Relevant bibliographies by topics / Gene and Molecular Therapy

Academic literature on the topic 'Gene and Molecular Therapy'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Gene and Molecular Therapy"

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M. Gordon, Erlinda, Joshua R. Ravicz, Sant P. Chawla, Christopher W. Szeto, Sant P. Chawla, Michael A. Morse, Frederick L. Hall, and Erlinda M. Gordon. "CCNG1 oncogene: a novel biomarker for cancer therapy /gene therapy." Cancer Research and Cellular Therapeutics 5, no. 4 (August 30, 2021): 01–09. http://dx.doi.org/10.31579/2640-1053/090.

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Background: Metastatic cancer is associated with an invariably fatal outcome. However, DeltaRex-G, a tumor-targeted retrovector encoding a gene-edited dominant-negative CCNG1 inhibitor gene, has induced long term (>10 years) survival of patients with chemo-resistant metastatic pancreatic adenocarcinoma, malignant peripheral nerve sheath tumor, osteosarcoma, B-cell lymphoma, and breast carcinoma. Objective: To evaluate the level of CCNG1 expression in tumors as a potential biomarker for CCNG1 (Cyclin G1-blocking) inhibitor therapy. Methods: CCNG1 RNA expression levels that were previously measured as part of whole genome molecular profiling of tumors (TCGA, N=9161), adjacent “tissues” (TCGA, N=678) and GTEx normal tissues (N=7187) across 22 organ sites were analyzed. Differential expression of CCNG1 and Ki-67 in primary (N= 9161) vs metastatic (N= 393) tumors were also compared in primary (N=103) vs. metastatic (N=367) skin cancers (i.e., melanoma). Statistical Analysis: To detect systematically differential expression of CCNG1 and Ki-67 expression between populations (e.g. tumor vs. normal), unpaired Student's t-tests were performed. Results: Enhanced CCNG1 RNA and Cyclin G1 protein expression were noted in tumors compared to normal analogous counterparts, and CCNG1 expression correlated significantly with that of Ki-67. Moreover, CCNG1 expression tended to be higher than that of Ki-67 in metastatic vs primary tumors. Conclusions: Taken together with the emerging Cyclin G1 / Cdk / Myc / Mdm2 / p53 Axis governing Cancer Stem Cell Competence, this supportive data indicates: (1) CCNG1 expression is frequently enhanced in tumors when compared to their normal analogous counterparts, (2) CCNG1 and Ki-67 expressions are higher in metastatic vs primary tumors, (3) CCNG1 expression is significantly correlated with that of Ki-67, and (4) CCNG1 may actually be a stronger prognostic marker of stem cell competence, chemo-refractoriness, and EMT/metastasis than Ki-67. Phase 2 studies are planned to identify patients most likely to respond favorably to CCNG1 inhibitor therapy.
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Chung, Hesson, Ick Chan Kwon, and Seo Young Jeong. "Gene Therapy and Molecular Imaging." Journal of the Korean Medical Association 47, no. 2 (2004): 139. http://dx.doi.org/10.5124/jkma.2004.47.2.139.

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Das, Dipak K., Richard M. Engelman, Nilanjana Maulik, John A. Rousou, Joseph E. Flack, and David W. Deaton. "Molecular targets of gene therapy." Annals of Thoracic Surgery 68, no. 5 (November 1999): 1929–33. http://dx.doi.org/10.1016/s0003-4975(99)01015-2.

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Escobar Fernandez, H., A. Zhogov, E. Metzler, R. Kühn, and S. Spuler. "GENE EDITING AND MOLECULAR THERAPY." Neuromuscular Disorders 29 (October 2019): S150. http://dx.doi.org/10.1016/j.nmd.2019.06.399.

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Robbins, Jeffrey. "Gene Therapy and Molecular Toxicology." Cardiovascular Toxicology 1, no. 1 (2001): 03–06. http://dx.doi.org/10.1385/ct:1:1:03.

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Pálffy, R., R. Gardlík, J. Hodosy, M. Behuliak, P. Reško, J. Radvánský, and P. Celec. "Bacteria in gene therapy: bactofection versus alternative gene therapy." Gene Therapy 13, no. 2 (September 15, 2005): 101–5. http://dx.doi.org/10.1038/sj.gt.3302635.

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Tanaka, N., N. Matsubara, M. Ikeda, H. Takashima, T. Fujiwara, J. Shao, M. Ogawa, T. Fukazawa, and A. Hizuta. "Molecular colorectal tumorigenesis and gene therapy." Nippon Daicho Komonbyo Gakkai Zasshi 51, no. 9 (1998): 686–686. http://dx.doi.org/10.3862/jcoloproctology.51.686.

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Cehajic Kapetanovic, McClements, Martinez-Fernandez de la Camara, and MacLaren. "Molecular Strategies for RPGR Gene Therapy." Genes 10, no. 9 (September 4, 2019): 674. http://dx.doi.org/10.3390/genes10090674.

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Mutations affecting the Retinitis Pigmentosa GTPase Regulator (RPGR) gene are the commonest cause of X-linked and recessive retinitis pigmentosa (RP), accounting for 10%–20% of all cases of RP. The phenotype is one of the most severe amongst all causes of RP, characteristic for its early onset and rapid progression to blindness in young people. At present there is no cure for RPGR-related retinal disease. Recently, however, there have been important advances in RPGR research from bench to bedside that increased our understanding of RPGR function and led to the development of potential therapies, including the progress of adeno-associated viral (AAV)-mediated gene replacement therapy into clinical trials. This manuscript discusses the advances in molecular research, which have connected the RPGR protein with an important post-translational modification, known as glutamylation, that is essential for its optimal function as a key regulator of photoreceptor ciliary transport. In addition, we review key pre-clinical research that addressed challenges encountered during development of therapeutic vectors caused by high infidelity of the RPGR genomic sequence. Finally, we discuss the structure of three current phase I/II clinical trials based on three AAV vectors and RPGR sequences and link the rationale behind the use of the different vectors back to the bench research that led to their development.
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Glode, L. Michael. "The molecular bridge to gene therapy." Urology 44, no. 6 (December 1994): 81–88. http://dx.doi.org/10.1016/s0090-4295(94)80249-1.

