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Artykuły w czasopismach na temat "RANKL"
Stejskal, David, Josef Bartek, Radmila Pastorkova, Viktor Ruzicka, Ivo Oral i Dalimil Horalik. "OSTEOPROTEGERIN, RANK, RANKL". Biomedical Papers 145, nr 2 (1.12.2001): 61–64. http://dx.doi.org/10.5507/bp.2001.013.
Pełny tekst źródłaNagy, Vanja, i Josef M. Penninger. "The RANKL-RANK Story". Gerontology 61, nr 6 (2015): 534–42. http://dx.doi.org/10.1159/000371845.
Pełny tekst źródłaSale, Craig, David C. Hughes, Julie P. Greeves, Trent Stellingwerff, Craig Ranson, William D. Fraser i Ian Varley. "Rankl/rank/opg Pathway". Medicine & Science in Sports & Exercise 46 (maj 2014): 268. http://dx.doi.org/10.1249/01.mss.0000493990.33112.e2.
Pełny tekst źródłaHanada, Reiko, Toshikatsu Hanada, Verena Sigl, Daniel Schramek i Josef M. Penninger. "RANKL/RANK—beyond bones". Journal of Molecular Medicine 89, nr 7 (29.03.2011): 647–56. http://dx.doi.org/10.1007/s00109-011-0749-z.
Pełny tekst źródłaBoyce, Brendan F., i Lianping Xing. "The RANKL/RANK/OPG pathway". Current Osteoporosis Reports 5, nr 3 (wrzesień 2007): 98–104. http://dx.doi.org/10.1007/s11914-007-0024-y.
Pełny tekst źródłaHofbauer, L. C. "Bedeutung des RANK/RANKL/OPGSignalwegs für den Knochenstoffwechsel". Osteologie 19, nr 04 (2010): 354–57. http://dx.doi.org/10.1055/s-0037-1619956.
Pełny tekst źródłaHooshiar, Saeedeh Hosseini, Mohammad Tobeiha i Sadegh Jafarnejad. "Soy Isoflavones and Bone Health: Focus on the RANKL/RANK/OPG Pathway". BioMed Research International 2022 (25.10.2022): 1–10. http://dx.doi.org/10.1155/2022/8862278.
Pełny tekst źródłaAslan, Figen, i Ülkü Küçük. "RANK and RANKL Expression in Salivary Gland Tumors". Ear, Nose & Throat Journal 99, nr 7 (11.06.2020): 475–80. http://dx.doi.org/10.1177/0145561320930640.
Pełny tekst źródłaXing, Lianping, Edward M. Schwarz i Brendan F. Boyce. "Osteoclast precursors, RANKL/RANK, and immunology". Immunological Reviews 208, nr 1 (grudzień 2005): 19–29. http://dx.doi.org/10.1111/j.0105-2896.2005.00336.x.
Pełny tekst źródłaBoyce, Brendan F., i Lianping Xing. "Biology of RANK, RANKL, and osteoprotegerin". Arthritis Research & Therapy 9, Suppl 1 (2007): S1. http://dx.doi.org/10.1186/ar2165.
Pełny tekst źródłaRozprawy doktorskie na temat "RANKL"
Navet, Benjamin. "Homéogènes Dlx, signalisation RANK/RANKL et ostéosarcomes". Thesis, Nantes, 2016. http://www.theses.fr/2016NANT1018/document.
