Relevant bibliographies by topics / Endosidin2

Academic literature on the topic 'Endosidin2'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Endosidin2"

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Zhang, Chunhua, Michelle Q. Brown, Wilhelmina van de Ven, Zhi-Min Zhang, Bin Wu, Michael C. Young, Lukáš Synek, et al. "Endosidin2 targets conserved exocyst complex subunit EXO70 to inhibit exocytosis." Proceedings of the National Academy of Sciences 113, no. 1 (November 25, 2015): E41—E50. http://dx.doi.org/10.1073/pnas.1521248112.

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The exocyst complex regulates the last steps of exocytosis, which is essential to organisms across kingdoms. In humans, its dysfunction is correlated with several significant diseases, such as diabetes and cancer progression. Investigation of the dynamic regulation of the evolutionarily conserved exocyst-related processes using mutants in genetically tractable organisms such as Arabidopsis thaliana is limited by the lethality or the severity of phenotypes. We discovered that the small molecule Endosidin2 (ES2) binds to the EXO70 (exocyst component of 70 kDa) subunit of the exocyst complex, resulting in inhibition of exocytosis and endosomal recycling in both plant and human cells and enhancement of plant vacuolar trafficking. An EXO70 protein with a C-terminal truncation results in dominant ES2 resistance, uncovering possible distinct regulatory roles for the N terminus of the protein. This study not only provides a valuable tool in studying exocytosis regulation but also offers a potentially new target for drugs aimed at addressing human disease.
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Huang, Lei, Xiaohui Li, Yang Li, Xianglin Yin, Yong Li, Bin Wu, Huaping Mo, et al. "Endosidin2-14 Targets the Exocyst Complex in Plants and Fungal Pathogens to Inhibit Exocytosis." Plant Physiology 180, no. 3 (May 9, 2019): 1756–70. http://dx.doi.org/10.1104/pp.18.01457.

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Zhao, Yujie, Xiaoting Hong, Xiong Chen, Chun Hu, Weihong Lu, Baoying Xie, Linhai Zhong, et al. "Deregulation of Exo70 Facilitates Innate and Acquired Cisplatin Resistance in Epithelial Ovarian Cancer by Promoting Cisplatin Efflux." Cancers 13, no. 14 (July 11, 2021): 3467. http://dx.doi.org/10.3390/cancers13143467.

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Whilst researches elucidating a diversity of intracellular mechanisms, platinum-resistant epithelial ovarian cancer (EOC) remains a major challenge in the treatment of ovarian cancer. Here we report that Exo70, a key subunit of the exocyst complex, contributes to both innate and acquired cisplatin resistance of EOC. Upregulation of Exo70 is observed in EOC tissues and is related to platinum resistance and progression-free survival of EOC patients. Exo70 suppressed the cisplatin sensitivity of EOC cells through promoting exocytosis-mediated efflux of cisplatin. Moreover, cisplatin-induced autophagy-lysosomal degradation of Exo70 protein by modulating phosphorylation of AMPK and mTOR, thereby reducing the cellular resistance. However, the function was hampered during prolonged cisplatin treatment, which in turn stabilized Exo70 to facilitate the acquired cisplatin resistance of EOC cells. Knockdown of Exo70, or inhibiting exocytosis by Exo70 inhibitor Endosidin2, reversed the cisplatin resistance of EOC cells both in vitro and in vivo. Our results suggest that Exo70 overexpression and excessive stability contribute to innate and acquired cisplatin resistance through the increase in cisplatin efflux, and targeting Exo70 might be an approach to overcome cisplatin resistance in EOC treatment.
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Sharda, Anish V., Alexandra M. Barr, Joshua A. Harrison, Adrian R. Wilkie, Chao Fang, Lourdes M. Mendez, Ionita C. Ghiran, Joseph E. Italiano, and Robert Flaumenhaft. "VWF maturation and release are controlled by 2 regulators of Weibel-Palade body biogenesis: exocyst and BLOC-2." Blood 136, no. 24 (December 10, 2020): 2824–37. http://dx.doi.org/10.1182/blood.2020005300.