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Orkin, Stuart H. "Molecular genetics and potential gene therapy." Clinical Immunology and Immunopathology 40, no. 1 (July 1986): 151–56. http://dx.doi.org/10.1016/0090-1229(86)90080-2.

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Dissertations / Theses on the topic "Gene and Molecular Therapy"

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Chen, Ian Ying-Li. "Molecular imaging of cardiac gene therapy /." May be available electronically:, 2008. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Lau, Cara Jean. "Gene therapy for malignant gliomas." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18478.

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Gliomas are the most common primary brain tumours found in adults. The median survival of patients diagnosed with the most malignant form, glioblastoma multiforme (GBM), is 9-12 months and has changed little over the years despite advances in medical technology. Gene therapy may offer new solutions to treat this resistant disease. Hence, we tested three different gene therapy strategies. In our first study, we tested the efficacy of targeted therapy to correct common aberrations found in gliomas including amplification/mutation of receptor tyrosine kinases (RTK) and loss of PTEN, which result in an overactive PI3K/Akt pathway. Without PTEN, FOXO transcription factors are inactivated, and the cell becomes resistant to apoptosis and cell cycle arrest. By using an adenoviral vector (AdV) expressing an activated FOXO1 mutant (AdFOXO1;AAA), we restored apoptosis and cell cycle arrest, reduced tumour volume and prolonged survival in an intracerebral xenograft model. Secondly, we examined the therapeutic capacity of a novel replicating/non-disseminating AdV expressing the fusion protein of cytosine deaminase and uracil phosphoribosyltransferase (CU). CU can convert the non-toxic pro-drug, 5-fluorocytosine (5-FC) to the tissue diffusible chemotherapeutic drug, 5-fluorouracil (5-FU) to target dividing cells. In vitro, the replicating vectors were superior to the non-replicating vectors, but the fully replicating/disseminating vector did not perform considerably better than the replicating/non-disseminating vector suggesting that dissemination may not be advantageous. In vivo, the replicating/non-disseminating vector administered in conjunction with 5-FC prolonged survival in both an athymic and an immunocompetent mouse model. Moreover, an immune bystander effect in vivo was mediated by macrophages and T cells. Lastly, we investigated a method to harness a tool of the immune system, IFN-ß; this cytokine is known to have anti-angiogenic, anti-proliferative, and immunomo
Les gliomes sont des tumeurs primaires de cerveau les plus communes retrouvées dans les adultes. La survie médiane des patients diagnostiqués avec la forme la plus maligne, le glioblastome multiforme (GBM), est de 9 à 12 mois et a peu changé au cours des années en dépit des avances en technologie médicale. La thérapie génique peut offrir de nouvelles solutions pour traiter cette maladie résistante. Durant nos travaux, nous avons examiné trois stratégies différentes de thérapie génique Dans notre première étude, nous avons examiné l'efficacité de la thérapie visée à corriger des anomalies communes retrouvées dans les gliomes, comprenant l'amplification/mutation de récepteurs de type tyrosine kinase (RTK) et la perte de PTEN, qui mènent en conséquence à une voie activée de PI3K/Akt. Sans PTEN, les facteurs de transcription FOXO sont inactivés, et la cellule devient résistante à l'arrêt du cycle cellulaire et à l'apoptose. En utilisant un vecteur adénoviral (AdV) exprimant une protéine activée du mutant FOXO1 (AdFOXO1;AAA.), nous avons reconstitué les signaux pour l'arrêt du cycle cellulaire et l'apoptose in vitro ainsi que in vivo. Deuxièmement, nous avons examiné la capacité thérapeutique d'un nouveau vecteur adénovirale qui a la capacité de se répliquer sans provoquer de lyse cellulaire et qui exprime en plus la protéine de fusion uracile phosphoribosyltransférase/cytosine déaminase (CU). La protéine CU peut convertir le promédicament non-toxique, le 5-fluorocytosine (5-FC) à la drogue chimiothérapeutique diffusible, le 5-fluorouracile (5-FU) qui a comme cible des cellules en division cellulaire. In vitro, les vecteurs à capacité de répliquation étaient meilleurs que ceux qui ne pouvaient pas se répliquer. In vivo, le vecteur en présence du 5-FC a prolongé la survie de deux modès animaux (avec et sans sytèmes immunitaires). Dans un dernier temps, nous avons étudié une méthode pour exprimer l'IF
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Katabi, Maha M. "Transcriptional targeting of suicide genes in cancer gene therapy." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0021/NQ55345.pdf.

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Wallace, Lindsay M. "Gene Therapy for Facioscapulohumeral Muscular Dystrophy." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1338315498.

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Rohatgi, Priyanka. "Engineering Protein Molecular Switches To Regulate Gene Expression with Small Molecules." Diss., Georgia Institute of Technology, 2006. http://hdl.handle.net/1853/19852.

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Small molecule dependent molecular switches that control gene expression are important tool in understanding biological cellular processes and for regulating gene therapy. Nuclear receptors are ligand activated transcription factors that have been engineered to selectively respond to synthetic ligands and used as regulators of gene expression. In this work the retinoid X receptor (RXR), has been used to develop an inducible molecular switch with a near drug like compound LG335. Three RXR variants (Q275C; I310M; F313I), (I268A; I310A; F313A; L436F), (I268V; A272V; I310M; F313S; L436M) were created via site-directed mutagenesis and a structure based approach, such that they preferentially bind to the synthetic ligand LG335 and not its natural ligand, 9-cis retinoic acid. These variants show reverse ligand specificity as designed and have an EC50 for LG335 of 80 nM, 30 nM, 180 nM, respectively. The ligand binding domains of the RXR variants were fused to a yeast transcription factor Gal4 DNA binding domain. This modified chimeric fusion protein showed reverse response element specificity as designed and recognized the Gal4 response element instead of the RXR response element. The modified RXR protein did not heterodimerize with wild type RXR or with other nuclear receptor such as retinoic acid receptor. These RXR-based molecular switches were tested in retroviral vectors using firefly luciferase and green fluorescence protein and they maintain their inducible behavior with LG335. These experiments demonstrate the orthogonality of RXR variants and their possible use in regulating gene therapy.
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Yoshida, Jun. "Molecular Neurosurgery Using Gene Therapy to Treat Malignant Glinoma." 名古屋大学医学部, 1996. http://hdl.handle.net/2237/6179.

