Academic literature on the topic 'Caveolina-1'

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Journal articles on the topic "Caveolina-1"

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Pereira-Prado, Vanesa, Gabriel Tapia, and Ronell Bologna-Molina. "CAVEOLINA-1 implicaciones fisiológicas y patológicas." Odontoestomatología 19, no. 30 (2017): 92–98. http://dx.doi.org/10.22592/ode2017n30a10.

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Llaverias, G., J. C. Laguna, and M. Alegret. "Regulación de la expresión de caveolina-1 en macrófagos por agonistas PPAR." Clínica e Investigación en Arteriosclerosis 17, no. 5 (2005): 213–22. http://dx.doi.org/10.1016/s0214-9168(05)73345-3.

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Mora García, Gustavo, María Stephany Ruiz Díaz, Ángelo Alario Bello, Doris Gómez Camargo, and Claudio Gómez Alegría. "Asociación entre el gen de caveolina 1 (cav1) y el riesgo cardiovascular en adultos." Revista Colombiana de Endocrinología, Diabetes & Metabolismo 5, no. 1 (2018): 15–21. http://dx.doi.org/10.53853/encr.5.1.337.

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La caveolina 1 es una proteína estructural que interviene en diversos procesos metabólicos. En estudios de asociación genética, el gen que la codifica CAV1 (7q31.2) se ha asociado a resistencia a la insulina, hipertensión, hipertrigliceridemia y c-HDL bajo. Sin embargo, se desconoce si variantes en CAV1 se asocian a obesidad e incremento en el riesgo cardiovascular (RCV).
 Objetivo: Analizar la posible asociación entre variantes en CAV1 con el RCV en población del caribe colombiano.Metodología: Se realizó un estudio de asociación genética con 595 adultos de Cartagena de Indias. Se hizo la
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Rodríguez, Héctor, Iván Silva, Leonella Jiménez, et al. "Presencia cualitativa y distribución de caveolina 1 (cav-1) en la celularidad y estadios del ciclo de la espermatogénesis." Revista Internacional de Andrología 7, no. 2 (2009): 92–97. http://dx.doi.org/10.1016/s1698-031x(09)71613-9.

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Sotgia, Federica, Babak Razani, Gloria Bonuccelli, et al. "Intracellular Retention of Glycosylphosphatidyl Inositol-Linked Proteins in Caveolin-Deficient Cells." Molecular and Cellular Biology 22, no. 11 (2002): 3905–26. http://dx.doi.org/10.1128/mcb.22.11.3905-3926.2002.

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ABSTRACT The relationship between glycosylphosphatidyl inositol (GPI)-linked proteins and caveolins remains controversial. Here, we derived fibroblasts from Cav-1 null mouse embryos to study the behavior of GPI-linked proteins in the absence of caveolins. These cells lack morphological caveolae, do not express caveolin-1, and show a ∼95% down-regulation in caveolin-2 expression; these cells also do not express caveolin-3, a muscle-specific caveolin family member. As such, these caveolin-deficient cells represent an ideal tool to study the role of caveolins in GPI-linked protein sorting. We sho
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Isvoran, Adriana, Dana Craciun, Alecu Ciorsac, et al. "A bioinformatics study concerning structural and functional properties of human caveolin proteins." Journal of the Serbian Chemical Society 79, no. 2 (2014): 133–50. http://dx.doi.org/10.2298/jsc130716100i.

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We performed a bioinformatics study to predict and compare the structural and functional properties of human caveolins: caveolin-1, -2 and -3. The computed local physico-chemical properties, predictions of their secondary structure elements and interacting partners of caveolin-2 and -3 are compared to experimentally proved structural and functional properties of caveolin-1. These data combined with the sequences alignment of the three caveolins, allowed predicting and characterizing the functional domains of caveolin-2 and -3. The hydrophobic regions of these proteins are highly similar in seq
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Costa, Maria José, Maximin Senou, Fabienne Van Rode, et al. "Reciprocal Negative Regulation between Thyrotropin/3′,5′-Cyclic Adenosine Monophosphate-Mediated Proliferation and Caveolin-1 Expression in Human and Murine Thyrocytes." Molecular Endocrinology 21, no. 4 (2007): 921–32. http://dx.doi.org/10.1210/me.2006-0328.

