Literatura académica sobre el tema "CaVβ1"
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Artículos de revistas sobre el tema "CaVβ1"
Cohen, Risa M., Jason D. Foell, Ravi C. Balijepalli, Vaibhavi Shah, Johannes W. Hell y Timothy J. Kamp. "Unique modulation of L-type Ca2+ channels by short auxiliary β1d subunit present in cardiac muscle". American Journal of Physiology-Heart and Circulatory Physiology 288, n.º 5 (mayo de 2005): H2363—H2374. http://dx.doi.org/10.1152/ajpheart.00348.2004.
Texto completoFoell, Jason D., Ravi C. Balijepalli, Brian P. Delisle, Anne Marie R. Yunker, Seth L. Robia, Jeffrey W. Walker, Maureen W. McEnery, Craig T. January y Timothy J. Kamp. "Molecular heterogeneity of calcium channel β-subunits in canine and human heart: evidence for differential subcellular localization". Physiological Genomics 17, n.º 2 (13 de abril de 2004): 183–200. http://dx.doi.org/10.1152/physiolgenomics.00207.2003.
Texto completoDespang, Patrick, Sarah Salamon, Alexandra Breitenkamp, Elza Kuzmenkina y Jan Matthes. "Inhibitory effects on L- and N-type calcium channels by a novel CaVβ1 variant identified in a patient with autism spectrum disorder". Naunyn-Schmiedeberg's Archives of Pharmacology 395, n.º 4 (5 de febrero de 2022): 459–70. http://dx.doi.org/10.1007/s00210-022-02213-7.
Texto completoTraoré, Massiré, Christel Gentil, Chiara Benedetto, Jean-Yves Hogrel, Pierre De la Grange, Bruno Cadot, Sofia Benkhelifa-Ziyyat et al. "An embryonic CaVβ1 isoform promotes muscle mass maintenance via GDF5 signaling in adult mouse". Science Translational Medicine 11, n.º 517 (6 de noviembre de 2019): eaaw1131. http://dx.doi.org/10.1126/scitranslmed.aaw1131.
Texto completoBelkacemi, Anouar, Andreas Beck, Barbara Wardas, Petra Weissgerber y Veit Flockerzi. "IP3-dependent Ca2+ signals are tightly controlled by Cavβ3, but not by Cavβ1, 2 and 4". Cell Calcium 104 (junio de 2022): 102573. http://dx.doi.org/10.1016/j.ceca.2022.102573.
Texto completoHeneghan, John F., Tora Mitra-Ganguli, Lee F. Stanish, Liwang Liu, Rubing Zhao y Ann R. Rittenhouse. "The Ca2+ channel β subunit determines whether stimulation of Gq-coupled receptors enhances or inhibits N current". Journal of General Physiology 134, n.º 5 (26 de octubre de 2009): 369–84. http://dx.doi.org/10.1085/jgp.200910203.
Texto completoBrown, Betty, M. Steven Oberste, Kaija Maher y Mark A. Pallansch. "Complete Genomic Sequencing Shows that Polioviruses and Members of Human Enterovirus Species C Are Closely Related in the Noncapsid Coding Region". Journal of Virology 77, n.º 16 (15 de agosto de 2003): 8973–84. http://dx.doi.org/10.1128/jvi.77.16.8973-8984.2003.
Texto completoTaylor, Jackson, Tan Zhang, Laura Messi, Jiang Qian, Cristina Furdui, Claudia Hereñú y Osvaldo Delbono. "The Cavβ1 Subunit Regulates Gene Expression in Muscle Progenitor Cells". Biophysical Journal 102, n.º 3 (enero de 2012): 365a. http://dx.doi.org/10.1016/j.bpj.2011.11.1993.
Texto completoTraore, M., C. Gentil, C. Benedetto, J. Hogrel, P. De la Grange, S. Benkhelifa-Ziyyat, L. Julien, M. Lemaitre, A. Ferry y S. Falcone. "P.133A novel CaVβ1 isoform connecting voltage sensing with muscle mass homeostasis". Neuromuscular Disorders 29 (octubre de 2019): S87. http://dx.doi.org/10.1016/j.nmd.2019.06.189.
Texto completoBuraei, Zafir y Jian Yang. "The β Subunit of Voltage-Gated Ca2+ Channels". Physiological Reviews 90, n.º 4 (octubre de 2010): 1461–506. http://dx.doi.org/10.1152/physrev.00057.2009.