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Thraser, Adrian James. "Molecular studies towards gene therapy for chronic granulomatous disease." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307515.

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Tiwari, Swati. "Gene Therapy Approaches for Hemophagocytic Lymphohistiocytosis." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1447690858.

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Mckiver, Bryan D. "SND1-Targeted Gene Therapy for Hepatocellular Carcinoma." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5676.

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Staphylococcal nuclease and tudor-domain containing 1 (SND1) is an oncogene for a wide variety of cancers, including hepatocellular carcinoma (HCC). SND1 is a multifunctional protein regulating gene expression of proto-oncogenes and tumor suppressor genes, making SND1 a prime target for developing cancer therapeutics. This notion is especially attributed to HCC as most patients are diagnosed in advanced stages and the therapeutic options available for these patients are severely limited. In this study, we evaluated the therapeutic potential of a replication-defective adenovirus vector delivering SND1 shRNA (Ad.SND1sh) to human HCC cell lines, HepG3, HuH-7, and Hep3B. Adenovirus infection in HCC cells was confirmed by Western blotting and immunofluorescence. The efficacy of Ad.SND1sh to knockdown SND1 expression was confirmed via Western blot, qRT-PCR, and immunofluorescence. Ad.SND1sh did not significantly affect proliferation of the three human HCC cells but significantly inhibited their invasive and migratory capacities, as determined by wound healing and Matrigel invasion assays, respectively. As a corollary, Ad.SND1sh treatment resulted in a decrease in mesenchymal markers, such as N-cadherin, Twist, Snail, and Slug, without affecting levels of epithelial marker E-Cadherin, indicating that SND1 knockdown induces mesenchymal conversion in HCC cells. Additionally, reductions in liver cancer stem cell marker CD133 and HCC marker α-fetoprotein (AFP) were observed with SND1 knockdown. HCC cells with aberrant expression of these markers are associated with tumor initiation, recurrence, and multi-drug resistance. Our findings indicate that Ad.SND1sh may potentially be an effective therapy for advanced HCC and needs to be studied further for its clinical application.
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Perri, Sabrina R. "Exploiting the use of plasminogen kringle domains for cancer gene therapy." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103176.

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Angiostatin is one of the most widely studied inhibitors of angiogenesis and encompasses the first 3 or 4 kringle domains of human plasminogen (Plg). Of particular interest, is the fifth kringle of human Plg (KS), which displays higher anti-angiogenic potency than angiostatin. In fact, kringles 1 to 5 exhibit greater inhibitory activity against endothelial cells than angiostatin, and this finding suggests that K5 domain acts synergistically to enhance the anti-angiogenic effect of angiostatin. Therefore, we proposed that the K5 domain---on its own---could act as a potent anti-angiogenic and anti-tumor protein within the context of a cancer gene therapy strategy.
In our first study, we assessed the angiostatic properties of the K5 peptide domain in an orthotopic brain cancer model. We demonstrated that the disulfide bridging conformation of K5, necessary to maintain its functionality, is conserved upon secretion by gene-modified mammalian cells. Kringle 5 retrovirally gene-engineered human U87 glioma cells produced functional soluble K5 protein capable of suppressing growth factor-induced endothelial cell migration in vitro and inhibiting glioma-induced angiogenesis in vivo. Interestingly, secreted K5 protein blocked the recruitment of tumor-associated CD45+Mac3 +Grl- macrophages in vivo and inhibited the migration of CD206+ human monocyte-derived macrophages in vitro. Moreover, in a clinically relevant orthotopic glioma model, soluble K5 induced long-term survival in a majority of test animals. Thus, these findings validate the use of a gene therapy approach to deliver Plg K5 protein and suggest that K5 acts as a novel 2-pronged anti-tumor agent, mediating its inhibitory effect via its action on host-derived endothelial cells and tumor-associated macrophages.
To determine if K5 mediated its anti-tumor effect by modulating other immune effector cells, we tested the use of soluble K5 in a murine DA/3 mammary adenocarcinoma model. Soluble K5 produced by retrovirally gene-modified DA/3 cells led to long-term survival (over 1 year) of immunocompetent BALB/c mice however, we failed to observe tumor rejection in immunodeficient NOD-SCID and BALB/c nude mice. Further analysis revealed that K5 enhances the recruitment of tumor-infiltrating CD3+ lymphoid cells, in particular the natural killer T (NKT)-lymphocyte phenotype. Consistent with our previous findings, we demonstrated that K5 led to a significant decrease in tumor-associated microvessel length and density. Interestingly, K5 tumors were characterized by a robust neutrophilic infiltrate. This may be explained by the ability of K5 to act as a strong chemotactic agent for human neutrophils in vitro as well as its ability to promote CD64+ activation within the CD11b+ neutrophil phenotype. These findings confirm that K5 acts as a potent angiostatic agent and possesses a novel pro-inflammatory role via its ability to recruit tumor-associated neutrophils and NKT-lymphocytes, leading to a strong anti-tumor response.
Tumor-associated macrophages (TAM) are key immune effector cells implicated in promoting tumor progression and metastasis. It would thus be desirable to explore strategies to reduce TAM infiltration within the tumor microenvironment. In our first study, we demonstrated that soluble K5 protein blocks macrophage recruitment. In addition, the recent observation that angiostatin reduces macrophage infiltration in an atherosclerosis model prompted our laboratory to further explore the use of angiostatin as an anti-macrophage agent. We demonstrated that angiostatin suppresses the in vitro migration of both murine peritoneal macrophages and human monocyte-derived CD206 + macrophages. Furthermore, we showed that angiostatin led to a decrease in the gelatinolytic activity of macrophage-produced matrix metalloproteinase-9, which may explain, in part, the observed angiostatin-mediated inhibition of migration. Additionally, we detected the presence of the beta-subunit of ATP synthase on the cell-surface of macrophages. ATP synthase was previously found to be a receptor for angiostatin on the cell-surface endothelial cells. We propose that the presence of ATP synthase on the surface of macrophages may promote interaction with angiostatin and prevent migration, similar to what has been reported with endothelial cells. Our findings suggest that angiostatin holds promise as an inhibitory agent against macrophages.
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Books on the topic "Gene and Molecular Therapy"

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B, Burck Kathy, ed. Gene therapy: Application of molecular biology. New York: Elsevier, 1991.