Pełny tekst źródłaOsteosarcoma (OS), the most common malignant primary bone tumor, is characterized by an osteoid formation occasionally associated with osteolysis. De-spite therapeutic advances, the 5-years survival rate remains low (30% in case of metastasis or drug-resistance). New therapeutic approaches targeting the tumor cell and its environment are needed. Presented studies focused on potential pro-tumor factors namely Dlx genes and a key signaling pathway of the bone environment (RANKL / RANK) that may influence tumor aggressiveness. The OS is an osteo-blastic tumor and Dlx family was chosen due to its in-volvement in osteoblastogenesis. RANKL / RANK path-way was selected as it constitutes a main element in the coupling between osteoblasts and osteoclasts. A link between Dlx genes and RANK signaling was suspected. Dlx1, Dlx4 and Rank genes are not normally ex-pressed in osteoblasts but are present in the OS cell lines. Dlx and Rank expression modulations were real-ized to assess the impact on tumor cells. RANK / RANKL signaling involvement in the tumor microenvi-ronment was analyzed. Disruption of remodeling is in favor of the tumor taking part in the establishment of a vicious circle between tumor and environment. This work established the involvement of Dlx, espe-cially DLX4 to which a new coding transcript has been characterized. However, additional studies are needed. Regarding the RANK / RANKL signaling, it turns out that beyond the vicious circle, leading to tumor initiation stage, the RANK expression by the tumor proves to be pro-metastatic elements
Yoskovitz, Guy. "Genetic Polymorphisms of RANK, RANKL and their relation to osteoporosis (Polimorfismos genéticos de RANK y RANKL y su relación con la osteoporosis)". Doctoral thesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/98294.
Pełny tekst źródłaLa osteoporosis es la enfermedad metabólica ósea más frecuente. Está definida como un trastorno esquelético sistémico caracterizado por una disminución de la densidad mineral ósea (DMO) y alteraciones en la microarquitectura del tejido óseo, con un consecuente incremento de la fragilidad ósea y del riesgo de fractura. Su complejidad genética permanece incompletamente definida. La DMO viene marcada por un remodelado óseo basado en ciclos de resorción y formación que suceden a lo largo de toda la vida del organismo. Este proceso, está regulado en parte por un conjunto de reacciones proteicas pertenecientes al sistema conocido como RANK/RANKL/OPG. La especial importancia de RANK, así como la interacción de éste con su ligando RANKL, recae en el hecho que, son factores clave tanto en el desencadenamiento de la diferenciación como de la supervivencia osteoclástica. El estudio se centra en el análisis detallado de variantes pertenecientes a ambos genes, seguido del estudio funcional correspondiente. Se ha replicado la asociación del SNP rs9594738 con la DMO, una variante genética localizada a 184 kb 5' del gen RANKL. Los resultados del estudio funcional muestran que la región que engloba dicha variante actúa como un regulador distal de RANKL, ejerciendo efectos en su expresión que varían en presencia ó ausencia de vitamina D. Además, se identificaron dos SNPs (rs78326403 y rs884205) en el 3’UTR de RANK, asociados con fracturas por bajo traumatismo en nuestra cohorte. Por último, una interacción significativa entre rs78326403 y rs9594738 en la determinación del riesgo de fractura, pone de relieve la importancia de la DMO baja y de la microarquitectura como predictores genéticamente determinados del riesgo de fractura que se deben evaluar con el uso de diversas técnicas.
Hamoudi, Dounia. "Implication de la voie RANK/RANKL/OPG dans la physiopathologie musculaire et potentiel thérapeutique de l’anti-RANKL pour la dystrophie musculaire de Duchenne". Doctoral thesis, Université Laval, 2021. http://hdl.handle.net/20.500.11794/69507.
Pełny tekst źródłaManfrin, Thais Mara [UNESP]. "Imunomarcação das proteínas OPG, RANK e RANKL em dentes reimplantados de rato". Universidade Estadual Paulista (UNESP), 2007. http://hdl.handle.net/11449/101206.