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Abstract The expression of caveolins is down-regulated in tissue samples of human thyroid autonomous adenomas and in the animal model of this disease. Because several cell types present in thyroid express caveolins, it remained unclear if this down-regulation occurs in thyrocytes and which are the mechanism and role of this down-regulation in the tumor context. Here we show that prolonged stimulation of isolated human thyrocytes by TSH/cAMP/cAMP-dependent protein kinase inhibits caveolins’ expression. The expression of caveolins is not down-regulated by activators of other signaling pathways r
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Ratajczak, Philippe, Patricia Oliviéro, Françoise Marotte, Frantisek Kolar, Bohuslav Ostadal, and Jane-Lise Samuel. "Expression and localization of caveolins during postnatal development in rat heart: implication of thyroid hormone." Journal of Applied Physiology 99, no. 1 (2005): 244–51. http://dx.doi.org/10.1152/japplphysiol.01292.2004.

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Caveolins modulate signaling pathways involved in cardiac development. Caveolin-1 exists in two isoforms: the β-isoform derivates from an alternative translational start site that creates a protein truncated by 31 amino acids, mainly expressed in endothelial cells, whereas caveolin-3 is present in muscle cells. Our aim was to define caveolin distribution and expression during cardiac postnatal development using immunofluorescence and Western blotting. Caveolin-3 sarcolemmal labeling appeared as dotted lines from days 1 to 5 and as continuous lines after 14 days of age. Caveolin-3 expression, l
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Pol, Albert, Sally Martin, Manuel A. Fernandez, et al. "Dynamic and Regulated Association of Caveolin with Lipid Bodies: Modulation of Lipid Body Motility and Function by a Dominant Negative Mutant." Molecular Biology of the Cell 15, no. 1 (2004): 99–110. http://dx.doi.org/10.1091/mbc.e03-06-0368.

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Caveolins are a crucial component of caveolae but have also been localized to the Golgi complex, and, under some experimental conditions, to lipid bodies (LBs). The physiological relevance and dynamics of LB association remain unclear. We now show that endogenous caveolin-1 and caveolin-2 redistribute to LBs in lipid loaded A431 and FRT cells. Association with LBs is regulated and reversible; removal of fatty acids causes caveolin to rapidly leave the lipid body. We also show by subcellular fractionation, light and electron microscopy that during the first hours of liver regeneration, caveolin
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Razani, B., A. Schlegel, and M. P. Lisanti. "Caveolin proteins in signaling, oncogenic transformation and muscular dystrophy." Journal of Cell Science 113, no. 12 (2000): 2103–9. http://dx.doi.org/10.1242/jcs.113.12.2103.

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In adult animals and humans, signal transduction maintains homeostasis. When homeostatic mechanisms are interrupted, an illness or disease may ensue. Caveolae are plasma membrane specializations that contain the structural proteins caveolins, and appear to be important for normal signal transduction. The caveolin scaffolding domain interacts with several signaling molecules, sequestering them in the absence of activating signals, and thereby reducing the signal-to-noise ratio. Deletion and mutation of genes that encode caveolins is implicated in the pathogenesis of several human diseases. Down
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Dissertations / Theses on the topic "Caveolina-1"

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Zampier, Carolina da Paz. "Papel de caveolina-1 na produção de mediadores inflamatórios." Instituto Oswaldo Cruz, 2012. https://www.arca.fiocruz.br/handle/icict/7031.

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Submitted by Alessandra Portugal (alessandradf@ioc.fiocruz.br) on 2013-10-01T21:53:22Z No. of bitstreams: 1 Carolina da Paz Zampier.pdf: 2134379 bytes, checksum: d822f378a88e2cf44b02c5ea60f52ea0 (MD5)<br>Made available in DSpace on 2013-10-01T21:53:22Z (GMT). No. of bitstreams: 1 Carolina da Paz Zampier.pdf: 2134379 bytes, checksum: d822f378a88e2cf44b02c5ea60f52ea0 (MD5) Previous issue date: 2012<br>Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil<br>A caveolina-1 (Cav-1), uma proteína essencial para a formação de cavéolas, apresenta atividade na modulação da sinali
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Lagares, Tena Laura María. "Caveolina-1 en la progresión metastásica del Sarcoma de Ewing." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/145475.