Texto completoTesis sobre el tema "CaVβ1"
Traoré, Massiré. "Maintien de la masse musculaire et vieillissement : rôle de Cavβ1". Thesis, Université de Paris (2019-....), 2020. http://www.theses.fr/2020UNIP7046.
Texto completoSkeletal muscle atrophy caused by disuse, nerve damage or other diseases are characterized by an increased protein breakdown leading to the progressive loss of muscle mass and function. However, it has been shown that skeletal muscle is able to activate a compensatory response in order to limit excessive muscle wasting. These compensatory mechanisms are still poorly described and the factors involved are not fully understood. To date, an important component of the compensatory response has been identified in mice : GDF5 (Growth Differenciation Factor 5), a member of the BMP (Bone Morphogenetic Protein) family, playing a critical role in muscle maintenance after a nerve damage. However, the first trigger of this molecular response remains unknown. We have hypothesized that this player could be a protein sensitive to electrical activity in skeletal muscle. We therefore focused our study on Cavβ1 protein, a regulatory subunit of the DHPR, a calcium channel described as essential in excitationcontraction coupling in skeletal muscle. Our study revealed the existence of a novel embryonic isoform of Cavβ1 (Cavβ1-E) in adult skeletal muscle, which expression increases after denervation. We discovered that Cavβ1-E stimulates GDF5 gene expression in skeletal muscle to counteract atrophy induced by nerve damage. Since we demonstrated that Cavβ1-E plays a key role in muscle maintenance, we studied its function during age-related muscle wasting. We observed that aged mouse muscle expresses lower quantity of Cavβ1-E and displays an altered Cavβ1-E/GDF5-dependent response to denervation compared to young muscle. These evidences suggested the involvement of this axis in skeletal muscle mass and function decline during ageing. Indeed, we found that overexpression of Cavβ1-E or GDF5 counteracts muscle mass loss and prevents the decrease of force generation in aged muscles. We also identified the human analogous of Cavβ1-E (hCavβ1-E) and our data showed a positive correlation between hCavβ1-E expression in human muscle and subject’s lean mass. These results suggest that strategies targeting Cavβ1-E or GDF5 could contribute to prevent agerelated skeletal muscle wasting
Vergnol, Amélie. "Les isoformes CaVβ1 : rôle dans la formation de la jonction neuromusculaire et implication dans la physiopathologie de la Dystrophie Myotonique de type 1". Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS305.
Texto completoFour CaVβ proteins (CaVβ1 to CaVβ4) are described as regulatory subunit of Voltage-gated Ca2+ channel (VGCC), each exhibiting specific expression pattern in excitable cells based on their function. While primarily recognized for their role in VGCC regulation, CaVβ proteins also function independently of channels, acting as regulators of gene expression. Among these, CaVβ1 is expressed in skeletal muscle as different isoforms. The adult constitutive isoform, CaVβ1D, is located at the sarcolemma and more specifically at the triad, where it plays a crucial role in regulating CaV1 to control Excitation-Contraction Coupling (ECC) mechanism, essential for muscle contraction.In this thesis, we further explored the less studied CaVβ1 isoforms, with a particular focus on embryonic/perinatal variants, including the previously described CaVβ1E. We investigated their roles in the neuromuscular and muscular systems. Indeed, CaVβ1 proteins have been showed as essential for NeuroMuscular Junction (NMJ) development, though the involvement of specific isoform remains unclear. Our investigation assessed the role of CaVβ1 isoforms at different stages of NMJ formation and maturation/maintenance. Additionally, given the deregulation of CaVβ1 in Myotonic Dystrophy Type 1 (DM1), we explored its functional role in this muscular pathological context.First, we identified CaVβ1A as another isoform expressed during embryogenesis and perinatal stages. Our findings revealed that CaVβ1 isoforms expressions are regulated by the differential activation of promoters during development: a promoter1 in exon 1 drives CaVβ1A/E expressions, while a promoter2 in exon 2B controls CaVβ1D expression. Interestingly, nerve damage in adult muscle triggers a shift toward the promoter1 activation and leading to the re-expression of CaVβ1A/E transcripts. Furthermore, we found that CaVβ1 embryonic/perinatal isoforms are critical for proper in vitro pre-patterning of myotubes and that their postnatal expressions influences NMJ maturation/maintenance. In the pathological context of DM1, we observed the increased expression of CaVβ1A/E, which appears to mitigate myotonia symptoms. In addition, we found that the modulation of their expression is linked with MBNL proteins, which are central in the pathophysiology of DM1. In conclusion, this thesis work has clarified knowledge of the various CaVβ1 isoforms in skeletal muscle and provides new insights into their role in two independent contexts of NMJ development and DM1 pathophysiology. Understanding CaVβ1 protein regulation in skeletal muscle is essential to decipher muscle homeostasis mechanisms and potentially identify new therapeutic targets to face muscular disorders
Marshall, Misty. "Brain Cav1 Channel/AKAP15 signaling complexes and the role of the distal C-terminus in Cav1 channel regulation in vivo /". Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/6297.