Pełny tekst źródłaO sistema OPG, RANK e RANKL é uma das mais importantes descobertas da biologia óssea. Essas proteínas regulam as atividades celulares na remodelação do tecido ósseo e na literatura há diversas investigações nos tecidos dentários. No entanto, no reimplante dentário, ainda não foram encontrados relatos. Foi objetivo deste trabalho, avaliar a imunomarcação das proteínas OPG, RANK e RANKL em dentes reimplantados de rato. Um grupo controle foi formado com quatro ratos no qual o reimplante dentário não foi realizado. Vinte e quatro ratos (Rattus norvegicus, albinus) tiveram seu incisivo superior extraído e depois reimplantado formando os seguintes grupos: grupo I – reimplante imediato; grupo II - reimplante tardio sem tratamento e grupo III - reimplante tardio com tratamento endodôntico (ressecção da papila dentária e preenchimento do canal com pasta de hidróxido de cálcio) e tratamento da superfície radicular (raspagem mecânica do ligamento periodontal necrosado e imersão em solução de flúor fosfato acidulado de sódio a 2,5%). Ao final dos períodos experimentais (10 e 60 dias) os ratos foram eutanasiados. Foram obtidos cortes longitudinais parafinados com 6μm de espessura. Os cortes foram submetidos à reação imunoístoquímica mediante a utilização de anticorpos primários para OPG, RANK e RANKL. Os resultados mostraram que a imunomarcação de OPG e RANKL ocorreu em todos os grupos e períodos estudados, muito embora RANKL não tenha sido observada no grupo reimplante imediato aos 60 dias. RANK foi observada somente aos 10 dias de todos os grupos no qual o reimplante foi realizado. A análise qualitativa dos resultados demonstrou que o sistema OPG, RANK e RANKL apresentou marcação evidente no reimplante tardio, sugerindo a efetiva participação no início do processo de reabsorção radicular, uma vez que aos 60 dias a imunomarcação foi discreta.
The OPG, RANK and RANKL system is one of the most important discoveries in bone biology. These proteins are key regulators of bone remodeling and in the literature there are several studies of tooth resorption. However, in tooth replantation, reports have not been found. The purpose of this study was to determine the immunolabeling of OPG, RANK and RANKL in replanted teeth in rats, using immunohistochemistry methodology. A control group (no replanted teeth) was formed by four rats. Twenty-four rats (Rattus norvegicus, albinus) were submitted to the extraction of their upper right incisors. The replantation was performed according to the groups below: group I – immediate replantation; group II – delay replantation without treatment and group III – delay replantation with endodontic treatment (extirpation of papilla and the root canal filled with calcium hydroxide) and root surface treatment (periodontal ligament was removed with scalpel and teeth were immersed in 2% acidulated phosphate sodium fluoride). The animals were euthanized at the end of the experimental periods (10 and 60 days). Longitudinal 6μm slices embedded in paraffin were obtained. The slices were submitted to immunohistochemistry reaction by means of the primary antibodies for OPG, RANK and RANKL proteins. The results showed the expression of OPG in all groups and periods. RANKL expression was observed in all groups, except in the immediate replanted teeth group (60 days). RANK expression was observed only at 10 days in all groups which replantation was performed. The qualitative analysis of our findings indicated that the system OPG, RANK and RANKL presented strong expression in delayed replantation, suggesting effective participation at the beginning of root resorption, since at 60 days the immunostained cells were discreet.
Manfrin, Thais Mara. "Imunomarcação das proteínas OPG, RANK e RANKL em dentes reimplantados de rato /". Araçatuba : [s.n.], 2007. http://hdl.handle.net/11449/101206.
Pełny tekst źródłaAbstract: The OPG, RANK and RANKL system is one of the most important discoveries in bone biology. These proteins are key regulators of bone remodeling and in the literature there are several studies of tooth resorption. However, in tooth replantation, reports have not been found. The purpose of this study was to determine the immunolabeling of OPG, RANK and RANKL in replanted teeth in rats, using immunohistochemistry methodology. A control group (no replanted teeth) was formed by four rats. Twenty-four rats (Rattus norvegicus, albinus) were submitted to the extraction of their upper right incisors. The replantation was performed according to the groups below: group I - immediate replantation; group II - delay replantation without treatment and group III - delay replantation with endodontic treatment (extirpation of papilla and the root canal filled with calcium hydroxide) and root surface treatment (periodontal ligament was removed with scalpel and teeth were immersed in 2% acidulated phosphate sodium fluoride). The animals were euthanized at the end of the experimental periods (10 and 60 days). Longitudinal 6μm slices embedded in paraffin were obtained. The slices were submitted to immunohistochemistry reaction by means of the primary antibodies for OPG, RANK and RANKL proteins. The results showed the expression of OPG in all groups and periods. RANKL expression was observed in all groups, except in the immediate replanted teeth group (60 days). RANK expression was observed only at 10 days in all groups which replantation was performed. The qualitative analysis of our findings indicated that the system OPG, RANK and RANKL presented strong expression in delayed replantation, suggesting effective participation at the beginning of root resorption, since at 60 days the immunostained cells were discreet.
