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Статті в журналах з теми "NBEAL2":
1
Noetzli, Leila, Natalie Smith, Gary Brodsky, and Jorge Di Paola. "Expression Patterns Of NBEAL2 In Human Tissues and a Megakaryocytic Cell Line." Blood 122, no. 21 (November 15, 2013): 1075. http://dx.doi.org/10.1182/blood.v122.21.1075.1075.
Анотація:
Abstract Gray platelet syndrome (GPS) is a rare autosomal recessive bleeding disorder characterized by thrombocytopenia, large platelets, and deficient alpha granules in platelets and megakaryocytes. The genetic cause of GPS was recently elucidated by our lab and others, and deleterious mutations were found in the gene NBEAL2 in several affected individuals. NBEAL2 stands for Neurobeachin-like 2 and is a large (30kb, 54 exon) gene on human chromosome 3p21.31. NBEAL2 is a member of a family of proteins that contain a BEACH (Beige and Chediak Higashi) domain which is a highly conserved domain that has been associated with protein functions such as vesicular trafficking, membrane dynamics, and receptor signaling. Very little is known about NBEAL2 other than its involvement with GPS. The relative expression of the NBEAL2 transcript, both in tissues and in subcellular compartments, is not known. It has previously been published that NBEAL2 protein coding isoforms are present in a variety of human tissues, but the abundance of NBEAL2 transcript in each tissue is not known. Furthermore, there is currently no available antibody that recognizes the 302 kDa NBEAL2 protein to validate that mRNA presence translates to protein expression. We have examined the relative transcript abundance of NBEAL2 in a human cDNA library and have validated a novel NBEAL2 antibody in a human megakaryocytic cell line (Dami) and human platelets. We obtained a human mRNA tissue library from Invitrogen which was reverse transcribed to cDNA. Tissues analyzed include bladder, brain, cervix, colon, esophagus, heart, kidney, liver, lung, ovary, placenta, prostate, skeletal muscle, small intestine, spleen, testes, thymus, thyroid, trachea, bone marrow, peripheral leukocytes, CD33+, and CD36+. To investigate relative transcript abundance, we used a Taqman qPCR probe designed to identify all six protein coding isoforms, as determined by Ensembl (http://uswest.ensembl.org). Highest NBEAL2 expression was seen in CD33+ cells, which was 54.3 fold higher than the tissue with lowest expression (skeletal muscle). Relatively high expression was also seen in the peripheral leukocytes, bone marrow, lung, esophagus, and cervix. Alternatively, NBEAL2 expression was low in the brain, despite the homology to the Neurobeachin (NBEA) brain specific protein. While high transcript abundance may infer function, relative protein expression is necessary to validate these findings. Therefore, we designed a novel NBEAL2 antibody against a 14 amino acid peptide (SLEPRRPEEAGAEVC) encoded by exon 1 of NBEAL2 that is 100% conserved between human and mouse. Western blot characterization of this antibody showed the expected approximately 300 kDa band in both soluble and insoluble Dami lysates and human platelet rich plasma lysates. Furthermore, the NBEAL2 antibody was also used for immunofluorescence of Dami cells to determine the approximate subcellular localization of the protein. Preliminary results suggest that NBEAL2 is localized to the cytoplasm, a finding that is consistent with a subcellular localization prediction program (Euk-mPLoc 2.0). In conclusion, we have determined the relative abundance of NBEAL2 transcript in several human tissues, and have begun to characterize a novel antibody against NBEAL2 using the human megakaryocytic Dami cell line and human platelets. Ongoing studies with this novel tool in the Nbeal2 knockout mouse model will likely provide new information about this elusive protein. Disclosures: Di Paola: CSL Behring: Consultancy; Pfizer: DSMB, DSMB Other.
2
Lo, Richard W., Ling Li, Fred G. Pluthero, Richard Leung, Koji Eto та Walter H. A. Kahr. "The endoplasmic reticulum protein SEC22B interacts with NBEAL2 and is required for megakaryocyte α-granule biogenesis". Blood 136, № 6 (6 серпня 2020): 715–25. http://dx.doi.org/10.1182/blood.2019004276.