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El sarcoma de Ewing (SE) es el segundo tumor óseo maligno infantil más frecuente y presenta una alta incidencia de enfermedad metastásica. Este tipo de tumores presentan una translocación génica característica que da origen a una proteína de fusión, normalmente EWS/FLI1. Esta proteína de fusión actúa como factor de transcripción aberrante, regulando la expresión de diferentes genes implicados en la iniciación, mantenimiento y progresión del tumor. Nuestro grupo describió como uno de estos genes diana a caveolina 1 (CAV1), describiendo además su papel determinante en el fenotipo maligno del SE,
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Díaz, Valdivia Natalia. "E-cadherina reduce la habilidad promotora de migración y metástasis de caveolina-1 por la disminución de la fosforilación de caveolina-1 en células metastásicas." Tesis, Universidad de Chile, 2016. http://repositorio.uchile.cl/handle/2250/140680.

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Tesis para optar al grado de Doctora en Bioquímica<br>El cáncer corresponde a la segunda causa de muerte en Chile y el mundo, pero los pacientes con cáncer no mueren debido al crecimiento del tumor primario, sino a la diseminación de las células tumorales y posterior colonización de éstas en nuevos órganos o metástasis. En términos generales, el cáncer es la consecuencia de un proceso multifactorial que lleva a la transformación progresiva de células normales en células altamente malignas. La amplia variedad de fenotipos del cáncer se debe a la manifestación de alteraciones esenciales e
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González, Muñoz Elena. "Papel de las caveolas/caveolina-1 en la fisiologia del adipocito." Doctoral thesis, Universitat de Barcelona, 2007. http://hdl.handle.net/10803/1023.

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La función de las caveolas y de la caveolina in vivo ha sido motivo de controversia, de hecho se han implicado en procesos de endocitosis y transcitosis, transporte de colesterol y ácidos grasos, regulación de procesos de transducción de señales y tumorigénesis (Liu et al., 2002). Sin embargo, la generación de los ratones KO de caveolina-1 (Drab et al., 2001; Razani et al., 2001a) mostraba que estos ratones eran perfectamente viables y fértiles, aunque estudios posteriores relacionaban a caveolina-1 con la homeostasis lipídica (Razani et al., 2002a).<br/><br/>A partir de estos antecedentes, el
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Mateo, Lozano Silvia. "Sarcoma de Ewing: nuevas aproximaciones terapéuticas y búsqueda de dianas biológicas del oncogén EWS/FLI-1." Doctoral thesis, Universitat Autònoma de Barcelona, 2007. http://hdl.handle.net/10803/3571.

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La familia de tumores del sarcoma de Ewing (ESFT) incluye un grupo heterogéneo de neoplasias caracterizadas por la presencia de células redondas de pequeño tamaño con mínima evidencia morfológica de diferenciación. ESFT es el segundo tumor óseo más frecuente, afectando fundamentalmente a niños y adolescentes. A pesar del uso de terapias agresivas combinando quimioterapia, radioterapia y cirugía, la supervivencia de pacientes con metástasis es aproximadamente del 30%, mientras que en ausencia de enfermedad metastásica alcanza valores del 70 %. Debido a esto, son necesarias nuevas aproximaciones
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Sáinz, Jaspeado Miguel Guillermo. "Regulación del aporte vascular en el Sarcoma de Ewing: Papel de la Caveolina-1." Doctoral thesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/107820.

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Como otros tumores sólidos, el sarcoma de Ewing (SE) requiere de un aporte vascular adecuado que permita nutrir y oxigenar a las células tumorales. En el SE, la vascularización tumoral se encuentra caracterizada principalmente por los procesos de vasculogenesis, mimetismo vascular y angiogénesis. Considerando la participación de CAV1 en el aporte vascular, nos planteamos demostrar que CAV1 juega un papel importante en el desarrollo vascular de la enfermedad. Estableciendo tres nuevos modelos de baja expresión de CAV1 en células se SE (RDES, SKES1 y TC71), fue posible observar la reducción e
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Ilha, Mariana. "Papel da caveolina-1 na capacidade de migração e proliferação de células estreladas hepáticas." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/117581.