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Wiwanitkit, Viroj. Cell, gene, and molecular therapy: New concepts. Hauppauge, NY: Nova Science Publishers, 2009.

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Greenwell, Pamela. Molecular therapeutics: 21st-century medicine. Chichester, England: J. Wiley, 2007.

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The new healers: The promise and problems of molecular medicine in the twenty-first century. New York: Oxford University Press, 1997.

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Bo, Xuenong, and Joost Verhaagen. Gene delivery and therapy for neurological disorders. New York: Humana Press, 2015.

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Monaco), Miami Bio/Technology European Symposium (1994. Advances in gene technology: Molecular biology of human genetic disease. Oxford: IRL Press at Oxford University Press, 1994.

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Falk Symposium (88th 1995 Basel, Switzerland). Molecular diagnosis and gene therapy: Proceedings of the 88th Falk Symposium (part III of the Basel Liver Week), held in Basel, Switzerland, October 22-23, 1995. Dordrecht: Kluwer Academic Publishers, 1996.

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Shulin, Li, ed. Electroporation protocols: Experimental and clinical gene medicine. Totowa, N.J: Humana, 2008.

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The lung: Molecular basis of disease. Philadelphia: W.B. Saunders Co., 1998.

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Boulikas, Teni. Gene Therapy and Molecular Biology. Gene Therapy Press, 1998.

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Book chapters on the topic "Gene and Molecular Therapy"

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Cornetta, Kenneth. "Gene Therapy." In Molecular Genetic Pathology, 717–29. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-405-6_29.

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Weber, Georg F. "Gene Therapy." In Molecular Therapies of Cancer, 283–96. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13278-5_8.

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Douglas, Joanne T., and David T. Curiel. "Gene Therapy." In Molecular Biology of the Lung, 1–20. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8784-7_1.

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Nakai, Hiroyuki. "Hepatic Gene Therapy." In Molecular Pathology Library, 343–70. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7107-4_23.

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Liu, Ning, and Rhonda Bassel-Duby. "Molecular Basis of Muscle Disease." In Muscle Gene Therapy, 13–39. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03095-7_2.

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Schepelmann, Silke, Ion Niculescu-Duvaz, and Caroline J. Springer. "Suicide Gene Therapy." In Principles of Molecular Oncology, 367–82. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-470-4_18.

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Hoffman, Robert M., Kenji Miki, Waddah Al-Refaie, Mingxu Xu, and Yuying Tan. "Methioninase Gene Therapy." In Methods in Molecular Biology, 173–97. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8796-2_14.

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Niculescu-Duvaz, Ion, and Caroline J. Springer. "Suicide Gene Therapy." In Principles of Molecular Oncology, 675–94. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-664-5_20.

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Vassalli, Giuseppe, and David A. Dichek. "Cardiovascular Gene Therapy." In Principles of Molecular Medicine, 161–68. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-726-0_18.

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Hildebrand, Staffan, and Alexander Pfeifer. "Gene Therapy Vectors." In Encyclopedia of Molecular Pharmacology, 689–94. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_63.

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Conference papers on the topic "Gene and Molecular Therapy"

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"Advances in Gene Therapy." In International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916417.

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Prates, Pedro Emílio Gomes. "AVALIAÇÃO DA TERAPIA GÊNICA DO SUICÍDIO COM USO DE GENES SUICIDAS PARA O COMBATE AO CÂNCER: REVISÃO INTEGRATIVA." In II Congresso Brasileiro de Biologia Molecular On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/2334.

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Introdução: Durante décadas os tratamentos quimioterápicos convencionais foram empregados no câncer devido à eficácia em matar as células tumorais. Diante disso, a terapia gênica com uso de genes suicidas surge como uma das abordagens mais inovadoras para o desenvolvimento de agentes antineoplásicos com maior seletividade tumoral. Assim, entre os genes suicidas disponíveis, a timidina quinase é investigada em vários modelos de tumor. Contudo, o uso dessa enzima apresenta limitações devido ao sistema de imunogenicidade. Recentemente, pesquisadores passaram a utilizar o sistema de gene suicida da Caspase-9 induzível, a qual apresentou resultados mais favoráveis se comparado à timidina quinase. Objetivo: Objetiva-se construir uma revisão integrativa da literatura sobre a terapia gênica do suicídio avaliando o uso de genes suicidas, sobretudo da timidina quinase e da caspase-9 induzível para o combate ao câncer. Material e Métodos: Foi realizada uma revisão integrativa de literatura por meio de uma pesquisa nos bancos de dados PubMed, Scopus e LILACS com os seguintes descritores “terapia gênica de genes suicidas”, “câncer”, “avaliação”, “timidina quinase” e “caspase-9 induzível” simultaneamente às correspondentes em inglês, em intervalo de 11 anos (2010-2021), com critérios de inclusão preestabelecidos. Para o cruzamento dos descritores, utilizou-se um protocolo com os seguintes booleanos: Gene Therapy of Suicide Gene AND Cancer AND Assessment AND Thymidine Kinase AND Inducible Caspase-9. Ao final, 4 artigos foram selecionados. Resultados: Foi selecionado 1 artigo (n = 25%) que abordava o tema da avaliação na terapia de genes suicidas. Em contrapartida, os critérios de exclusão foram estudos que não contemplavam o efeito avaliativo desses genes na terapia gênica, resumindo-se a 3 artigos selecionados (n = 75%). Com isso, observou-se que a avaliação do uso de genes suicidas ainda é uma abordagem recente, necessitando de mais estudos que contemplem essa temática. Conclusão: A avaliação da terapia gênica do suicídio pautada no uso de genes suicidas para o combate ao câncer é promissora, mesmo que recente e dos mínimos estudos publicados. Além disso, o sistema de entrega utilizando a caspase-9 induzível é mais viável do que o sistema de entrega da timidina quinase, já que esse sistema se limita à imunogenicidade do transgene viral.
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Deng, Xu-Bin, Li Xiao, Fang Jin, Joseph Testa, and Guang-Hui Xiao. "Abstract A64: Adenovirus-mediated NK4 gene therapy for malignant mesothelioma." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a64.