Анотація:
Abstract Studies of inherited platelet disorders have provided many insights into platelet development and function. Loss of function of neurobeachin-like 2 (NBEAL2) causes gray platelet syndrome (GPS), where the absence of platelet α-granules indicates NBEAL2 is required for their production by precursor megakaryocytes. The endoplasmic reticulum is a dynamic network that interacts with numerous intracellular vesicles and organelles and plays key roles in their development. The megakaryocyte endoplasmic reticulum is extensive, and in this study we investigated its role in the biogenesis of α-granules by focusing on the membrane-resident trafficking protein SEC22B. Coimmunoprecipitation (co-IP) experiments using tagged proteins expressed in human HEK293 and megakaryocytic immortalized megakaryocyte progenitor (imMKCL) cells established binding of NBEAL2 with SEC22B, and demonstrated that NBEAL2 can simultaneously bind SEC22B and P-selectin. NBEAL2-SEC22B binding was also observed for endogenous proteins in human megakaryocytes using co-IP, and immunofluorescence microscopy detected substantial overlap. SEC22B binding was localized to a region of NBEAL2 spanning amino acids 1798 to 1903, where 2 GPS-associated missense variants have been reported: E1833K and R1839C. NBEAL2 containing either variant did not bind SEC22B coexpressed in HEK293 cells. CRISPR/Cas9-mediated knockout of SEC22B in imMKCL cells resulted in decreased NBEAL2, but not vice versa. Loss of either SEC22B or NBEAL2 expression resulted in failure of α-granule production and reduced granule proteins in imMKCL cells. We conclude that SEC22B is required for α-granule biogenesis in megakaryocytes, and that interactions with SEC22B and P-selectin facilitate the essential role of NBEAL2 in granule development and cargo stability.
3
Kahr, Walter H. A., Richard W. Lo, Ling Li, Fred G. Pluthero, Hilary Christensen, Ran Ni, Nima Vaezzadeh, et al. "Abnormal megakaryocyte development and platelet function in Nbeal2−/− mice." Blood 122, no. 19 (November 7, 2013): 3349–58. http://dx.doi.org/10.1182/blood-2013-04-499491.
Анотація:
Key Points Nbeal2 −/− mice are a model of human GPS, characterized by macrothrombocytopenia and α-granule-deficient platelets. NBEAL2 is required for normal platelet function and megakaryocyte development.
4
Darling, Thayer K., Michael P. Schenk, Chengjing C. Zhou, Franklin M. Maloba, Patrice N. Mimche, Jonathan M. Gibbins, Shawn M. Jobe та Tracey J. Lamb. "Platelet α-granules contribute to organ-specific pathologies in a mouse model of severe malaria". Blood Advances 4, № 1 (31 грудня 2019): 1–8. http://dx.doi.org/10.1182/bloodadvances.2019000773.
Анотація:
Key Points Nbeal2 deficiency leads to significantly reduced lung and brain pathology and enhanced survival in a mouse model of malaria. Both antibody-dependent and antibody-independent platelet depletion in mice recapitulate the findings observed in Nbeal2−/− mice.
5
Mayer, Louisa, Maria Jasztal, Mercedes Pardo, Salvadora Aguera de Haro, Janine Collins, Tadbir K. Bariana, Peter A. Smethurst, et al. "Nbeal2 interacts with Dock7, Sec16a, and Vac14." Blood 131, no. 9 (March 1, 2018): 1000–1011. http://dx.doi.org/10.1182/blood-2017-08-800359.
Анотація:
Key Points Nbeal2 interacts with Dock7, Sec16a, and Vac14; and missense variants that cause GPS disrupt the binding of Dock7 and Vac14. The level of the α-granule protein Dock7 in platelets from Nbeal2−/− mice and GPS cases is reduced and its signaling pathway is dysregulated.
6
Aarts, Cathelijn E. M., Kate Downes, Arie J. Hoogendijk, Evelien G. G. Sprenkeler, Roel P. Gazendam, Rémi Favier, Marie Favier, et al. "Neutrophil specific granule and NETosis defects in gray platelet syndrome." Blood Advances 5, no. 2 (January 25, 2021): 549–64. http://dx.doi.org/10.1182/bloodadvances.2020002442.