Orientador: Wilson Roberto Poi
Coorientador: Roberta Okamoto
Banca: Sônia Regina Panzarini Barioni
Banca: Celso Koogi Sonoda
Banca: Luiz Guilherme Brentegani
Banca: Mirian Marubayashi Hidalgo
Doutor
Cordeiro, Olga. "From lymph node embryogenesis to homeostasis : new insights into the functions of stromal RANKL (TNFSF11)". Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ075/document.
Pełny tekst źródłaRANKL and RANK are members of the TNF-superfamily and TNF-receptor superfamily, respectively. They are known to play an important role in the regulation of bone mass and in the development and the function of the immune system. However questions still remain. We have used genetically modified mice to address some of these questions, in particular by using a mouse whose lymph node marginal reticular stromal cells lack RANKL. The results obtained during this PhD provide important new insights into the positive impact of stromal RANKL on lymph node macrophages concomitant with enhanced B cell function and reduced viral pathogenicity. We found that stromal RANKL regulates lymphotoxin and CXCL13 expression, two key molecules for B cell homeostasis and secondarylymphoid organ cellular integrity. RANKL activity seems to follow a temporal hierarchy over lymphotoxin/TNFα, as the phenotype caused by stromal RANKL-deficiency has increased penetrance with age. Furthermore, we demonstrate that RANKL activates lymph node lymphatic endothelial cells and found that the integrin ITGA2b is a new indicator for activated lymphatic endothelial cells. Thus, together with MAdCAM-1, ITGA2b serves as a novel marker for those lymphatic endothelial cells that are constitutively activated by stromal RANKL. Altogether, the data reinforce the importance of RANKL for the lymph node homeostasis and uncover here to unknown mechanisms of RANKL functions.In light of this and the fact that RANKL is responsive to female hormones, we studied the role of RANKL in the Sjögrens syndrome, a chronic inflammatory disease of salivary and lacrimal glands with a strong female sex bias. We provide evidence that RANKL neutralization reduces tertiary lymphoid organ size. On the perspective side, a possible cross talk between lymph node lymphatic endothelial cells and macrophages or marginal reticular cells remains to be clarified.Furthermore, further work is required to elucidate the mechanism by which RANKL stimulates chronic inflammatory diseases presenting tertiary lymphoid structures, in order to make RANKL a new target for therapy
Nascimento, Mariele Andrade do. "Associação entre polimorfismos genéticos em RANK, RANKL e OPG com alterações nas dimensões craniofaciais". Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/58/58135/tde-20112017-095844/.