Texto completoRima, Mohamad. "Le rôle de Cavβ4 dans la prolifération cellulaire et la régulation génique". Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV062/document.
Texto completoThe voltage gated calcium channels are involved in many cellular processes such as muscle contraction, neurotransmitter release and regulation of gene expression. These channels consist of the pore-forming subunit α1 usually associated with different regulatory subunits: α2δ, β and γ. The auxiliary subunit β (Cavβ) plays a key role in regulating membrane trafficking of the channel and its biophysical properties. Recent studies describe this subunit as a multifunctional protein that can also perform calcium channel-independent functions such as gene regulation. Four different isoforms of Cavβ are encoded by 4 different genes and are characterized by structural similarities but different tissue distribution. Cavβ4 isoform is mainly expressed in the brain and cerebellum, thus, playing an important role in the regulation of neuronal calcium currents. The importance of Cavβ4 neuronal functions has been highlighted by its R482X mutation that was associated to a form of human epilepsy.The aim of my thesis was to study the role of Cavβ4 in the control of cell division and its involvement in the Wnt signaling pathway. I also studied the influence of the R482X mutation on this new function of Cavβ4.To this end, CHO cells stably expressing Cavβ4, or its epileptic mutant (Cavβ1-481), were generated and the subcellular localization of the two proteins and their implication in the proliferation and cell cycle progression were studied. In these cells, Cavβ4 undergoes nuclear translocation and is found preferentially in the nucleoli. However, the deletion of 38 amino acids in the C-terminus domain of Cavβ4, corresponding to the R482X mutation, prevents its nucleolar translocation. In addition, the expression of Cavβ4 significantly reduces the proliferative rate of the cells. This reduction seems to be linked to Cavβ4 nuclear localization because the epileptic mutant is unable to slow down cell proliferation. On the other hand, the expression of each of these proteins is able to deregulate cell cycle progression and to alter the expression of many genes linked to the cycle.Since the Wnt/β-catenin pathway is known as one of the most important pathways controlling cell proliferation, I studied the effect of Cavβ4 expression on this signaling pathway. Indeed, Cavβ4, but not Cavβ1-481, substantially reduces the transcription of β-catenin-dependant genes and therefore slows down cell proliferation. This inhibition is due to a direct interaction between Cavβ4 and TCF4 that prevents the interaction of TCF4 with β-catenin, and thereafter negatively regulates the transcription of targeted genes.These findings suggest that Cavβ4 can play a role in the control of proliferation during development, particularly in neuronal cells
Tadmouri, Abir. "Les déterminants moléculaires et cellulaires de la mutation humaine R482X de la sous-unité Cavb4 impliqués dans l’épilepsie". Université Joseph Fourier (Grenoble), 2007. http://www.theses.fr/2007GRE10081.