Анотація:
Abstract Gray platelet syndrome (GPS) is an autosomal recessive bleeding disorder characterized by a lack of α-granules in platelets and progressive myelofibrosis. Rare loss-of-function variants in neurobeachin-like 2 (NBEAL2), a member of the family of beige and Chédiak-Higashi (BEACH) genes, are causal of GPS. It is suggested that BEACH domain containing proteins are involved in fusion, fission, and trafficking of vesicles and granules. Studies in knockout mice suggest that NBEAL2 may control the formation and retention of granules in neutrophils. We found that neutrophils obtained from the peripheral blood from 13 patients with GPS have a normal distribution of azurophilic granules but show a deficiency of specific granules (SGs), as confirmed by immunoelectron microscopy and mass spectrometry proteomics analyses. CD34+ hematopoietic stem cells (HSCs) from patients with GPS differentiated into mature neutrophils also lacked NBEAL2 expression but showed similar SG protein expression as control cells. This is indicative of normal granulopoiesis in GPS and identifies NBEAL2 as a potentially important regulator of granule release. Patient neutrophil functions, including production of reactive oxygen species, chemotaxis, and killing of bacteria and fungi, were intact. NETosis was absent in circulating GPS neutrophils. Lack of NETosis is suggested to be independent of NBEAL2 expression but associated with SG defects instead, as indicated by comparison with HSC-derived neutrophils. Since patients with GPS do not excessively suffer from infections, the consequence of the reduced SG content and lack of NETosis for innate immunity remains to be explored.
7
Tang, Yuling, Hongping Wu, Caiyun Huo, Shumei Zou, Yanxin Hu, and Hanchun Yang. "Transcriptomic Profiling of Mouse Mast Cells upon Pathogenic Avian H5N1 and Pandemic H1N1 Influenza a Virus Infection." Viruses 14, no. 2 (January 29, 2022): 292. http://dx.doi.org/10.3390/v14020292.
Анотація:
Mast cells, widely residing in connective tissues and on mucosal surfaces, play significant roles in battling against influenza A viruses. To gain further insights into the host cellular responses of mouse mast cells with influenza A virus infection, such as the highly pathogenic avian influenza A virus H5N1 and the human pandemic influenza A H1N1, we employed high-throughput RNA sequencing to identify differentially expressed genes (DEGs) and related signaling pathways. Our data revealed that H1N1-infected mouse mast P815 cells presented more up- and down-regulated genes compared with H5N1-infected cells. Gene ontology analysis showed that the up-regulated genes in H1N1 infection were enriched for more degranulation-related cellular component terms and immune recognition-related molecular functions terms, while the up-regulated genes in H5N1 infection were enriched for more immune-response-related biological processes. Network enrichment of the KEGG pathway analysis showed that DEGs in H1N1 infection were specifically enriched for the FoxO and autophagy pathways. In contrast, DEGs in H5N1 infection were specifically enriched for the NF-κB and necroptosis pathways. Interestingly, we found that Nbeal2 could be preferentially activated in H5N1-infected P815 cells, where the level of Nbeal2 increased dramatically but decreased in HIN1-infected P815 cells. Nbeal2 knockdown facilitated inflammatory cytokine release in both H1N1- and H5N1-infected P815 cells and aggravated the apoptosis of pulmonary epithelial cells. In summary, our data described a transcriptomic profile and bioinformatic characterization of H1N-1 or H5N1-infected mast cells and, for the first time, established the crucial role of Nbeal2 during influenza A virus infection.
8
Di Paola, Jorge. "Novel Congenital Platelet Disorders." Blood 128, no. 22 (December 2, 2016): SCI—39—SCI—39. http://dx.doi.org/10.1182/blood.v128.22.sci-39.sci-39.