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A fibrose hepática é uma característica comum de diversas doenças crônicas do fígado e é caracterizada pela deposição excessiva de matriz extracelular no órgão. Em última instância, essa alteração anormal do parênquima hepático acarreta em hipertensão portal, cirrose e insuficiência do fígado, o que pode levar o paciente à morte. As células estreladas hepáticas (HSC) participam ativamente deste processo, modificando seu fenótipo quiescente, rico em gotas lipídicas no citoplasma, para o fenótipo ativado, em resposta a um insulto hepático. A linhagem GRX é um modelo de HSC ativadas. As caveolas
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Cruz, Gómez Sebastián Matías. "Rol de caveolina-1 en la quimiotaxis de las células dendríticas hacia los nódulos linfáticos." Tesis, Universidad de Chile, 2017. http://repositorio.uchile.cl/handle/2250/150211.

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Tesis para optar al grado de Magister en Bioquímica<br>Las células dendríticas (DCs) son células presentadoras de antígeno capaces de capturar y procesar antígenos que luego son presentados a linfocitos T específicos en órganos linfoides. Para activar a los linfocitos T, las DCs deben pasar por un proceso de maduración y migración hacia los nódulos linfáticos. Para esto, las DCs deben percibir el rastro de quimioquinas como CCL21, a través de receptores como CCR7, que las dirigen hacia los vasos linfáticos y finalmente al nódulo linfático. Dicho proceso se denomina quimiotaxis y es dependiente
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Sanhueza, Muñoz Carlos Joaquín. "Caveolina-1 reduce la transcripción dependiente de hif1α en un mecanismo dependiente del óxido nítrico en células tumorales". Tesis, Universidad de Chile, 2013. http://repositorio.uchile.cl/handle/2250/114871.

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Doctor en Farmacología<br>Autorizada por el autor, pero con restricción para ser publicada a texto completo en el Portal de Tesis Electrónicas, hasta diciembre de 2018<br>El cáncer es la 2° causa de muerte en Chile. El desarrollo del cáncer se ha propuesto que es consecuencia de la pérdida de función de los genes supresores de tumores beneficiando la acción de los oncogenes (genes que promueven el crecimiento de tumores). La activación del Factor inducible por hipoxia 1α (HIF1α) en un ambiente reducido en oxígeno (hipoxia) o por óxido nítrico (NO), permiten la proliferación y adaptación metabó
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Díaz, Morales María Inés. "Rol de la respuesta a proteínas mal plegadas en la actividad supresora de tumores de Caveolina-1." Tesis, Universidad de Chile, 2015. http://repositorio.uchile.cl/handle/2250/136641.

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Doctora en Bioquímica<br>Autor no autoriza el acceso a texto completo de su documento<br>El cáncer es la segunda causa de muerte a nivel mundial y en Chile luego de las enfermedades cardiovasculares. Importantemente, las muertes por cáncer van en aumento. Los avances más recientes en el entendimiento de las vías de señalización involucradas en cáncer, ha permitido la identificación de marcadores tempranos y tardíos de la carcinogénesis, los cuales son fundamentales para el diagnóstico y la prognosis del paciente. Basados en estos descubrimientos, existen disponibles nuevas terapias para el tra
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Books on the topic "Caveolina-1"

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Mercier, Isabelle, Jean-François Jasmin, and Michael P. Lisanti. Caveolins in cancer pathogenesis, prevention and therapy. Springer, 2012.

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Mercier, Isabelle, Michael P. Lisanti, and Jean-François Jasmin. Caveolins in Cancer Pathogenesis, Prevention and Therapy. Springer, 2011.

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Book chapters on the topic "Caveolina-1"

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Routray, Samapika, Niharika Swain, and Rashmi Maruti Hosalkar. "Caveolin-1." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101931.

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Routray, Samapika, Niharika Swain, and Rashmi Maruti Hosalkar. "Caveolin-1." In Encyclopedia of Signaling Molecules. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101931-1.

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Senetta, Rebecca, and Paola Cassoni. "Caveolin-1 in Brain Tumors." In Caveolins in Cancer Pathogenesis, Prevention and Therapy. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-1001-0_4.

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Bonuccelli, Gloria, and Michael P. Lisanti. "Caveolin-1 and Breast Cancer." In Caveolins in Cancer Pathogenesis, Prevention and Therapy. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-1001-0_7.

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Pavlides, Stephanos, Jorge L. Gutierrez-Pajares, Christiane Danilo, Michael P. Lisanti, and Philippe G. Frank. "Atherosclerosis, Caveolae and Caveolin-1." In Advances in Experimental Medicine and Biology. Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-1222-9_9.

