Literatura científica selecionada sobre o tema "Cdc42 isoforms"
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Artigos de revistas sobre o assunto "Cdc42 isoforms"
Ravindran, Priyadarshini, e Andreas W. Püschel. "An isoform-specific function of Cdc42 in regulating mammalian Exo70 during axon formation". Life Science Alliance 6, n.º 3 (21 de dezembro de 2022): e202201722. http://dx.doi.org/10.26508/lsa.202201722.
Texto completo da fonteJansson, Thomas, Marisol Castillo-Castrejon, Madhulika B. Gupta, Theresa L. Powell e Fredrick J. Rosario. "Down-regulation of placental Cdc42 and Rac1 links mTORC2 inhibition to decreased trophoblast amino acid transport in human intrauterine growth restriction". Clinical Science 134, n.º 1 (janeiro de 2020): 53–70. http://dx.doi.org/10.1042/cs20190794.
Texto completo da fonteFediuk, Jena, Anurag S. Sikarwar, Nora Nolette e Shyamala Dakshinamurti. "Thromboxane-induced actin polymerization in hypoxic neonatal pulmonary arterial myocytes involves Cdc42 signaling". American Journal of Physiology-Lung Cellular and Molecular Physiology 307, n.º 11 (1 de dezembro de 2014): L877—L887. http://dx.doi.org/10.1152/ajplung.00036.2014.
Texto completo da fonteKolyada, Alexey Y., Kathleen N. Riley e Ira M. Herman. "Rho GTPase signaling modulates cell shape and contractile phenotype in an isoactin-specific manner". American Journal of Physiology-Cell Physiology 285, n.º 5 (novembro de 2003): C1116—C1121. http://dx.doi.org/10.1152/ajpcell.00177.2003.
Texto completo da fonteZhou, Rihong, Zhen Guo, Charles Watson, Emily Chen, Rong Kong, Wenxian Wang e Xuebiao Yao. "Polarized Distribution of IQGAP Proteins in Gastric Parietal Cells and Their Roles in Regulated Epithelial Cell Secretion". Molecular Biology of the Cell 14, n.º 3 (março de 2003): 1097–108. http://dx.doi.org/10.1091/mbc.e02-07-0425.
Texto completo da fonteFotiadou, Poppy P., Chiaki Takahashi, Hasan N. Rajabi e Mark E. Ewen. "Wild-Type NRas and KRas Perform Distinct Functions during Transformation". Molecular and Cellular Biology 27, n.º 19 (16 de julho de 2007): 6742–55. http://dx.doi.org/10.1128/mcb.00234-07.
Texto completo da fonteWang, Lin, William A. Rudert, Anatoly Grishin, Patrice Dombrosky-Ferlan, Kevin Sullivan, Xiaoying Deng, David Whitcomb e Seth Corey. "Identification and genetic analysis of human and mouse activated Cdc42 interacting protein-4 isoforms". Biochemical and Biophysical Research Communications 293, n.º 5 (maio de 2002): 1426–30. http://dx.doi.org/10.1016/s0006-291x(02)00398-4.
Texto completo da fonteJaiswal, Mamta, Eyad Kalawy Fansa, Radovan Dvorsky e Mohammad Reza Ahmadian. "New insight into the molecular switch mechanism of human Rho family proteins: shifting a paradigm". Biological Chemistry 394, n.º 1 (1 de janeiro de 2013): 89–95. http://dx.doi.org/10.1515/hsz-2012-0207.
Texto completo da fonteTcherkezian, Joseph, Eric I. Danek, Sarah Jenna, Ibtissem Triki e Nathalie Lamarche-Vane. "Extracellular Signal-Regulated Kinase 1 Interacts with and Phosphorylates CdGAP at an Important Regulatory Site". Molecular and Cellular Biology 25, n.º 15 (1 de agosto de 2005): 6314–29. http://dx.doi.org/10.1128/mcb.25.15.6314-6329.2005.
Texto completo da fonteLorenzi, Matthew V., Paola Castagnino, Qiong Chen, Yasuhiro Hori e Toru Miki. "Distinct expression patterns and transforming properties of multiple isoforms of Ost, an exchange factor for RhoA and Cdc42". Oncogene 18, n.º 33 (agosto de 1999): 4742–55. http://dx.doi.org/10.1038/sj.onc.1202851.
Texto completo da fonteTeses / dissertações sobre o assunto "Cdc42 isoforms"
Ravichandran, Yamini. "Cdc42 isoforms : localization, functions and regulation". Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS405.
Texto completo da fonteMutations in proteins cause diverse developmental disorders, particularly for individuals with rare diseases or for whom a unifying clinical diagnosis is unknown. Cdc42 is one such protein; vital for establishing cell polarity, a crucial step in many biological processes such as cell migration, division and immune responses. Not surprisingly, mutations in Cdc42 cause a range of diseases such as growth dysregulation, facial dysmorphism and neurodevelopmental, immunological, and hematological abnormalities. In vertebrates there are two isoforms of Cdc42. The first being the ubiquitous isoform, has almost exclusively been studied and the role of the second isoform, being the brain isoform, is largely unknown. We have shown that the two isoforms are localized differently in cells. The ubiquitous isoform is mostly found in the cell cytoplasm and at the plasma membrane, while the Brain isoform localizes at the Golgi apparatus and on intracellular vesicles. We have also shown that the two isoforms carry out different functions during cell migration, suggesting that the differences between these two isoforms which only differs by the last 10 amino acids are responsible for their distinct localisation and function. Interestingly, a mutation in the C-ter sequence of Cdc42 ubiquitous isoform alters Cdc42 localisation and causes a generalized pustular psoriasis disease. Two main objectives have been studied in this project 1) the impact of the last amino acids of the protein in Cdc42 localization; and 2) new regulatory mechanisms of Cdc42 responsible for its intracellular localization. These findings will bring a better understanding of pathologies related to Cdc42 mutations
Fediuk, Jena. "Thromboxane receptor signaling and Rho GTPase activation on actin polymerization and contraction in hypoxic neonatal pulmonary arterial myocytes". Am J Physiol Lung Cell Mol Physiol, 2012. http://hdl.handle.net/1993/23862.
Texto completo da fonteKiso, Marina. "Long isoform of VEGF stimulates cell migration of breast cancer by filopodia formation via NRP1/ARHGAP17/Cdc42 regulatory network". Kyoto University, 2018. http://hdl.handle.net/2433/235980.
Texto completo da fonteTrabalhos de conferências sobre o assunto "Cdc42 isoforms"
Kiso, Marina, Sunao Tanaka, Masakazu Toi e Fumiaki Sato. "Abstract 2862: Long isoform of VEGF stimulates cell migration of breast cancer by filopodia formation via NRP1/ARHGAP17/Cdc42 regulatory network". In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2862.
Texto completo da fonteKiso, Marina, Sunao Tanaka, Masakazu Toi e Fumiaki Sato. "Abstract 2862: Long isoform of VEGF stimulates cell migration of breast cancer by filopodia formation via NRP1/ARHGAP17/Cdc42 regulatory network". In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2862.
Texto completo da fonte