Pełny tekst źródłaThe objective of the present study was to evaluate, in humans, the association between genetic polymorphisms in the RANK/ RANKL/OPG system with alterations in craniofacial dimensions. A total of 100 unrelated Brazilian Caucasians were included in this study. DNA was extracted from the saliva of each of the participants and the polymorphisms rs3826620, rs9594738 and rs2073618 in RANK, RANKL and OPG, respectively, were analyzed by real-time PCR. To evaluate the craniofacial dimensions, three angular measurements (SNA, SNB and ANB) and four linear measurements (Co-Gn, Go-Pg, Co-Go and PTM-A) were obtained from cephalometric tracings. To compare the difference between the means of the linear and angular measurements according to the genotype, Kruskal-Wallis followed by Dunn post test or ANOVA followed by the Tukey post test was used. Linear regression analysis was also used to adjust the possible influence of age and gender on each linear maxillary and mandibular measure. The Hardy-Weinberg equilibrium was also evaluated using the chi-square test within each polymorphism. The level of significance was 5%. The results demonstrated that there were no statistically significant association between the genotypic distribution of RANK, RANKL, OPG, and the angules SNA, SNB and according to the phenotypic distribution (Class I, Class II or Class III of skeletal pattern) (p> 0.05). A statistically significant difference was observed between the distribution of mandibular base length measurements according to the RANK genotypes, where the GG genotype showed a higher Go-Pg measurement (p=0.039). In the multivariate analysis, a statistically significant association was found for RANK and mandibular (Go-Pg and Co-Gn) polymorphisms (p<0.05). Measurement of the maxilla was not associated with any polymorphism. It was concluded that there was an association between genetic polymorphism rs3826620 in RANK with a greater mandibular dimension, in which the length of the mandible (Co-Gn) and the length of the base of the mandible (Go-Pg) were increased.
Dumont, Nicolas. "Atrophie, croissance et fonction musculaire : l'impact des leucocytes et de la triade RANK/RANKL/OPG". Thesis, Université Laval, 2013. http://www.theses.ulaval.ca/2013/29749/29749.pdf.
Pełny tekst źródłaMuscle atrophy and dysfunction are characterized by a loss of muscle mass and force, which are commonly found in many pathologies or conditions such as AIDS, cancers, chronic obstructive pulmonary diseases, cast immobilization, hypogravity, bed rest or aging, to name a few. Muscle atrophy/dysfunction have also very high social and economic costs, but very few laboratories have investigated the cellular and molecular mechanisms behind these muscular problems. The aim of this thesis is therefore to enhance our understanding of different mechanisms governing muscle atrophy/dysfunction and regrowth by using different models of disuse and dystrophy. Thus, we have initially explored the roles of different leucocytes in atrophied and reloaded soleus muscle. Firstly, we looked at the role of mast cells and showed that the mechanical stress associated with muscle reloading is able to stimulate mast cell degranulation, which orchestrates the recruitment of neutrophils and monocytes/macrophages. Secondly, our experiments revealed that neutrophil activity is adaptable and that neutrophil-induced tissue damage is dependent on the microenvironment. In atrophied and reloaded muscles, the presence of neutrophils is not associated with secondary damage or promotion of muscle recovery. Thirdly, we demonstrated that the presence of macrophages is essential for optimal muscle force recovery from atrophy. Fourthly, we showed that the macrophage-colony stimulating factor (M-CSF) promote the myogenic activity of macrophages by stimulating their anti-inflammatory phenotype. Finally, we investigated the impact of the receptor activator of NF-kB (RANK) and its ligand RANKL, a signalling pathway involved in bone remodelling and osteoporosis, on muscle atrophy and dysfunction. Our results showed that the specific deletion of RANK in the muscle or the blockage of RANKL with osteoprotegerin increased significantly force production in denervated and dystrophic muscles. These results were associated with various modifications in calcium handling protein expression favouring efficient calcium uptake. Moreover, we also demonstrated that RANK activation gives preference to the reconversion from fast-to-slow muscle fibers following hindlimb unloading/reloading. Overall, our results bring a better understanding of different mechanisms related to muscle atrophy, dysfunction and regrowth and potentially open new avenues for the treatment of several debilitating skeletal muscle conditions.
Loureiro, Melina Bezerra. "Estudo da associa??o dos genes RANk, RANKL e OPG com a osteopatia diab?tica". Universidade Federal do Rio Grande do Norte, 2014. http://repositorio.ufrn.br/handle/123456789/19413.
