Auswahl der wissenschaftlichen Literatur zum Thema „Myosin 1g“
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Zeitschriftenartikel zum Thema "Myosin 1g"
Estrada-Abreo, Laura A., Leonor Rodríguez-Cruz, Yanelly Garfias-Gómez, Janeth E. Araujo-Cardenas, Gabriela Antonio-Andrés, Alfonso R. Salgado-Aguayo, Darío Orozco-Ruiz et al. „High expression of Myosin 1g in pediatric acute lymphoblastic leukemia“. Oncotarget 12, Nr. 19 (14.09.2021): 1937–45. http://dx.doi.org/10.18632/oncotarget.28055.
Der volle Inhalt der QuelleDart, A. E., S. Tollis, M. D. Bright, G. Frankel und R. G. Endres. „The motor protein myosin 1G functions in Fc R-mediated phagocytosis“. Journal of Cell Science 125, Nr. 24 (04.10.2012): 6020–29. http://dx.doi.org/10.1242/jcs.109561.
Der volle Inhalt der QuelleMéndez, Irene, Ana Isabel Fernández, Maria Ángeles Espinosa, Sofía Cuenca, Rebeca Lorca, José Fernando Rodríguez, Maria Tamargo et al. „Founder mutation in myosin-binding protein C with an early onset and a high penetrance in males“. Open Heart 8, Nr. 2 (September 2021): e001789. http://dx.doi.org/10.1136/openhrt-2021-001789.
Der volle Inhalt der QuelleKonno, Tetsuo, Masami Shimizu, Hidekazu Ino, Noboru Fujino, Katsuharu Uchiyama, Tomohito Mabuchi, Kenji Sakata et al. „A novel mutation in the cardiac myosin-binding protein C gene is responsible for hypertrophic cardiomyopathy with severe ventricular hypertrophy and sudden death“. Clinical Science 110, Nr. 1 (12.12.2005): 125–31. http://dx.doi.org/10.1042/cs20050189.
Der volle Inhalt der QuelleRodríguez-Téllez, Rosa Isela, Rosa María Ribas-Aparicio und Genaro Patiño-López. „Detection of Myosin 1g Overexpression in Pediatric Leukemia by Novel Monoclonal Antibodies“. International Journal of Molecular Sciences 23, Nr. 7 (01.04.2022): 3912. http://dx.doi.org/10.3390/ijms23073912.
Der volle Inhalt der QuelleOlety, Balaji, Mike Wälte, Ulrike Honnert, Hermann Schillers und Martin Bähler. „Myosin 1G (Myo1G) is a haematopoietic specific myosin that localises to the plasma membrane and regulates cell elasticity“. FEBS Letters 584, Nr. 3 (04.12.2009): 493–99. http://dx.doi.org/10.1016/j.febslet.2009.11.096.
Der volle Inhalt der QuelleMaravillas-Montero, José L., Orestes López-Ortega, Genaro Patiño-López und Leopoldo Santos-Argumedo. „Myosin 1g regulates cytoskeleton plasticity, cell migration, exocytosis, and endocytosis in B lymphocytes“. European Journal of Immunology 44, Nr. 3 (16.01.2014): 877–86. http://dx.doi.org/10.1002/eji.201343873.
Der volle Inhalt der QuellePatino Lopez, Genaro, E. Michael Ostap und Stephen Shaw. „Myosin 1G is a hematopoietic-restricted protein highly enriched in lymphocyte plasma membrane/microvilli whose deficiency impairs lymphocyte activation (35.40)“. Journal of Immunology 182, Nr. 1_Supplement (01.04.2009): 35.40. http://dx.doi.org/10.4049/jimmunol.182.supp.35.40.
Der volle Inhalt der QuellePicquet, F., V. Bouet, L. Cochon, M. Lacour und M. Falempin. „Changes in rat soleus muscle phenotype consecutive to a growth in hypergravity followed by normogravity“. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, Nr. 1 (Juli 2005): R217—R224. http://dx.doi.org/10.1152/ajpregu.00596.2004.
Der volle Inhalt der QuellePatino-Lopez, Genaro, L. Aravind, Xiaoyun Dong, Michael J. Kruhlak, E. Michael Ostap und Stephen Shaw. „Myosin 1G Is an Abundant Class I Myosin in Lymphocytes Whose Localization at the Plasma Membrane Depends on Its Ancient Divergent Pleckstrin Homology (PH) Domain (Myo1PH)“. Journal of Biological Chemistry 285, Nr. 12 (12.01.2010): 8675–86. http://dx.doi.org/10.1074/jbc.m109.086959.