Texto completoHigh voltage-activated (HVA) calcium channels are hetero-multimeric complexes that translate electrical signals into Ca2+ influx, a secondary messenger that mediates essential neuronal processes such as neurotransmitter release and neuronal excitability. HVA calcium channels are composed of four subunits: Cavα1 subunit, the pore forming of the channel and the auxiliary subunits Cavβ, Cavα2δ and Cavγ. The Cavß subunit has focused much of the interest owing to its regulatory functions within the complex. By masking an endoplasmic retention signal on the Cavα1 subunit, Cavß subunit targets the mature calcium channel to the plasma membrane and contributes to the increase in number of functional calcium currents. In humans, pathologic mutations have been identified in CACNAB4 that produce epileptic phenotype. One of these mutations is a premature termination mutation (R482X). Mutations produced minor biophysical effects on calcium channels in spite of their preponderant pathological phenotypes, which tend to indicate that cellular functions other than channel regulation may be responsible for the predominant neurological effects of the R482X mutation. My thesis focuses on the molecular and cellular determinants of the Cavb4 mutant (R482X) inducing the human neurological phenotype. Studies were realized in hippocampal neurons which are particularly implicated in epilepsy. A translocation of endogenous Cavß4, from the cytoplasm to the nucleus is observed during neuronal differentiation and synaptogenesis. This translocation is conditioned by the native structural conformation of Cavß4 subunit; carboxy-terminal deletion inhibits the nuclear localization of the mutant. The 38 amino acids deletion disturbs the structure of Cavß4 by altering the intramolecular interaction between the two conserved domains in Cavß4 subunit. In hippocampal neurons, this structural distortion prevents the nuclear localization of the mutant Cavß4. In order to identify the impact of the nuclear localization of the Cavß4 subunit on transcriptional regulation, a study on gene expression generated by microarray is realized. Profiles of gene expression revealed a differential gene regulation between wild-type and mutant Cavß4. Cavß4 subunit seems to have a repressive action on gene regulation; on the other hand, the lack of nuclear localization of the mutant reverses this repressive impact. Among the specific transcripts differentially expressed, some genes are primordial keys in neuronal activities, thus alterations in the regulation of these genes could be involved in neuronal diseases. Since no NLS consensus sequence has been identified on Cavß4, two-hybrid assay was realized in order to identify partners responsible of the Cavß4 nuclear targeting. A specific protein holding a NLS sequence interacts specifically with Cavß4 subunit, but not with the mutant, and is able to target Cavß4 to the nucleus. The other protein which specifically interacts with the WT Cavß4 sequesters Cavß4 in the cytoplasm. Finally, the lack in nuclear targeting of the R482X mutant due to the structural distortion appears to alter the transcriptional gene regulation which is maybe implicated in the epileptic phenotype of patients holding the mutation
Grasset, Eloïse. "La rigidification de la matrice extracellulaire et la voie de signalisation de l’EGFR coopèrent pour induire l’expansion des carcinomes squameux par la régulation du canal calcique CaV1". Thesis, Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4091/document.
Texto completoEpidermal growth factor receptor (EGFR) is a rational target for squamous cell carcinoma (SCC) anticancer therapies, nevertheless; only a subset of patients shows clinical benefits. I demonstrated a cooperation between EGFR signaling and extracellular matrix (ECM) stiffness that could explain this phenomenon. I sought to resolve the molecular pathway underlying this cooperation in SCC proliferation and expansion in order to identify new pharmaceutical targets. Screening of pharmacological inhibitors, in an in vitro 3-D assay, identified verapamil and diltiazem, FDA approved L-type calcium channels inhibitors, as potent blockers of SCC invasion. Mechanistically, I revealed that tumor-derived ECM stiffness and EGFR signaling trigger increased of intracellular calcium through the L-type CaV1.1 channel in SCC. Blocking L-type calcium channels activity resulted in reduced SCC cells invasion and proliferation in vitro. More importantly, I also demonstrate a strong reduction in tumor development in two in vivo models, both head and neck patient derived xenograft and skin SCC mice model. Consequently, I suggest a repurpose of verapamil and diltiazem to anti-cancer agents
Triffaux, Emily. "Identification des canaux Cav1 impliqués dans la voie de signalisation calcique des lymphocytes Th2". Toulouse 3, 2013. http://thesesups.ups-tlse.fr/1959/.
Texto completoAsthma is an allergic pulmonary disease which affects around 10% of the population. Allergen-specific type 2 T helper lymphocytes Th2 have a crucial role in the asthma physiopathology by producing interleukin IL4,5,13. Previously, my team reported that mouse Th2 but not Th1 cells express voltage gated calcium CaV1 channels. CaV1 channel specific antisense oligonucleotide CaV1AS inhibit calcium response and Th2 cytokine production (IL4,5,13) upon TCR stimulation without any effect on Th1 cells in mice. In addition, CaV1AS prevent experimental allergic asthma. During my PhD, I showed the CaV1. 4 expression in human resting cells. Conversely, CaV1. 2 and CaV1. 3 predominated in Th2 cells and were lost in Th1 cells. CaV1 channel inhibitors, CaV1. 2 AS and CaVbAS decreased calcium signaling and cytokine production in Th2 but not in Th1 cells. Moreover, CaVbAS decrease the CaV1. 2 protein suggesting that CaVb is required for CaV1. 2 stability in Th2 cells. Finally selective PKCa/b inhibition decreased calcium response and cytokine production by Th2 but not Th1 cells suggesting that PKC may contribute to CaV1 regulation in Th2 cells. These results suggest that the inhibition of CaV1. 2 channels could be beneficial in allergic diseases while sparing Th1 cell responses
Rosa, Nicolas. "Rôle des sous-unités auxiliaires des canaux calciques Cav1 dans les lymphocytes Th2 : implications thérapeutiques dans l'asthme allergique". Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30359/document.
