3α-gp100 DNA vaccination with immunomodulatory αIL-10 and αPD-1 antibodies significantly enhances survival in a mouse melanoma model system." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2511.

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Palermo, Belinda, Ornella Franzese, Cosmo Di Donna, Mariangela Panetta, Isabella Sperduti, Antonella Soriani, Maria Laura Foddai, Angela Santoni, and Paola Nisticò. "Abstract A040: The low antitumor functionality of PD1-positive gp100-specific CD8+ T cell clones isolated from melanoma patients correlates with the presence of CD28 co-stimulatory molecule." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a040.

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Gordy, James, Kun Luo, and Richard Markham. "Abstract 1593: Neutralization of IL-10 enhances antitumor efficacy of dendritic cell-targeting MIP-3α-gp100 vaccine by way of type-I interferons in B16F10 mouse melanoma model." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1593.

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Carreno, Beatriz M., Michelle Becker-Hapak, Megan Chan, Wen-Rong Lie, and Gerald P. Linette. "Abstract 5519: Vaccination of melanoma patients with CD40L/IFN-γ activated dendritic cells reveals a correlation between IL-12p70 production and CD8+ T cell priming to the melanoma differentiation antigen gp100." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5519.

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Gordy, James T., Avinaash K. Sandhu, Samuel K. Ayeh, Aakanksha Kapoor, Emily Kim, Petros C. Karakousis, and Richard B. Markham. "Abstract 2198: The anti-tumor enhancement of a dendritic-cell targeting MIP3α-Gp100-Trp2 DNA vaccine by IFNα and 5-Aza-2'-deoxycytidine treatments correlates with intratumoral CCL19 but not CCL21 expression." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2198.

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Santos, Matheus Filipe, Guilherme Augusto Roza, and Wendell Sérgio Ferreira Meira. "INVESTIGAÇÃO DA EXPRESSÃO DO GENE CODIFICADOR DA GP160 EM CEPA de Trypanosoma cruzi-like." In I Congresso Brasileiro de Parasitologia Humana On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/743.

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Introdução: Os tripanosomatídeos possuem grande importância para a saúde do ser humano, dentre estes destaca-se o Trypanosoma cruzi (T. cruzi), causador da Doença de Chagas. O Trypanosoma cruzi-like (T. cruzi-like) é considerado uma subespécie do T. cruzi e, este parasito está relacionado aos morcegos. Apesar do T. cruzi-like e do T. cruzi serem espécies distintas quanto algumas caraterísticas biológicas, genéticas e moleculares, uma análise do genoma mostra uma alta similaridade entre eles, o que corrobora para esta proximidade entre as espécies. O T. cruzi expressa uma glicoproteína essencial para conseguir realizar a infecção no ser humano, a gp160, que tem como função inibir a ação do sistema complemento, desta forma favorencendo a evasão do parasito frente a resposta imunológica do hospedeiro. Objetivo: avaliar a presença do gene que codifica a expressão da gp160 em cepas de T. cruzi-like. Material e métodos: Foram utilizadas duas cepas de T. cruzi-like, EM425 e EM242. Ambas as cepas foram cultivadas em meio LIT (Liver InfusionTryptose) para obter a massa parasitária de formas epimastigotas. Para obter as formas tripomastigotas de ambas as cepas, foram infectadas células epiteliais de rim de macaco Rhesus (MK2). As tripomastigotas foram recuperadas no sobrenadante das culturas após 10 dias da infecção. Após a obtenção das massas parasitárias das formas epimastigotas e tripomastigotas, foi realizado a extração de DNA genômico e, realizado reação em cadeia da polimerase (PCR) utilizando os iniciadores CRP-2F e CRP-2R, que detectam o gene codificador da gp160. Resultados: com este estudo foi possível demonstrar que as formas tripomastigotas de ambas as cepas avaliadas expressaram o gene codificador da proteína gp160. Conclusão: Conclui-se que as cepas EM425 e EM242 de T. cruzilike possuem o gene codificador da gp160 em suas tripomastigotas e, que assim como o T. cruzi, este parasito pode evadir da resposta imune do hospedeiro. Além disso, podese sugerir que esta proteína venha a ser expressa e ser alguns dos antígenos que estes dois protozoários, T. cruzi e T. cruzi-like podem estar compartilhando e, que estudos devem ser feitos para avaliar essa expressão da proteína e sua função de inibir o sistema complemento.
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Reports on the topic "Gp100"

1

Knudsen, Beatrice. Gp140/CDCPI in the Development pf Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada569430.

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Knudsen, Beatrice. GP140/CDCPI in the Development of Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada594061.

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Carter, William G. GP140/CDCPI in the Development of Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada562491.

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Li, Chenglong, James Fuchs, and Jiayuh Lin. Novel Small Molecules Disabling the IL-6/IL-6R/GP130 Heterohexamer Complex. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada606135.

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Li, Chenglong, James Fuchs, and Jiayuh Lin. Novel Small Molecules Disabling the IL-6/IL-6R/GP130 Heterohexamer Complex. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada584824.

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Redvers, Richard P. The Role of Interleukin-6/GP130 Signaling in Prostate Cancer Progression and Its Contribution to Bone Metastasis Morbidity. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ada469521.

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