Анотація:
The processes of megakaryocyte differentiation, proplatelet formation, and the daily release of 1011 platelets into the bloodstream are tightly regulated. Genetic disturbances can lead to a cascade of downstream molecular alterations that markedly affect the function of megakaryocytes and platelets. Therefore, identifying new genes and their function in megakaryocytes and platelets is critical for understanding how these unique cells contribute to health and disease. Over the last decade advances in genomics, specifically next generation sequencing, have allowed for the discovery of several mutations and genetic variants that cause disease or influence associated hematological traits. By performing platelet RNA-Seq we were among the first to identify NBEAL2 as the causative gene for gray platelet syndrome (GPS) and showed that NBEAL2 regulates megakaryocyte development and platelet function.1-3 Mice carrying targeted Nbeal2 null alleles not only replicated the thrombocytopenia and lack of alpha granules observed in humans, but also provided new information about the role of platelets in thromboinflammation, wound healing, myelofibrosis and metastasis dissemination.4-7 More recently, we and others found that germline mutations in ETV6 lead to thrombocytopenia, red cell macrocytosis, and predisposition to lymphoblastic leukemia.8,9ETV6 encodes an ETS family transcriptional repressor, which exerts its activity by binding a consensus sequence in the promoter regions of DNA. Mice with conditional Etv6 knockout in megakaryocytic-erythroid cells are thrombocytopenic indicating the involvement of Etv6 in thrombopoiesis.10 Several of the families recently described have a missense mutation in the central domain of ETV6 (p.P214L). This mutation results in aberrant cellular localization of ETV6, decreased transcriptional repression, and impaired megakaryocyte maturation. The bone marrow of individuals affected by this mutation show hyperplasia of immature megakaryocytes suggesting a differentiation arrest. Deep sequencing of the platelet transcriptome also revealed significant differences in mRNA expression levels between patients with the ETV6 p.P214L mutation and non-affected family members, indicating that ETV6 is critically involved in defining the molecular phenotype and function of platelets. Consistent with this notion, individuals with the ETV6 p.P214L mutation experience bleeding that is disproportionate to their mild thrombocytopenia. We have also used CRISPR/Cas9 technology to generate a mouse colony where the human p.P214L ETV6 mutation was inserted into the conserved site of Etv6. Mice with this mutation (Etv6H.P214L) have reduced platelet counts. In summary, advances in human genetics that led to the discovery of novel congenital platelet disorders coupled with relevant animal models will likely contribute to our understanding of megakaryopoiesis and platelet function. References 1. Kahr WH, Hinckley J, Li L, et al. Mutations in NBEAL2, encoding a BEACH protein, cause gray platelet syndrome. Nature genetics. 2011;43(8):738-740. 2. Gunay-Aygun M, Falik-Zaccai TC, Vilboux T, et al. NBEAL2 is mutated in gray platelet syndrome and is required for biogenesis of platelet alpha-granules. Nature genetics. 2011;43(8):732-734. 3. Albers CA, Cvejic A, Favier R, et al. Exome sequencing identifies NBEAL2 as the causative gene for gray platelet syndrome. Nature genetics. 2011;43(8):735-737. 4. Deppermann C, Cherpokova D, Nurden P, et al. Gray platelet syndrome and defective thrombo-inflammation in Nbeal2-deficient mice. The Journal of clinical investigation. 2013. 5. Kahr WH, Lo RW, Li L, et al. Abnormal megakaryocyte development and platelet function in Nbeal2(-/-) mice. Blood. 2013;122(19):3349-3358. 6. Guerrero JA, Bennett C, van der Weyden L, et al. Gray platelet syndrome: proinflammatory megakaryocytes and alpha-granule loss cause myelofibrosis and confer metastasis resistance in mice. Blood.2014;124(24):3624-3635. 7. Tomberg K, Khoriaty R, Westrick RJ, et al. Spontaneous 8bp Deletion in Nbeal2 Recapitulates the Gray Platelet Syndrome in Mice. PLoS One. 2016;11(3):e0150852. 8. Noetzli L, Lo RW, Lee-Sherick AB, et al. Germline mutations in ETV6 are associated with thrombocytopenia, red cell macrocytosis and predisposition to lymphoblastic leukemia. Nature Genetics. 2015;47(5):535-538. 9. Zhang MY, Churpek JE, Keel SB, et al. Germline ETV6 mutations in familial thrombocytopenia and hematologic malignancy. Nature genetics. 2015;47(2):180-185. 10. Wang LC, Swat W, Fujiwara Y, et al. The TEL/ETV6 gene is required specifically for hematopoiesis in the bone marrow. Genes & development. 1998;12(15):2392-2402. Disclosures Di Paola: CSL BEhring: Consultancy; Biogen: Consultancy.
9
Kim, Dongjune A., Katrina J. Ashworth, Jorge Di Paola та David N. Ku. "Platelet α-granules are required for occlusive high-shear-rate thrombosis". Blood Advances 4, № 14 (22 липня 2020): 3258–67. http://dx.doi.org/10.1182/bloodadvances.2020002117.