Der volle Inhalt der QuelleDissertationen zum Thema "Myosin 1g"
Janardhana, Kurup Akshai. „Étude de la myosine nonconventionelle myosine1g dans l'asymétrie droite-gauche du poisson zèbre“. Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://www.theses.fr/2022COAZ6028.
Der volle Inhalt der QuelleLeft-Right (LR) asymmetry refers to the asymmetric placement of organs across the midline. Dysregulation of LR asymmetry establishment during animal development can lead to misplaced organs - a situation that can be lethal.I use zebrafish as a model to study the mechanisms that establish LR asymmetry. In zebrafish, a ciliated organ - Kupffer's Vesicle (KV) acts as a central LR organizer (LRO). The Nodal ligand Southpaw (Spaw) and its antagonist Dand5 are initially expressed in a symmetric fashion around the LRO. The beating of cilia in the LRO establishes a directional fluid flow that represses Dand5 on the left, allowing Spaw to spread on the left side through auto-induction and thereby direct the laterality of heart, brain and viscera.In contrast to many vertebrates, Drosophila establishes LR asymmetry independently of cilia using chiral cell remodeling controlled by the unconventional Myosin Myo1D. Our group showed previously that zebrafish Myo1D regulates LR asymmetry by orienting KV cilia and promoting the formation of a symmetry-breaking fluid flow. In addition to myo1d, the zebrafish genome encodes the closely related gene myo1g. The objective of my PhD work has been to study the contribution of Myo1G to the establishment of zebrafish LR asymmetry.KV acts as a central LRO that controls the laterality of the different organs of the animal. Accordingly, myo1d mutants that have an altered LRO flow present LR defects at the level of the heart, brain and viscera. In contrast, myo1g mutants present LR defects in heart and brain but not viscera, suggesting that myo1g may exert a flow-independent function in LR asymmetry.In order to directly test this hypothesis, I inactivated myo1g in dnaaf1 mutants which lack ciliary motility and present therefore no LRO flow. While the asymmetric movement of cardiac precursors is randomized to either the left or right side in dnaaf1 single mutants, asymmetric precursor cell movement is altogether lost in myo1g ; dnaaf1 double mutants, demonstrating thereby that myo1g functions indeed independently of the LRO flow.My work reveals that in contrast to Myo1D which regulates LRO cilia orientation, Myo1G is required for the Nodal-mediated transfer of laterality information from the central LRO to different target tissues. In myo1g mutants, spaw expression remains limited to the posterior of the embryo, properly guiding the laterality establishment of the posterior viscera, whereas the anterior heart and brain fail to establish laterality.In the context of the establishment of Zebrafish LR asymmetry, the Nodal ligand Spaw binds to a receptor complex formed by Acvr2, Alk4 and the co-receptor Oep. Productive ligand/receptor interactions trigger the phosphorylation of the downstream transcription factors Smad2/3, which then translocate into the nucleus to activate downstream genes. Nodal signal transduction induces spaw itself (which therefore propagates through auto-induction) as well the Nodal antagonist lefty1.When I injected equal amounts of spaw mRNA in WT and myo1g mutants and assessed the response by monitoring lefty1 activation, myo1g mutant embryos displayed a weaker response to spaw overexpression than their WT siblings, indicating thereby an impairment in Nodal signal transduction. In contrast, misexpression of constitutively activated smad2 produced equivalent responses in WT and myo1g mutant animals.Of particular interest, previous studies have implicated Myosin1 proteins in the endocytic trafficking of TGFβ receptor molecules. Different endocytic pathways have been shown to either promote TGFβ receptor signal transduction or conversely trigger receptor degradation. My work shows that myo1g mutants present a decrease in the number of Nodal-receptor positives endosomes, suggesting thereby that Myo1G may regulate LR asymmetry by controlling TGFβ receptor trafficking
Konferenzberichte zum Thema "Myosin 1g"
Souza, Taís Aparecida Matozo de, Letícia Kogachi, Maria Clara Martins Ferreira, Tania Carolina Reis und Bruna Alencar. „Myosin 1g involvement in HIV-1 entry and infection in Jurkat cells“. In Anais do XXXII Congresso Brasileiro de Virologia: Virologia em Casa. Recife, Brasil: Even3, 2021. http://dx.doi.org/10.29327/146355.32-11.
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