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Abstract von Willebrand factor (VWF) is an essential hemostatic protein that is synthesized in endothelial cells and stored in Weibel-Palade bodies (WPBs). Understanding the mechanisms underlying WPB biogenesis and exocytosis could enable therapeutic modulation of endogenous VWF, yet optimal targets for modulating VWF release have not been established. Because biogenesis of lysosomal related organelle-2 (BLOC-2) functions in the biogenesis of platelet dense granules and melanosomes, which like WPBs are lysosome-related organelles, we hypothesized that BLOC-2–dependent endolysosomal trafficking is essential for WPB biogenesis and sought to identify BLOC-2–interacting proteins. Depletion of BLOC-2 caused misdirection of cargo-carrying transport tubules from endosomes, resulting in immature WPBs that lack endosomal input. Immunoprecipitation of BLOC-2 identified the exocyst complex as a binding partner. Depletion of the exocyst complex phenocopied BLOC-2 depletion, resulting in immature WPBs. Furthermore, releasates of immature WPBs from either BLOC-2 or exocyst-depleted endothelial cells lacked high-molecular weight (HMW) forms of VWF, demonstrating the importance of BLOC-2/exocyst-mediated endosomal input during VWF maturation. However, BLOC-2 and exocyst showed very different effects on VWF release. Although BLOC-2 depletion impaired exocytosis, exocyst depletion augmented WPB exocytosis, indicating that it acts as a clamp. Exposure of endothelial cells to a small molecule inhibitor of exocyst, Endosidin2, reversibly augmented secretion of mature WPBs containing HMW forms of VWF. These studies show that, although BLOC-2 and exocyst cooperate in WPB formation, only exocyst serves to clamp WPB release. Exocyst function in VWF maturation and release are separable, a feature that can be exploited to enhance VWF release.
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Wilkop, Thomas E., Minmin Wang, Angelo Heringer, Jaideep Singh, Florence Zakharov, Viswanathan V. Krishnan, and Georgia Drakakaki. "NMR spectroscopy analysis reveals differential metabolic responses in arabidopsis roots and leaves treated with a cytokinesis inhibitor." PLOS ONE 15, no. 11 (November 6, 2020): e0241627. http://dx.doi.org/10.1371/journal.pone.0241627.

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In plant cytokinesis, de novo formation of a cell plate evolving into the new cell wall partitions the cytoplasm of the dividing cell. In our earlier chemical genomics studies, we identified and characterized the small molecule endosidin-7, that specifically inhibits callose deposition at the cell plate, arresting late-stage cytokinesis in arabidopsis. Endosidin-7 has emerged as a very valuable tool for dissecting this essential plant process. To gain insights regarding its mode of action and the effects of cytokinesis inhibition on the overall plant response, we investigated the effect of endosidin-7 through a nuclear magnetic resonance spectroscopy (NMR) metabolomics approach. In this case study, metabolomics profiles of arabidopsis leaf and root tissues were analyzed at different growth stages and endosidin-7 exposure levels. The results show leaf and root-specific metabolic profile changes and the effects of endosidin-7 treatment on these metabolomes. Statistical analyses indicated that the effect of endosidin-7 treatment was more significant than the developmental impact. The endosidin-7 induced metabolic profiles suggest compensations for cytokinesis inhibition in central metabolism pathways. This study further shows that long-term treatment of endosidin-7 profoundly changes, likely via alteration of hormonal regulation, the primary metabolism of arabidopsis seedlings. Hormonal pathway-changes are likely reflecting the plant’s responses, compensating for the arrested cell division, which in turn are leading to global metabolite modulation. The presented NMR spectral data are made available through the Metabolomics Workbench, providing a reference resource for the scientific community.
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Lockhart, Jennifer. "Endosidin20: A Key to Unlock the Secrets of Cellulose Biosynthesis." Plant Cell 32, no. 7 (May 14, 2020): 2061–62. http://dx.doi.org/10.1105/tpc.20.00382.

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Huang, Lei, Xiaohui Li, and Chunhua Zhang. "Endosidin20‐1 is more potent than endosidin20 in inhibiting plant cellulose biosynthesis and molecular docking analysis of cellulose biosynthesis inhibitors on modeled cellulose synthase structure." Plant Journal 106, no. 6 (April 21, 2021): 1605–24. http://dx.doi.org/10.1111/tpj.15258.

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Huang, Lei, Xiaohui Li, Weiwei Zhang, Nolan Ung, Nana Liu, Xianglin Yin, Yong Li, et al. "Endosidin20 Targets the Cellulose Synthase Catalytic Domain to Inhibit Cellulose Biosynthesis." Plant Cell 32, no. 7 (April 23, 2020): 2141–57. http://dx.doi.org/10.1105/tpc.20.00202.

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Huang, Lei, and Chunhua Zhang. "Endosidin20 does not affect cellulose synthase complex transport from ER to the Golgi." Plant Signaling & Behavior 15, no. 8 (June 21, 2020): 1780039. http://dx.doi.org/10.1080/15592324.2020.1780039.

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Park, Eunsook, Sara M. Díaz-Moreno, Destiny J. Davis, Thomas E. Wilkop, Vincent Bulone, and Georgia Drakakaki. "Endosidin 7 Specifically Arrests Late Cytokinesis and Inhibits Callose Biosynthesis, Revealing Distinct Trafficking Events during Cell Plate Maturation." Plant Physiology 165, no. 3 (May 23, 2014): 1019–34. http://dx.doi.org/10.1104/pp.114.241497.

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Book chapters on the topic "Endosidin2"

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Huang, Lei, and Chunhua Zhang. "Use Endosidin2 to Study Plant Exocytosis and Vacuolar Trafficking." In Plant Vacuolar Trafficking, 167–75. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7856-4_13.

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