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Little, Annette S., Jessica Hunt, David Hughes, Ruth Feltell, Daniel Gitterman, Rachel Leah, Holly Astley, Ramu Mangena, Kyla Grimshaw, and Christopher Torrance. "Abstract A148: Modeling patient responses to targeted therapy with rAAV mediated gene editing." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a148.

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Zhang, Xue-Qing, Mark Chen, Robert Lam, Xiaoyang Xu, Eiji Osawa, and Dean Ho. "A Platform Approach to Gene Delivery via Surface Modified Nanodiamonds." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13340.

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The purpose of gene therapy is to introduce foreign genetic material into host cells to either supplement aberrant genes or to endow additional biological functions. To date, however, there has been only modest progress towards this goal, mainly due to the lack of safe, effective and broadly applicable delivery methods. Functional nanodiamonds (NDs) are rapidly emerging as promising platform carriers for next-generation therapeutics due to their innate biocompatibility, scalability, precise particle distribution, high surface area-to-volume ratio, near-spherical aspect ratio, and easily adaptable carbon surface for bioagent attachment. NDs have been functionalized with a range of therapeutics, proteins, antibodies, DNA, polymers, and other assorted biological agents. Furthermore, NDs are stable and dispersible in water, making them a promising and clinically important modality in improving the efficacy of the treatment of diseases and even some cancers at the molecular level. Mitochondrial function (MTT) and luminescent ATP production assays have demonstrated that NDs are not toxic to a wide variety of cell types. In this study, we functionalized NDs with amine groups via either covalent attachment of (3-aminopropyl) trimethoxysilane or surface immobilization of 800 Da low molecular weight polyethyleneimine (LMW PEI800) for plasmid DNA delivery. The latter delivery approach combines complementary characteristics of PEI800 and NDs to create a hybrid material that exhibits the high transfection efficiency of high molecular weight PEI, but without the inherent high cytotoxicity.
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Pinho, Rafaela Seixas, Afonso Moraes Melo Junior, Rafael Silva Lemos, Amanda da Silva Furtado, and Luís Eduardo Werneck de Carvalho. "Gliomas: tumor markers and prognosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.538.

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Background: Gliomas are classified based from the molecular parameters involved in their pathogenesis, which influence their prognosis. The parameters are based on the mutation of the genes encoding the enzyme isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2), on the codelection of the arms of chromosome 1p/19q and the promoting hypermethylation of the MGMT gene. Objectives: identify tumor markers related to gliomas and their prognostic values. Methods: integrative review of the literature based on pubmed, lilacs and scielo platforms. Articles published in English, Portuguese and Spanish between 2016 and 2021 were included. Articles that were not related to the theme were excluded from the analysis. Results: The IDH1 and 2 genes are traditional markers and mutations in these genes are associated with a better prognosis. The codeletion 1p/19q, on the other hand, is indicative of a more favorable prognosis when related to tumors without codeletion. MGMT gene hypermethylation has strong prognostic value in patients treated with radiotherapy and chemotherapy with alkyl agentes, because the low expression of the MGMT gene allows better efficacy of the therapy, which would be prevented by the MGMT enzyme. The circulating marker microRNA – 221 (miRNA), obtained by less invasive techniques, is an indicator of poor prognosis, however, it has not yet obtained clinical validation for use. Conclusion: It is concluded that the tumor markers that indicate a better prognosis are the genes IDH-I and II, the codelection 1p / 19q and the hypermethylation of the MGMT gene. While miRNA showed a worse prognosis.
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Li, Jianbo, and Hao Lin. "The Role of Ion Electrophoresis in Electroporation-Mediated Molecular Delivery." In ASME 2009 Second International Conference on Micro/Nanoscale Heat and Mass Transfer. ASMEDC, 2009. http://dx.doi.org/10.1115/mnhmt2009-18495.

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Electroporation is a widely applied technique to deliver active molecules into the cellular compartment, to perform tasks such as gene therapy and directed stem cell differentiation, among many others. In this technique, an electric field transiently permeabilizes the cellular membrane to facilitate molecular exchange. While the permeabilization process is relatively well understood, the transport mechanisms for molecular delivery are still under debate. In this work, the role of ion electrophoresis in electroporation-mediated molecular delivery is investigated using numerical simulation. The Nernst-Planck equations for ionic transport in the extracellular and intracellular spaces are solved, respectively, and are coupled through a permeabilization model on the membrane. For the latter, an asymptotic Smoluchowski equation system is adopted, following the work of Krassowska and co-authors. The simulation is used to investigate the delivery of calcium ions into Chinese hamster ovary cells. The results indicate that ion electrophoresis is the dominant mode of transport in the delivery of small charged molecules. Furthermore, the achievable intracellular concentration is strongly influenced by the conductivity difference between the cytoplasm and the buffer, a phenomenon known as “field-amplified sample stacking”. The results agree qualitatively with the fluorescence measurements by Gabriel and Teissie´ (1999), and suggest a new possibility to simultaneously improve cell viability and efficiency in electroporation-mediated molecular delivery.
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Gurskaya, N. A., and K. V. Kobets. "THE RELATIONSHIP OF POLYMORPHIC VARIANTS OF ESTROGEN RECEPTOR GENES WITH THE DEVELOPMENT OF OSTEOPOROSIS IN THE BELARUSIAN POPULATION." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute, 2021. http://dx.doi.org/10.46646/sakh-2021-1-245-248.