Анотація:
Abstract von Willebrand factor (VWF) is essential for the induction of arterial thrombosis. In this study, we investigated the critical role of platelet VWF in occlusive thrombosis formation at high shear in mice that do not express platelet VWF (Nbeal2−/−). Using in silico modeling, in vitro high-shear microfluidics, and an in vivo Folts model of arterial thrombosis we reproduced the platelet dynamics that occur under pathological flow in a stenosed vessel. Computational fluid dynamics (CFDs) simulated local hemodynamics in a stenosis based on arterial geometries. The model predicted shear rates, time course of platelet adhesion, and time to occlusion. These predictions were validated in vitro and in vivo. Occlusive thrombosis developed in wild-type control mice that had normal levels of plasma VWF and platelet VWF in vitro and in vivo. Occlusive thrombosis did not form in the Nbeal2−/− mice that had normal plasma VWF and an absence of platelet VWF. Occlusive thrombosis was corrected in Nbeal2−/− microfluidic assays by the addition of exogenous normal platelets with VWF. Combining model and experimental data, we demonstrated the necessary requirement of platelet VWF in α-granules in forming an occlusive thrombus under high shear. These results could inspire new pharmacological targets specific to pathological conditions and prevent arterial thrombosis.
10
Guerrero, Jose A., Cavan Bennett, Louise van der Weyden, Harriet McKinney, Melody Chin, Paquita Nurden, Zoe McIntyre та ін. "Gray platelet syndrome: proinflammatory megakaryocytes and α-granule loss cause myelofibrosis and confer metastasis resistance in mice". Blood 124, № 24 (4 грудня 2014): 3624–35. http://dx.doi.org/10.1182/blood-2014-04-566760.
Анотація:
Key Points Proinflammatory MKs from mice with GPS drive the extension of myelofibrosis, splenomegaly, and emperipolesis. The lack of preformed α-granules in Nbeal2−/− platelets leads to protection against cancer metastasis.
Дисертації з теми "NBEAL2":
1
Delage, Laure. "Des déficiences génétiques comme modèles naturels pour l'étude de la régulation des checkpoints immunitaires et la caractérisation des réponses auto-immunes." Electronic Thesis or Diss., Université Paris Cité, 2021. http://www.theses.fr/2021UNIP5190.
Анотація:
Des mutations récessives de NBEAL2 ont été décrites chez des patients atteints du syndrome des plaquettes grises (SPG). Ce syndrome se caractérise par une macro-thrombopénie, avec des plaquettes dénuées de granules-alpha, conduisant à des troubles de la coagulation, souvent associés à une splénomégalie. Ainsi, NBEAL2 a un rôle crucial dans le trafic des granules-alpha plaquettaires. En outre, notre laboratoire a montré que les patients avec un déficit en NBEAL2 peuvent présenter des caractéristiques cliniques semblables aux syndromes lymphoprolifératifs auto-immuns ; suggérant un rôle de NBEAL2 dans l'homéostasie immunitaire et la tolérance. Une cohorte internationale plus large de patients SPG a confirmé et décrit de nouvelles anomalies immunitaires chez ces patients (maladies auto-immunes, autoanticorps, lymphopénies). Si le rôle de NBEAL2 dans le trafic des granules est souvent étudié, le mécanisme exact conduisant au développement des manifestations auto-immunes chez les patients SPG reste inconnu. NBEAL2 appartient à une famille de protéines, impliquées dans le trafic vésiculaire, et possédant toutes un domaine BEACH conservé. Dans cette famille de protéines à domaine BEACH, une des protéines les plus proche de NBEAL2 est LRBA. LRBA est impliqué dans le recyclage de CTLA-4, un checkpoint immunitaire inhibiteur. CTLA-4 joue un rôle crucial dans la régulation des réponses immunitaires et la tolérance. Des mutations récessives de LRBA conduisent à des caractéristiques cliniques semblables aux déficiences partielles en CTLA-4 : auto-immunité, infiltrations lymphocytaires et lymphopénie B progressive. En condition physiologique, LRBA empêche la dégradation lysosomale de CTLA-4 et permet son recyclage à la membrane plasmatique. Par analogie avec LRBA, nous avons étudié l'importance de NBEAL2 dans le trafic intracellulaire des checkpoints immunitaires et nous avons apporté un nouveau regard sur son rôle dans les lymphocytes. NBEAL2 est ainsi une protéine d'échafaudage, se liant à LRBA, et impliquée dans le trafic de CTLA-4 ainsi que le trafic vésiculaire en général. Ces travaux apportent de nouvelles