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Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior - CAPES
Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico - CNPq
O objetivo do presente trabalho foi avaliar a express?o de RNAm e os polimorfismos dos genes RANK, RANKL e OPG de crian?as, adolescentes e adultos jovens com DM1, bem como estudar a associa??o dos mesmos com o desenvolvimento de altera??es no metabolismo ?sseo.No total, foram inclu?dos no estudo 119 crian?as e adolescentes com DM1 e 161 indiv?duos normoglic?micos (NG) da mesma faixa et?ria. Foram pesquisados os polimorfismos dos genes OPG (1181 G>C e 163 A>G), RANK (575 C>T e 3'UTR C>A) e RANKL (?ntron A>G) e determinadas as express?es g?nicas de OPG, RANK e RANKL. Al?m disso, foram avaliados o controle glic?mico e par?metros laboratoriais de fun??o ?ssea, al?m da densitometria ?ssea. Os indiv?duos com DM1 apresentaram um controle glic?mico insatisfat?rio e valores diminuidos de c?lcio total, propept?deo do col?geno tipo 1 (CTX), como tamb?m baixa densidade mineral ?ssea, quando comparados com os NG (p<0,05). O polimorfismo OPG 1181 G>C pode estar associado com susceptibilidade ao DM1 (p=0,054). Estudando apenas os indiv?duos com DM1, foi observado que os carreadores do gen?tipo OPG 1181 GG apresentaram maiores concentra??es de c?lcio ionizado no modelo recessivo (p<0,05). Esses resultados sugerem que o polimorfismo OPG 1181 G>C pode contribuir para o desenvolvimento do DM1 e da osteopatia diab?tica.
Camara, Abdouramane. "Control of lymphoid organ CD169+ macrophage differentiation by stromal cells through the RANK-RANKL axis". Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ102.
Pełny tekst źródłaLymph node CD169 + sinusoidal macrophages are sentinel cells that recognize the danger signals and initiate the protective immune responses. However, the signals and the mechanism underlying their formation are not well known. During my thesis, I have shown that the cytokine Receptor Activator of NF-kB Ligand (RANKL) is required for their differentiation, starting from the embryogenesis up to four weeks after birth. The lymphatic endothelial cells (LECs) activated by RANKL expressed by mesenchymal cells form the niches for the primary differentiation of these macrophages. Yet, in adults, RANKL-activated LECs are required for their niche replenishment after transient depletion induced by an inflammatory stimulus. Beyond lymph node, my research has revealed a general requirement of the double signal RANKL & lymphotoxin LTα1β2 for the differentiation of non-osteoclastic CD169 + macrophages of spleen and bone marrow
Książki na temat "RANKL"
Bingaman, Steven A. The history of American ranks and rank insignia. United States]: [publisher not identified ], 2013.
Znajdź pełny tekst źródłagroup), Fishamble (Theater, red. Rank. London: Nick Hern Books, 2008.
Znajdź pełny tekst źródłaCabban, Peter T. Breaking ranks. Milsons Point, N.S.W: Random House Australia, 2005.
Znajdź pełny tekst źródłaAylin, Clyde. Breaking ranks. Braunton: Merlin, 1989.
Znajdź pełny tekst źródłaMoprofesara ranko. Pretoria: Via Africa, 1992.
Znajdź pełny tekst źródłaRōhita, Bōgollāgama, i Eksat Jātika Pakṣaya (Sri Lanka), red. Nāyaka Ranil. Śrī Jayavardhanapura: Eksat Jātika Pakṣaya, 1996.
Znajdź pełny tekst źródłaGoga, Lamratu M. Inda ranka. Nigeria]: [s.n.], 1999.
Znajdź pełny tekst źródłaNakajima, Shigeo. Tadanai rankō. Tōkyō: Rippū Shobō, 1988.
Znajdź pełny tekst źródłaSchütt, Hans-Dieter. Uta Ranke. Berlin: Elefanten Press, 1993.
Znajdź pełny tekst źródłaClosing ranks. London: Viking, 1997.
Znajdź pełny tekst źródłaCzęści książek na temat "RANKL"
Nakashima, Tomoki, i Hiroshi Takayanagi. "RANK and RANKL". W Encyclopedia of Signaling Molecules, 4445–54. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_633.