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Rittenhouse, David W., Oeendree Mukherjee, Nathan G. Richards, Charles J. Yeo, Agnieszka K. Witkiewicz, and Jonathan R. Brody. "Caveolin-1 and Pancreatic Ductal Adenocarcinoma." In Caveolins in Cancer Pathogenesis, Prevention and Therapy. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-1001-0_3.

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Boscher, Cécile, and Ivan Robert Nabi. "CAVEOLIN-1: Role in Cell Signaling." In Advances in Experimental Medicine and Biology. Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-1222-9_3.

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Freeman, Michael R., Wei Yang, and Dolores Di Vizio. "Caveolin-1 and Prostate Cancer Progression." In Advances in Experimental Medicine and Biology. Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-1222-9_7.

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Reagan, Alaina, Xiaowu Gu, Stefanie M. Hauck, et al. "Retinal Caveolin-1 Modulates Neuroprotective Signaling." In Retinal Degenerative Diseases. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_54.

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Parat, Marie-Odile, and Paul L. Fox. "Oxidative Stress, Caveolae and Caveolin-1." In Membrane Dynamics and Domains. Springer US, 2004. http://dx.doi.org/10.1007/978-1-4757-5806-1_13.

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Conference papers on the topic "Caveolina-1"

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Radhakrishnan, V., L. Fan, A. S. Marudamuthu, et al. "Caveolin-1-Scaffolding Peptide Attenuates Pulmonary Fibrosis." In 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.a5392.

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Pabelick, Christina M., Michael A. Thompson, Lucas W. Meuchel, Elizabeth A. Townsend, and Y. S. Prakash. "Airway Reactivity In The Caveolin-1 Knockout Mouse." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1273.

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Brown, BJ, AM Pastva, B. Lo, et al. "AHR Is Attenuated in Caveolin-1 Deficient Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5093.

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Shetty, S., A. Marudamuthu, Y. Bhandary, et al. "Caveolin-1-Derived Peptide Limits Development of Pulmonary Fibrosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7881.

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Sanders, Yan Y., Hui Liu, Xiangyu Zhang, and Victor J. Thannickal. "Epigenetic Mechanisms Regulating Caveolin-1 Expression In Lung Fibroblasts." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3476.

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Fan, L., A. Kumar, and S. Shetty. "Caveolin-1-Scaffolding Peptide Attenuates Radiation-Induced Lung Injury." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6843.

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Xia, Hong, Wajahat Khalil, Judy Kahm, jose Jessurun, Jill Kleidon Kleidon, and Craig A. Henke. "Pathologic Caveolin-1 Regulation Of PTEN In Idiopathic Pulmonary Fibrosis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3507.

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Trimmer, Casey, Sanjay Katiyar, Richard G. Pestell, Michael P. Lisanti, and Franco Capozza. "Abstract 1083: Caveolin-1 in cutaneous squamous cell carcinoma development." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1083.

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Moon, Hyeongsun, C. Soon Lee, Sowmya Sharma, et al. "Abstract 3040: Cavin-1 alters oncogenic effects of caveolin-1 microdomains in prostate cancer." In 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.am2013-3040.

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Xia, H., W. Khalil, J. Kleidom, J. Kahm, and CA Henke. "Caveolin-1 Regulates PTEN in Idiopathic Pulmonary Fibrosis in Polymerized Collagen." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3463.

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Reports on the topic "Caveolina-1"

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Thompson, Timothy C. Role of Caveolin-1 in Prostate Cancer Angiogenesis. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada495845.

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Thompson, Timothy C. Role of Caveolin-1 in Prostate Cancer Angiogenesis. Defense Technical Information Center, 2009. http://dx.doi.org/10.21236/ada587089.

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Thompson, Timothy C. Role of Caveolin-1 in Prostate Cancer Angiogenesis. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada466161.

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Thompson, Timothy C. Role of Caveolin-1 in Prostate Cancer Angiogenesis. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada481347.

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Lu, Michael L. Caveolin-1 Modulates Androgen Receptor Signaling in Advanced Prostate Cancer. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada434550.

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Lu, Michael L. Caveolin-1 Modulates Androgen Receptor Signaling in Advanced Prostate Cancer. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada414469.

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Lu, Michael L. Caveolin-1 Modulates Androgen Receptor Signaling in Advanced Prostate Cancer. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada427983.

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Lu, Michael L. Caveolin-1 Modulates Androgen Receptor Signaling in Advanced Prostate Cancer. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada459172.

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