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A violation of the hormonal balance is considered one of the factors affecting the development of osteoporosis (OP). The study of the molecular and genetic aspects of this fact will allow us to select a more effective course of OP therapy in the future. Sex hormones, as activators of the expression of a number of genes that regulate bone metabolism, act indirectly through specific receptors. We considered polymorphic variants of the estrogen receptor genes ESR1 and ESR2, encoding the a and в subunits of the estrogen receptor, respectively. Among the studied polymorphic variants of ESR1 (rs9340799, rs2234693, rs1801132) and ESR2 (rs3020444), we identified an association of the T/T genotype of the ESR1 (PvuII) rs2234693 gene with the risk of developing OP (p=0.026) in the Belarusian population.
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Ackerley, David F., Janine N. Copp, Elsie M. Williams, Alexandra M. Mowday, Christopher P. Guise, Gareth A. Prosser, Sophie P. Syddall, Jeff B. Smaill, and Adam V. Patterson. "Abstract B88: Discovery, characterization, and engineering of bacterial nitroreductases for gene-directed enzyme prodrug therapy." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-b88.

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Sadler, J. Evan. "THE MOLECULAR BIOLOGY OF VON WILLEBRAND FACTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643930.

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Human von Willebrand factor (vWF) is a plasma glycoprotein that is synthesized by endothelial cells and megakaryocytes, and perhaps by syncytiotrophoblast of placenta. The biosynthesis of vWF is very complex, involving proteolytic processing, glycosyla-tion, disulfide bond formation, and sulfation. Mature vWF consists of a single subunit of ∼ 250,000 daltons that is assembled into multimer ranging from dimers to species of over 10 million daltons. vWF performs its essential hemostatic function through several binding interactions, forming a bridge between specific receptors on the platelet surface and components of damaged vascular subendothelial connective tissue. Inherited deficiency of vWF, or von Willebrand disease (vWD), is the most common genetically transmitted bleeding disorder worldwide. The last two years has been a time of very rapid progress in understanding the molecular biology of vWF. Four research groups have independently isolated and sequenced the 9 kilobase full-length vWF cDNA. The predicted protein sequence has provided a foundation for understanding the biosynthetic processing of vWF, and has clarified the relationship between vWF and a 75-100 kilodalton plasma protein of unknown function, von Willebrand antigen II (vWAgll)/ vWAgll is co-distributed with vWF in endothelial cells and platelets, and is deficient in patients with vWD. The cDNA sequence of vWF shows that vWAgll is a rather large pro-peptide for vWF, explaining the biochemical and genetic association between the two proteins. vWF has a complex evolutionary history marked by many separate gene segment duplications. The primary structure of the protein contains four distinct types of repeated domains present in two to four copies each. Repeated domains account for over 90 percent of the protein sequence. This sequence provides a framework for ordering the functional domains that have been defined by protein chemistry methods. A tryptic peptide from the amino-terminus of vWF that overlaps domain D3 binds to factor VIII and also appears to bind to heparin. Peptides that include domain A1 bind to collagens, to heparin, and to platelet glycoprotein Ib. A second collagen binding site appears to lie within domain A3. The vWF cDNA has been expressed in heterologous cells to produce small amounts of functionally and structurally normal vWF, indicating that endothelial cells are not unique in their ability to process and assemble vWF multimers. Site-directed mutagenesis has been used to show that deletion of the propeptide of vWF prevents the formation of multimers. Cloned cDNA probes have been employed to isolate vWF genomic DNA from cosmid and λ-phage libraries, and the size of the vWF gene appears to be ∼ 150 kilobases. The vWF locus has been localized to human chromosome 12p12—pter. Several intragenic RFLPs have been characterized. With them, vWF has been placed on the human genetic linkage map as the most telomeric marker currently available for the short arm of chromosome 12. A second apparently homologous locus has been identified on chromosome 22, but the relationship of this locus to the authentic vWF gene is not yet known. The mechanism of vWD has been studied by Southern blotting of genomic DNA with cDNA probes in a few patients. Three unrelated pedigrees have been shown to have total deletions of the vWF gene as the cause of severe vWD (type III). This form of gene deletion appears to predispose to the development of inhibitory alloantibodies to vWF during therapy with cryoprecipitate. During the next several years recombinant DNA methods will continue to contribute our understanding of the evolution, biosynthesis, and structure-function relationships of vWF, as well as the mechanism of additional variants of vWD at the level of gene structure.
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Reports on the topic "Gene and Molecular Therapy"

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Mohan, Subburaman. Molecular Genetic and Gene Therapy Studies of the Musculoskeletal System. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada512941.

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Mohan, Subburaman. Molecular Genetic and Gene Therapy Studies of the Musculoskeletal System. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ada469196.

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Mohan, Subburaman. Molecular Genetic and Gene Therapy Studies of the Musculoskeletal System. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada469369.

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Wahl, Geoffrey M. Amplified Genes in Breast Cancer: Molecular Targets for Investigation and Therapy. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada382811.

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Gomer, Charles J. Photodynamic Therapy Oxidative Stress as a Molecular Switch Controlling Therapeutic Gene Expression for the Treatment of Locally Recurrent Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada396793.

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Gaugler, Randy, Itamar Glazer, Daniel Segal, and Sarwar Hashmi. Molecular Approach for Improving the Stability of Insecticidal Nematodes. United States Department of Agriculture, November 2002. http://dx.doi.org/10.32747/2002.7580680.bard.

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Our overall goal is to improve insecticidal nematodes by genetically engineering strains capable of entering an enhanced state of dormancy that provides improved stability. Objectives: 1. Clone and sequence tps-l homologue from Steinernema carpocapsae. (Revised: A failure to isolate the tps gene group from Steinernema precipitated a redirection to identifying other genes involved in insecticidal nematode desiccation process.) 2. Incorporate cloned tps-l gene into S. carpocapsae to obtain overexpression, thereby, enhancing desiccation tolerance. (Revised: Other stress genes in addition to tps-l genes were cloned and efforts at expression in S. carpocapsae were conducted) 3. Characterize the transgenic strains. No other biological control agent offers more impressive attributes than insecticidal nematodes. However, their potential is limited by the bane of nearly all biological control agents: poor stability. This leads to inadequate shelf-life and ultimately reduced field efficacy. Nematode storage is based on desiccation, yet insecticidal species are only capable of partial desiccation termed quiescent anhydrobiosis. Overwhelming evidence has shown that when the disaccharide compound trehalose is elevated in anhydrobiotic organisms such as yeast, plants, and nematodes it enables these organisms the ability to survive environmental stresses i.e., desiccation. Armed with this information our goal was to improve insecticidal nematodes stability by engineering trehalose overexpression.
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Meir, Shimon, Michael S. Reid, Cai-Zhong Jiang, Amnon Lers, and Sonia Philosoph-Hadas. Molecular Studies of Postharvest Leaf and Flower Senescence. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7592657.bard.