Pełny tekst źródłaLeibbrandt, Andreas, i Josef M. Penninger. "RANK–RANKL Signaling". W Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_4945-2.
Pełny tekst źródłaMartemyanov, Kirill A., Pooja Parameswaran, Irene Aligianis, Mark Handley, Marga Gual-Soler, Tomohiko Taguchi, Jennifer L. Stow i in. "RANK and RANKL". W Encyclopedia of Signaling Molecules, 1581–89. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_633.
Pełny tekst źródłaLeibbrandt, Andreas, i Josef M. Penninger. "RANK–RANKL Signaling". W Encyclopedia of Cancer, 3899–903. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_4945.
Pełny tekst źródłaLeibbrandt, Andreas, i Josef M. Penninger. "RANK-RANKL Signaling". W Encyclopedia of Cancer, 3165–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4945.
Pełny tekst źródłaStein, Nicola, Martina Rauner i Lorenz C. Hofbauer. "RANKL Inhibition: Clinical Data". W Principles of Osteoimmunology, 217–40. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0520-7_10.
Pełny tekst źródłaSipos, Wolfgang. "RANKL Inhibition: Preclinical Data". W Principles of Osteoimmunology, 197–215. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0520-7_9.
Pełny tekst źródłaHofbauer, Lorenz, i Tilman Rachner. "Die Rolle des RANK/RANKL/OPG-Signalwegs im Knochenstoffwechsel". W Fortbildung Osteologie, 118–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-05385-6_26.
Pełny tekst źródłaBrown, Julie M., Jian Zhang i Evan T. Keller. "OPG, RANKL, and RANK in Cancer Metastasis: Expression and Regulation". W Cancer Treatment and Research, 149–72. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9129-4_7.
Pełny tekst źródłaLeibbrandt, Andreas, i Josef M. Penninger. "TNF Conference 2009: Beyond Bones – RANKL/RANK in the Immune System". W Advances in Experimental Medicine and Biology, 5–22. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6612-4_2.
Pełny tekst źródłaStreszczenia konferencji na temat "RANKL"
Remoto, Júlia Maranghetti, Maria Eduarda Ramos Cezine, Paulo Henrique Cavalcanti De Araújo i Mariana Kiomy Osako. "EXPRESSÃO DE RANK-RANKL-OPG NA DIFERENCIAÇÃO DE CÉLULAS MUSCULARES ESQUELÉTICAS". W I Congresso Nacional On-line de Biologia Celular e Estrutural. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1947.
Pełny tekst źródłaSun, Y. "IL-17A-Dependent Lymphoid Neogenesis in COPD Involves RANKL-RANK Expression". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3768.
Pełny tekst źródłaSharma, Bhawna, Michelle L. Varney i Rakesh K. Singh. "Abstract 4968: Chemotherapy up-regulates RANK-RANKL signaling in breast cancer cells." W Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4968.
Pełny tekst źródłaSousa, Sofia, Evelyne Gineyts, Sandra Geraci, Martine Croset i Philippe Clézardin. "Abstract 29: RANK-RANKL signaling inhibition delays early breast cancer bone metastasis formation". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-29.
Pełny tekst źródłaIntemann, J., C. Wehmeyer, V. Kracke, E. Werbenko, P. Paruzel, I. Kramer, M. Kneissel, T. Pap i B. Dankbar. "P081 Sclerostin affects rankl-mediated osteoclast differentiation". W 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.98.
Pełny tekst źródłaBoorsma, Carian, Christina Draijer, Robbert Cool, Corry-Anke Brandsma, George Nossent, Peter Heukels, Bernt Van den Blink, David Brass, Wim Timens i Barbro Melgert. "The RANKL-OPG balance in pulmonary fibrosis". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3809.
Pełny tekst źródłaWieser, V., I. Tsibulak, C. Degasper, H. Welponer, K. Leitner, S. Sprung, J. Haybäck, H. Fiegl, C. Marth i AG Zeimet. "RANKL als unabhängiger Prognoseparameter für Patientinnen mit Ovarialkarzinom". W Kongressabstracts zur Wissenschaftlichen Tagung der Arbeitsgemeinschaft für gynäkologische Onkologie (AGO) der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG). Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1682001.