connaissances sur la régulation de CTLA-4 dans les lymphocytes T activés, une nouvelle liste de partenaires pour la protéine NBEAL2 ainsi qu'un nouveau modèle pour le trafic vésiculaire dans lequel est impliqué NBEAL2. Enfin, une meilleure compréhension des mécanismes conduisant à l'auto-immunité chez les patients atteints du syndrome des plaquettes grises pourrait conduire à un diagnostic plus précoce et un traitement adaptéRecessive NBEAL2 mutations have been reported in patients with Gray Platelet Syndrome (GPS). This syndrome is characterized by a macro-thrombocytopenia, with platelets lacking alpha-granules, leading to bleeding disorders, often associated with splenomegaly. Thus, NBEAL2 plays a crucial role in the trafficking of alpha-granules in platelets. Moreover, our lab has also described NBEAL2 deficiencies in patients presenting clinical features of the autoimmune lymphoproliferative syndrome, suggesting a role of NBEAL2 in immune homeostasis and tolerance. A broader international cohort of GPS patients has been described, revealing immune system abnormalities (autoimmune diseases, autoantibodies, lymphopenia). If the role of NBEAL2 in the traffic of granules is often investigated, the exact mechanism leading to the development of autoimmune manifestations in GPS patients remains unknown. NBEAL2 belongs to a protein family involved in vesicular trafficking, all of which possess a conserved BEACH domain. Within this BEACH-domain containing proteins family, one of the closest members to NBEAL2 is LRBA. LRBA is involved in the recycling of CTLA-4, an inhibitory immune checkpoint. CTLA-4 plays a crucial role in the regulation of immune responses and tolerance. Recessive mutations of LRBA lead to similar clinical features as partial CTLA-4 deficiency: autoimmunity, lymphocytic infiltrations, and progressive B lymphopenia. Physiologically, LRBA prevents the lysosomal degradation of CTLA-4 and allows its recycling to the membrane. By analogy with LRBA, we investigated the importance of NBEAL2 in immune checkpoints intracellular trafficking and we brought new insights on its role in lymphocytes. Thus, NBEAL2 is a scaffold protein, binding LRBA, and involved in CTLA-4 trafficking as well as in vesicular trafficking in general. This work brings new knowledge to the regulation of CTLA-4 in activated T lymphocytes, a list of new partners for NBEAL2 protein and a new model of vesicular trafficking in which NBEAL2 is involved. Finally, a better understanding of the mechanisms leading to autoimmunity in patients with gray platelets syndrome could lead to better diagnosis and treatment management
2
Chang, Meng-Hsuan, and 張孟璇. "Key Factors in Family Business Succession - Case Studies of Public Companies in Taiwan." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/nbezh2.
Анотація:
碩士國立臺灣科技大學
管理研究所
107
Companies in Taiwan are mainly family-owned businesses, which account for a high proportion of economic contribution, thus significantly affecting the economy. Whether the family business succession transition has been implemented successfully is sufficient to affect Taiwan’s overall economy. Thus far, relevant studies on the inheritance of family businesses have focused mainly on a single related topic, thereby resulting in an inadequate understanding of the scope and insufficient discussion. This thesis aims to outline a framework and thus emphasize key areas of attention when addressing the transfer of a family business; it seeks to assist family members in conceptualizing and understanding this issue extensively for them to allow self-development of a comprehensive transfer plan that best suits the specificities of their families and businesses. This research uses “The Three-Circle Model of the Family Business System” framework (i.e., family members, shareholders, and enterprise) to examine issues that affect family businesses during transfer. This research conducts extensive interviews with members of three family businesses involved in public trading in Taiwan. Each of these companies has been in operation for more than 50 years. These interviews are conducted to derive critical factors in the transfer of family businesses.
3
Tsai, Chung-Han, and 蔡崇瀚. "The study of NbEILP from Nicotiana benthamiana involved in the cell-to-cell movement of Bamboo mosaic virus." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/65337367438434178777.