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Original objectives: To understand the regulation of abscission by exploring the nature of changes of auxin-related gene expression in tomato (Lycopersicon esculatumMill) abscission zones (AZs) following organ removal, and by analyzing the function of these genes. Our specific goals were: 1) To complete the microarray analyses in tomato flower and leaf AZs, for identifying genes whose expression changes early in response to auxin depletion; 2) To examine, using virus-induced gene silencing (VIGS), the effect of silencing target genes on ethylene sensitivity and abscission competence of the leaf and flower AZs; 3) To isolate and characterize promoters from AZ-specific genes to be used in functional analysis; 4) To generate stable transgenic tomato plants with selected genes silenced with RNAi, under the control of an AZ-specific promoter, for further characterization of their abscission phenotypes. Background: Abscission, the separation of organs from the parent plant, results in postharvest quality loss in many ornamentals and other fresh produce. The process is initiated by changes in the auxin gradient across the AZ, and is triggered by ethylene. Although changes in gene expression have been correlated with the ethylene-mediated execution of abscission, there is almost no information on the initiation of the abscission process, as the AZ becomes sensitized to ethylene. The present project was focused on elucidating these early molecular regulatory events, in order to gain a better control of the abscission process for agricultural manipulations. Major conclusions, solutions, achievements: Microarray analyses, using the Affymetrix Tomato GeneChip®, revealed changes in expression, occurring early in abscission, of many genes with possible regulatory functions. These included a range of auxin- and ethylene-related transcription factors (TFs), other TFs that are transiently induced just after flower removal, and a set of novel AZ-specific genes. We also identified four different defense-related genes, including: Cysteine-type endopeptidase, α- DOX1, WIN2, and SDF2, that are newly-associated with the late stage of the abscission process. This supports the activation of different defense responses and strategies at the late abscission stages, which may enable efficient protection of the exposed tissue toward different environmental stresses. To facilitate functional studies we implemented an efficient VIGS system in tomato, and isolated two abscission-specific promoters (pTAPG1 and pTAPG4) for gene silencing in stable transformation. Using the VIGS system we could demonstrate the importance of TAPGs in abscission of tomato leaf petioles, and evaluated the importance of more than 45 genes in abscission. Among them we identified few critical genes involved in leaf and flower abscission. These included: PTRP-F1, PRP, TKN4, KNOTTED-like homeobox TF, KD1, and KNOX-like homeodomain protein genes, the silencing of which caused a striking retardation of pedicel abscission, and ERF1, ERF4, Clavata-like3 protein, Sucrose transporter protein, and IAA10 genes, the silencing of which delayed petiole abscission. The importance of PRPand KD1 genes in abscission was confirmed also by antisense–silencing using pTAPG4. Experiments testing the effects of RNAi silencing of few other genes are still in progress, The analysis of the microarray results of flower and leaf AZs allowed us to establish a clear sequence of events occurring during acquisition of tissue sensitivity to ethylene, and to confirm our hypothesis that acquisition of ethylene sensitivity in the AZ is associated with altered expression of auxin-regulated genes in both AZs. Implication, both scientific and agricultural: Our studies had provided new insights into the regulation of the abscission process, and shaded light on the molecular mechanisms that drive the acquisition of abscission competence in the AZ. We pointed out some critical genes involved in regulation of abscission, and further expanded our knowledge of auxin-ethylene cross talk during the abscission process. This permits the development of novel techniques for manipulating abscission, and thereby improving the postharvest performance of ornamentals and other crops.
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Ohad, Nir, and Robert Fischer. Regulation of plant development by polycomb group proteins. United States Department of Agriculture, January 2008. http://dx.doi.org/10.32747/2008.7695858.bard.

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Our genetic and molecular studies have indicated that FIE a WD-repeat Polycomb group (PcG) protein takes part in multi-component protein complexes. We have shown that FIE PcG protein represses inappropriate programs of development during the reproductive and vegetative phases of the Arabidopsis life cycle. Moreover, we have shown that FIE represses the expression of key regulatory genes that promote flowering (AG and LFY), embryogenesis (LEC1), and shoot formation (KNAT1). These results suggest that the FIE PcG protein participates in the formation of distinct PcG complexes that repress inappropriate gene expression at different stages of plant development. PcG complexes modulate chromatin compactness by modifying histones and thereby regulate gene expression and imprinting. The main goals of our original project were to elucidate the biological functions of PcG proteins, and to understand the molecular mechanisms used by FIE PcG complexes to repress the expression of its gene targets. Our results show that the PcG complex acts within the central cell of the female gametophyte to maintain silencing of MEA paternal allele. Further more we uncovered a novel example of self-imprinting mechanism by the PgG complex. Based on results obtained in the cures of our research program we extended our proposed goals and elucidated the role of DME in regulating plant gene imprinting. We discovered that in addition to MEA,DME also imprints two other genes, FWA and FIS2. Activation of FWA and FIS2 coincides with a reduction in 5-methylcytosine in their respective promoters. Since endosperm is a terminally differentiated tissue, the methylation status in the FWA and FIS2 promoters does not need to be reestablished in the following generation. We proposed a “One-Way Control” model to highlight differences between plant and animal genomic imprinting. Thus we conclude that DEMETER is a master regulator of plant gene imprinting. Future studies of DME function will elucidate its role in processes and disease where DNA methylation has a key regulatory role both in plants and animals. Such information will provide valuable insight into developing novel strategies to control and improve agricultural traits and overcome particular human diseases.
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Rafaeli, Ada, and Russell Jurenka. Molecular Characterization of PBAN G-protein Coupled Receptors in Moth Pest Species: Design of Antagonists. United States Department of Agriculture, December 2012. http://dx.doi.org/10.32747/2012.7593390.bard.