Texto completoCalcium channels include store-operated (ORAI) and voltage-gated (Cav) channels that are considered to be important for calcium entry in non-excitable and excitable cells, respectively. Voltage-gated calcium channels such as Cav1 are essential for excitable cell function, including neuronal transmission, muscle contraction or hormone secretion. However, numerous studies show that Cav1 channels are expressed in non-excitable cells as well, and are important for T cell effector functions. Cav1 channels are composed of the a1 subunit forming the ion pore and auxiliary subunits ß and a2δ. These subunits are important for the electric activity of the channel but also for its regulation, its stability and its expression at the plasma membrane in excitable cells. Our group clearly identified the a1 subunit of Cav1.2 and Cav1.3 channels as essential for the function of Th2 lymphocytes, a T cell subset responsible for allergic diseases. Pharmacological and genetic inhibition of these channels significantly reduces the expression of cytokines in mouse Th2 cells, but not in Th1 cells. The goal of my work was to understand whether the auxiliary subunits of Cav channels, particularly the ß subunit, are necessary for the function of Cav1 channels in Th2 lymphocytes that are not excitable cells. We used antisense oligonucleotides targeting all ß subunits to reduce the expression of ß1 and ß3, the two subunits expressed in Th2 lymphocytes. Transfection of murine and human Th2 with these oligonucleotides decreases TCR-dependent calcium influx and cytokine expression. In addition, the effect of the Cavß antisense oligonucleotides seems to result from the loss of expression of the a1 subunit, as similarly described in neurons. In addition, the use of shRNA specific to ß1 and ß3 in mouse Th2 shows a critical role the ß1 subunit in the functional response of Th2 lymphocytes. Finally, the Cavß antisense oligonucleotides reduce the airway inflammation in an allergic asthma model in mice, as well as a pharmacological inhibitor of a2δ subunits. This work has identified auxiliary subunits of Cav channels as new potential therapeutic targets in allergic diseases such as asthma
Grasset, Eloïse. "La rigidification de la matrice extracellulaire et la voie de signalisation de l’EGFR coopèrent pour induire l’expansion des carcinomes squameux par la régulation du canal calcique CaV1". Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2017. http://theses.univ-cotedazur.fr/2017AZUR4091.
Texto completoEpidermal growth factor receptor (EGFR) is a rational target for squamous cell carcinoma (SCC) anticancer therapies, nevertheless; only a subset of patients shows clinical benefits. I demonstrated a cooperation between EGFR signaling and extracellular matrix (ECM) stiffness that could explain this phenomenon. I sought to resolve the molecular pathway underlying this cooperation in SCC proliferation and expansion in order to identify new pharmaceutical targets. Screening of pharmacological inhibitors, in an in vitro 3-D assay, identified verapamil and diltiazem, FDA approved L-type calcium channels inhibitors, as potent blockers of SCC invasion. Mechanistically, I revealed that tumor-derived ECM stiffness and EGFR signaling trigger increased of intracellular calcium through the L-type CaV1.1 channel in SCC. Blocking L-type calcium channels activity resulted in reduced SCC cells invasion and proliferation in vitro. More importantly, I also demonstrate a strong reduction in tumor development in two in vivo models, both head and neck patient derived xenograft and skin SCC mice model. Consequently, I suggest a repurpose of verapamil and diltiazem to anti-cancer agents
Gomes, Bruno. "Les canaux calciques Cav1 spécifiquement exprimés par les lymphocytes Th2 : une cible dans le traitement de l'asthme allergique". Toulouse 3, 2005. http://www.theses.fr/2005TOU30225.
