Littérature scientifique sur le sujet « Cdc42 isoformes »
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Articles de revues sur le sujet "Cdc42 isoformes"
Ravindran, Priyadarshini, et Andreas W. Püschel. « An isoform-specific function of Cdc42 in regulating mammalian Exo70 during axon formation ». Life Science Alliance 6, no 3 (21 décembre 2022) : e202201722. http://dx.doi.org/10.26508/lsa.202201722.
Texte intégralJansson, Thomas, Marisol Castillo-Castrejon, Madhulika B. Gupta, Theresa L. Powell et 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, no 1 (janvier 2020) : 53–70. http://dx.doi.org/10.1042/cs20190794.
Texte intégralKolyada, Alexey Y., Kathleen N. Riley et Ira M. Herman. « Rho GTPase signaling modulates cell shape and contractile phenotype in an isoactin-specific manner ». American Journal of Physiology-Cell Physiology 285, no 5 (novembre 2003) : C1116—C1121. http://dx.doi.org/10.1152/ajpcell.00177.2003.
Texte intégralFediuk, Jena, Anurag S. Sikarwar, Nora Nolette et 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, no 11 (1 décembre 2014) : L877—L887. http://dx.doi.org/10.1152/ajplung.00036.2014.
Texte intégralWirth, Alexander, Chen Chen-Wacker, Yao-Wen Wu, Nataliya Gorinski, Mikhail A. Filippov, Ghanshyam Pandey et Evgeni Ponimaskin. « Dual lipidation of the brain-specific Cdc42 isoform regulates its functional properties ». Biochemical Journal 456, no 3 (22 novembre 2013) : 311–22. http://dx.doi.org/10.1042/bj20130788.
Texte intégralZhou, Rihong, Zhen Guo, Charles Watson, Emily Chen, Rong Kong, Wenxian Wang et 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, no 3 (mars 2003) : 1097–108. http://dx.doi.org/10.1091/mbc.e02-07-0425.
Texte intégralFotiadou, Poppy P., Chiaki Takahashi, Hasan N. Rajabi et Mark E. Ewen. « Wild-Type NRas and KRas Perform Distinct Functions during Transformation ». Molecular and Cellular Biology 27, no 19 (16 juillet 2007) : 6742–55. http://dx.doi.org/10.1128/mcb.00234-07.
Texte intégralCARGINALE, Vincenzo, Rosaria SCUDIERO, Clemente CAPASSO, Antonio CAPASSO, Peter KILLE, Guido di PRISCO et Elio PARISI. « Cadmium-induced differential accumulation of metallothionein isoforms in the Antarctic icefish, which exhibits no basal metallothionein protein but high endogenous mRNA levels ». Biochemical Journal 332, no 2 (1 juin 1998) : 475–81. http://dx.doi.org/10.1042/bj3320475.
Texte intégralChen, Hung-Hsi, Yu-Chiuan Wang et Ming-Ji Fann. « Identification and Characterization of the CDK12/Cyclin L1 Complex Involved in Alternative Splicing Regulation ». Molecular and Cellular Biology 26, no 7 (1 avril 2006) : 2736–45. http://dx.doi.org/10.1128/mcb.26.7.2736-2745.2006.
Texte intégralScalia, Pierluigi, Carmen Merali, Carlos Barrero, Antonio Suma, Vincenzo Carnevale, Salim Merali et Stephen J. Williams. « Novel Isoform DTX3c Associates with UBE2N-UBA1 and Cdc48/p97 as Part of the EphB4 Degradation Complex Regulated by the Autocrine IGF-II/IRA Signal in Malignant Mesothelioma ». International Journal of Molecular Sciences 24, no 8 (17 avril 2023) : 7380. http://dx.doi.org/10.3390/ijms24087380.
Texte intégralThèses sur le sujet "Cdc42 isoformes"
Ravichandran, Yamini. « Cdc42 isoforms : localization, functions and regulation ». Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS405.
Texte intégralMutations 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.
Texte intégralKiso, 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.
Texte intégralActes de conférences sur le sujet "Cdc42 isoformes"
Kiso, Marina, Sunao Tanaka, Masakazu Toi et Fumiaki Sato. « Abstract 2862 : Long isoform of VEGF stimulates cell migration of breast cancer by filopodia formation via NRP1/ARHGAP17/Cdc42 regulatory network ». Dans 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.
Texte intégralKiso, Marina, Sunao Tanaka, Masakazu Toi et Fumiaki Sato. « Abstract 2862 : Long isoform of VEGF stimulates cell migration of breast cancer by filopodia formation via NRP1/ARHGAP17/Cdc42 regulatory network ». Dans 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.
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