Анотація:
碩士國立中興大學
生物科技學研究所
104
To study the interaction between the viral pathogens and their hosts, by cDNA-AFLP technique, we screened the differentially expressed genes from the Nicotiana benthamiana plants after inoculated with Bamboo mosaic virus (BaMV), a single-stranded positive-sense RNA virus. Among those differentially expressed genes, one of the upregulated genes ACCT8-1 is an ortholog of N. tabacum elicitor inducible leucine-rich repeats (LRR) protein gene (EILP) and Cladosporium fulvum resistance genes cf-2 and cf-5. In the previous study, by Tobacco rattle virus (TRV)-based silencing system, we knocked down the expression of ACCT8-1 in plants and resulting in reduced BaMV coat protein accumulation and lesion size on the inoculated leaves. Furthermore, the accumulation of BaMV coat protein in the ACCT8-1-knockdown protoplasts showed no significant difference to that in the control protoplasts. The results suggest that ACCT8-1 might be involved in the movement step of the BaMV infection cycle. Since the similarity of this gene is very similar to the EILP of N. tabacum, thus we designated this gene as NbEILP. To further reveal how the NbEILP is involved in the movement of BaMV, we fused the green fluorescent protein (GFP) at the C-terminus of the NbEILP. Unfortunately, because of the large gene size about 3.2 kb in length, the expression of this gene in plants was shown very difficult to detect. We then construct a deletion mutant removing the leucine-rich repeats domain (ΔLRR). The accumulation of BaMV coat protein is enhanced in the NbEILP/ΔLRR-GFP transient expressed leaves. The results indicate that the leucine-rich repeats domain is not essential in assisting BaMV movement. We then based on this construct NbEILP/ΔLRR-GFP to create a few deletion mutants such as NbEILP/ΔLRRΔTMD (without transmembrane domain), NbEILP/ΔLRRΔCD (without cytoplasmic domain), and NbEILP/ΔLRRΔSP (without signal peptide) to examine if these domains are involved in BaMV movement. The results of transient expression indicated that the two mutants NbEILP/ΔLRRΔTMD and NbEILP/ΔLRRΔSP could not enhance the accumulation of BaMV as that of NbEILP/ΔLRR. These results also suggest that NbEILP requires the signal peptide to target the right location and the transmembrane domain to associate the membrane in assisting the cell-to-cell movement of BaMV.
Книги з теми "NBEAL2":
1
(Editor), Clarice P. Brantley, and Bobbye J. Davis (Editor), eds. The Changing Dimensions of Business Education: 1997 Nbea Yearbook (National Business Education Yearbook). National Business Education Association, 1997.
2
Rerreault, Heidi R. Classroom Strategies - The Methodology of Business Education: 1996 Nbea Yearbook (National Business Education Yearbook). National Business Education Association, 1996.
Тези доповідей конференцій з теми "NBEAL2":
1
Wu, Weiji, Tao Zheng, and Xitong Ning. "NBean: A HeteroPastry-Based P2P Proxy System." In 2009 5th International Conference on Wireless Communications, Networking and Mobile Computing (WiCOM). IEEE, 2009. http://dx.doi.org/10.1109/wicom.2009.5303154.
2
Zheng, Yuxuan, Huiwen Deng, Jianjun Chen, Jiaxiang Hu, and Weihao Hu. "Degradation trajectories prognosis for fuel cell based on MP-NBEATS." In 2023 IEEE 4th China International Youth Conference On Electrical Engineering (CIYCEE). IEEE, 2023. http://dx.doi.org/10.1109/ciycee59789.2023.10401570.
3
Huang, Song, Danhong Zhang, Tuo Zheng, Guangbo Tong, Jianxin Xu, and Fangzheng Jia. "Studies of short-term load forecasting model based on LSTM-NBEATS." In 2022 China Automation Congress (CAC). IEEE, 2022. http://dx.doi.org/10.1109/cac57257.2022.10055018.
4
S., Naveenkumar, Paras Rawat, Aditya Ganesh, Ashwath Ramakrishnan, Suresh Sankaranarayanan, and Anis Salwa Binti Mohd Khairuddin. "Energy Generation Forecasting Based on Seasonality Using Deep Learning." In International Technical Postgraduate Conference 2022. AIJR Publisher, 2022. http://dx.doi.org/10.21467/proceedings.141.5.
Анотація:
Energy forecasting is affected by various factors like seasonality, abrupt weather changes, system malfunctions, and lack of efficient resource management. Hence, towards meeting the energy demand of consumers, there is a need to generate energy efficiently which can be from renewable or nonrenewable sources like coal, wind, solar etc. This requires the need of machine learning and deep learning technique to forecast the generation of energy efficiently and economically. This work focuses on solving the issue related to energy generation forecasting by analyzing energy generation from various fuel sources over the course of 8 years by applying various techniques such as Bi-LSTM, Nbeats, ETS, Xgboost and MLP. From the performance analysis for four seasons, it has been concluded that Bi-LSTM performed the best overall 4 seasons with an average SMAPE of 20.412. This would really benefit utility companies in forecasting the fuel generation effectively in meeting the consumer demand.