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The proposed research was directed at determining the activation/binding domains and gene regulation of the PBAN-R’s thereby providing information for the design and screening of potential PBAN-R-blockers and to indicate possible ways of preventing the process from proceeding to its completion. Our specific aims included: (1) The identification of the PBAN-R binding domain by a combination of: (a) in silico modeling studies for identifying specific amino-acid side chains that are likely to be involved in binding PBAN with the receptor and; (b) bioassays to verify the modeling studies using mutant receptors, cell lines and pheromone glands (at tissue and organism levels) against selected, designed compounds to confirm if compounds are agonists or antagonists. (2) The elucidation ofthemolecular regulationmechanisms of PBAN-R by:(a) age-dependence of gene expression; (b) the effect of hormones and; (c) PBAN-R characterization in male hair-pencil complexes. Background to the topic Insects have several closely related G protein-coupled receptors (GPCRs) belonging to the pyrokinin/PBAN family, one with the ligand pheromone biosynthesis activating neuropeptide or pyrokinin-2 and another with diapause hormone or pyrokinin-1 as a ligand. We were unable to identify the diapause hormone receptor from Helicoverpa zea despite considerable effort. A third, related receptor is activated by a product of the capa gene, periviscerokinins. The pyrokinin/PBAN family of GPCRs and their ligands has been identified in various insects, such as Drosophila, several moth species, mosquitoes, Triboliumcastaneum, Apis mellifera, Nasoniavitripennis, and Acyrthosiphon pisum. Physiological functions of pyrokinin peptides include muscle contraction, whereas PBAN regulates pheromone production in moths plus other functions indicating the pleiotropic nature of these ligands. Based on the alignment of annotated genomic sequences, the primary and secondary structures of the pyrokinin/PBAN family of receptors have similarity with the corresponding structures of the capa or periviscerokinin receptors of insects and the neuromedin U receptors found in vertebrates. Major conclusions, solutions, achievements Evolutionary trace analysisof receptor extracellular domains exhibited several class-specific amino acid residues, which could indicate putative domains for activation of these receptors by ligand recognition and binding. Through site-directed point mutations, the 3rd extracellular domain of PBAN-R was shown to be critical for ligand selection. We identified three receptors that belong to the PBAN family of GPCRs and a partial sequence for the periviscerokinin receptor from the European corn borer, Ostrinianubilalis. Functional expression studies confirmed that only the C-variant of the PBAN-R is active. We identified a non-peptide agonist that will activate the PBAN-receptor from H. zea. We determined that there is transcriptional control of the PBAN-R in two moth species during the development of the pupa to adult, and we demonstrated that this transcriptional regulation is independent of juvenile hormone biosynthesis. This transcriptional control also occurs in male hair-pencil gland complexes of both moth species indicating a regulatory role for PBAN in males. Ultimate confirmation for PBAN's function in the male tissue was revealed through knockdown of the PBAN-R using RNAi-mediated gene-silencing. Implications, both scientific and agricultural The identification of a non-peptide agonist can be exploited in the future for the design of additional compounds that will activate the receptor and to elucidate the binding properties of this receptor. The increase in expression levels of the PBAN-R transcript was delineated to occur at a critical period of 5 hours post-eclosion and its regulation can now be studied. The mysterious role of PBAN in the males was elucidated by using a combination of physiological, biochemical and molecular genetics techniques.
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Tucker, Mark L., Shimon Meir, Amnon Lers, Sonia Philosoph-Hadas, and Cai-Zhong Jiang. Elucidation of signaling pathways that regulate ethylene-induced leaf and flower abscission of agriculturally important plants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7597929.bard.

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The Problem: Abscission is a highly regulated process, occurring as a natural terminal stage of development, in which various organs are separated from the parent plant. In most plant species, the process is initiated by a decrease in active auxin in the abscission zone (AZ) and an increase in ethylene, and may be accelerated by postharvest or environmental stresses. Another potential key regulator in abscission is IDA (Inflorescence Deficient in Abscission), which was identified as an essential peptide signal for floral organ abscission in Arabidopsis. However, information is still lacking regarding the molecular mechanisms integrating all these regulators. In our previous BARD funded research we made substantial progress towards understanding these molecular events in tomato, and the study is still in progress. We established a powerful platform for analysis of genes for regulatory proteins expressed in AZ. We identified changes in gene expression for several transcription factors (TFs) directly linked to ethylene and auxin signaling and several additional regulatory proteins not so obviously linked to these hormones. Moreover, we demonstrated using a virus-induced gene silencing (VIGS) assay that several play a functional role in the onset of abscission. Based on these results we have selected 14 genes for further analysis in stably transformed tomato plants. All 14 genes were suppressed by RNA interference (RNAi) using a constitutive promoter, and 5 of them were also suppressed using an abscission-specific promoter. Transformations are currently at different stages of progress including some lines that already display an abscission phenotype. Objectives: We propose here to (1) complete the functional analysis of the stably transformed tomato plants with T2 lines and perform transcriptome analysis using custom abscission-specific microarrays; (2) conduct an indepth analysis of the role of IDA signaling in tomato leaf and flower abscission; (3) perform transcriptome and proteome analyses to extend the earlier gene expression studies to identify transcripts and proteins that are highly specific to the separation layer (i.e., target cells for cell separation) prior to the onset of abscission; (4) extend and compliment the work in tomato using a winnowed set of genes in soybean. Methodology: Next Generation Sequencing (NGS) of mRNA will be used to further increase the list of abscission-associated genes, and for preparation of a custom tomato abscission microarray to test altered gene expression in transgenic plants. Tandem mass spectrometry (LC-MS/MS) of protein extracts from leaf petiole, flower pedicel and their AZ tissues will be used to identify the proteome of the AZ before and during abscission. AZ-specific gene promoters will be used in stably transformed tomato plants to reduce non-target phenotypes. The bean pod mottle virus (BPMV) plasmid vectors will be used for VIGS analysis in soybean. Expected Contribution: Our study will provide new insights into the regulation of ethylene-induced abscission by further revealing the role of key regulators in the process. This will permit development of novel techniques for manipulating leaf and flower abscission, thereby improving the postharvest performance of agriculturally important crops.
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