Texto completoThe prevalence of asthma has risen drastically in the last two decades, with a worldwide impact on health care systems. T-helper (Th) lymphocytes orchestrate the immune response and are divided into two subsets, Th1 cells that produce IFN-g and Th2 cells which synthetize IL-4. Th2 lymphocytes play an important role in the pathogenesis of allergic asthma. We show that Th2 lymphocytes, unlike Th1 cells, express a unique profile of Cav1 calcium channels that control calcium influx and Th2 cytokine production upon TCR stimulation. Our results underline the therapeutic potential of Cav1 channel antagonists or specific inhibition of Cav1 expression by antisense oligonucleotides in Th2-dependent immunopathological disorders in mice and rats. Capitalizing on these unique attributes is important for drug development in allergic asthma
Capítulos de libros sobre el tema "CaVβ1"
Triggle, David J. "Pharmacology of Cav1 (L-Type) Channels". En Calcium Channel Pharmacology, 21–72. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9254-3_2.
Texto completoKoschak, Alexandra y Amy Lee. "Cav1 L-Type Calcium Channels in the Auditory and Visual Systems". En Voltage-Gated Calcium Channels, 475–89. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08881-0_17.
Texto completoNakao, Akito, Mitsuru Hirano, Yoshinori Takada, Shigeki Kiyonaka y Yasuo Mori. "Molecular Architecture of Ca2+ Channel Complexes Organized by CaVβ Subunits in Presynaptic Active Zones". En Modulation of Presynaptic Calcium Channels, 79–99. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6334-0_4.
Texto completoMoosmang, Sven y Franz Hofmann. "Cav1 Voltage-Gated Calcium Channels". En xPharm: The Comprehensive Pharmacology Reference, 1–5. Elsevier, 2009. http://dx.doi.org/10.1016/b978-008055232-3.60393-9.
Texto completoEyries, Mélanie, Barbara Girerd, David Montani, David-Alexandre Tregouët, Marc Humbert y Florent Soubrier. "Pulmonary hypertension genes as major diagnostic tools". En ESC CardioMed, editado por Marc Humbert, 2490–93. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0577.
Texto completoHadinnapola, Charaka y Nicholas Morrell. "Heritable pulmonary arterial hypertension". En ESC CardioMed, editado por Marc Humbert, 2527–28. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0590.
Texto completoActas de conferencias sobre el tema "CaVβ1"
Geletu, Mulu, Reva Mohan, Rozanne Arulanandam, Adina Vultur y Leda H. Raptis. "Abstract 4004: Reciprocal regulation of Stat3 and the caveolae protein, cav1". En 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.am10-4004.
Texto completoTrimmer, Casey y Franco Capozza. "Abstract 1631: Cav1 is a key mediator of tumor-stromal interactions in melanoma." En 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.am2013-1631.
Texto completoKanlikilicer, Pinar, Recep Bayraktar, Mohammed Rashed, Burcu Aslan, George A. Calin, Anil K. Sood y Gabriel Lopez-Berestein. "Abstract 1988: Exosome-mediated ovarian cancer tumorigenesis mediated by miR1246/Rb/Cav1 axis". En Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1988.
Texto completoDu, Xiaoli, Xiaolan Qian, Alex Papageorge, William C. Vass, Richard Braverman y Douglas R. Lowy. "Abstract 2184: Complex formation between the DLC1 START domain and Cav1 contributes to the tumor suppressor function of DLC1". En 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.am2011-2184.
Texto completoYamaguchi, Tomoya, Can Lu, Lisa Ida, Kiyoshi Yanagisawa, Jiro Usukura, Jinglei Cheng, Naoe Hotta et al. "Abstract 4585: ROR1 sustains caveolae and RTK-mediated survival signaling as a scaffold of cavin-1 and CAV1 in lung cancer". En Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4585.
Texto completoLee, Ji Shin, Nah Ihm Kim y Min Ho Park. "Abstract P3-02-12: CAV1, MCT1, and MCT4 expression in ductal carcinoma in situ of the breast and its association with clinicopathologic features". En Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p3-02-12.
Texto completoWang, Neng, Fengxue Zhang, Zhiyu Wang, Yifeng Zheng, Shengqi Wang y Bowen Yang. "Abstract 1230: Critical role of cav1 in high-throughput identification of gallic acid as a novel late-stage autophagy suppresser against invasive breast cancer". En Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1230.
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