Pełny tekst źródłaJacob, A., D. Branstetter, K. Rohrbach, A. Winters, R. Erwert, S. Allred, J. Jones i in. "P3-01-14: RANK and RANK Ligand (RANKL) Expression in Invasive Breast Carcinoma and Human Breast Cancer Cell Lines." W Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p3-01-14.
Pełny tekst źródłavan de Luijtgaarden, Addy, Manon Leus, Melissa Roeffen, Uta Flucke, Ingrid van der Geest, Winette van der Graaf i Yvonne Versleijen-Jonkers. "Abstract 655: Prognostic relevance of the RANK/RANKL/OPG triad and the IGF1R pathway in osteosarcoma". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-655.
Pełny tekst źródłaSILVA, AMANDA LORRAINE PEREIRA, i CINTIA GRAZIELY MIRANDA AZEVEDO. "A RELEVÂNCIA DO ESTROGÊNIO NO DESENVOLVIMENTO DA OSTEOPOROSE". W I Congresso Brasileiro de Doenças Crônicas On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/cronics/6633.
Pełny tekst źródłaRaporty organizacyjne na temat "RANKL"
Bhatia, Pardeep. Study of RANKL Expression in Metastatic Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2002. http://dx.doi.org/10.21236/ada405313.
Pełny tekst źródłaBhatia, Pardeep. Study of RANKL Expression in Metastatic Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2003. http://dx.doi.org/10.21236/ada418749.
Pełny tekst źródłaHossain, Niamat Ullah Ibne, Farjana Nur, Raed Jaradat, Seyedmohsen Hosseini, Mohammad Marufuzzaman, Stephen Puryear i Randy Buchanan. Metrics for assessing overall performance of inland waterway ports : a Bayesian Network based approach. Engineer Research and Development Center (U.S.), maj 2021. http://dx.doi.org/10.21079/11681/40545.
Pełny tekst źródłaWeber, G. F., i D. L. Laudal. Low-rank coal research. Office of Scientific and Technical Information (OSTI), styczeń 1989. http://dx.doi.org/10.2172/7045956.
Pełny tekst źródłaKryzhanivs'kyi, Evstakhii, Liliana Horal, Iryna Perevozova, Vira Shyiko, Nataliia Mykytiuk i Maria Berlous. Fuzzy cluster analysis of indicators for assessing the potential of recreational forest use. [б. в.], październik 2020. http://dx.doi.org/10.31812/123456789/4470.
Pełny tekst źródłaNybom, Martin, Toru Kitagawa i Jan Stuhler. Measurement error and rank correlations. The IFS, kwiecień 2018. http://dx.doi.org/10.1920/wp.cem.2081.2818.
Pełny tekst źródłaMann, M., M. Johnson, S. Selle i J. Gunderson. Low-rank coal slurry combustion. Office of Scientific and Technical Information (OSTI), maj 1988. http://dx.doi.org/10.2172/6936637.
Pełny tekst źródłaCucuringu, Mihai. Sync-rank: Robust Ranking, Constrained Ranking and Rank Aggregation via Eigenvector and SDP Synchronization. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2015. http://dx.doi.org/10.21236/ada625017.
Pełny tekst źródłaHenry, Marc, Alfred Galichon, Victor Chernozhukov i Marc Hallin. Monge-Kantorovich depth, quantiles, ranks and signs. IFS, styczeń 2015. http://dx.doi.org/10.1920/wp.cem.2015.0415.
Pełny tekst źródłaGalichon, Alfred, Marc Hallin, Victor Chernozhukov i Marc Henry. Monge-Kantorovich depth, quantiles, ranks and signs. Institute for Fiscal Studies, wrzesień 2015. http://dx.doi.org/10.1920/wp.cem.2015.5715.
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