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Добірка наукової літератури з теми "Kpnb1"

Автор: Grafiati

Опубліковано: 29 березня 2025

Оновлено: 31 липня 2025

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Статті в журналах з теми "Kpnb1"

Mihalas, Bettina P., Patrick S. Western, Kate L. Loveland, Eileen A. McLaughlin, and Janet E. Holt. "Changing expression and subcellular distribution of karyopherins during murine oogenesis." REPRODUCTION 150, no. 6 (2015): 485–96. http://dx.doi.org/10.1530/rep-14-0585.

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Mammalian oocyte growth and development is driven by a strict program of gene expression that relies on the timely presence of transcriptional regulators via nuclear pores. By targeting specific cargos for nucleo-cytoplasmic transport, karyopherin (KPN) proteins are key to the relocation of essential transcription factors and chromatin-remodelling factors into and out of the nucleus. Using multiple complementary techniques, here we establish that KPNA genes and proteins are dynamically expressed and relocalised throughout mouse oogenesis and folliculogenesis. Of the KPNAs examined (Kpna1, Kpna

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Sato, Kota, Hironori Yoshino, Yoshiaki Sato, Manabu Nakano та Eichi Tsuruga. "ΔNp63 Regulates Radioresistance in Human Head and Neck Squamous Carcinoma Cells". Current Issues in Molecular Biology 45, № 8 (2023): 6262–71. http://dx.doi.org/10.3390/cimb45080394.

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Radiation therapy is commonly used to treat head and neck squamous cell carcinoma (HNSCC); however, recurrence results from the development of radioresistant cancer cells. Therefore, it is necessary to identify the underlying mechanisms of radioresistance in HNSCC. Previously, we showed that the inhibition of karyopherin-β1 (KPNB1), a factor in the nuclear transport system, enhances radiation-induced cytotoxicity, specifically in HNSCC cells, and decreases the localization of SCC-specific transcription factor ΔNp63. This suggests that ΔNp63 may be a KPNB1-carrying nucleoprotein that regulates

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Hazawa, Masaharu, Hironori Yoshino, Yuta Nakagawa та ін. "Karyopherin-β1 Regulates Radioresistance and Radiation-Increased Programmed Death-Ligand 1 Expression in Human Head and Neck Squamous Cell Carcinoma Cell Lines". Cancers 12, № 4 (2020): 908. http://dx.doi.org/10.3390/cancers12040908.

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Nuclear transport receptors, such as karyopherin-β1 (KPNB1), play important roles in the nuclear-cytoplasmic transport of macromolecules. Recent evidence indicates the involvement of nuclear transport receptors in the progression of cancer, making these receptors promising targets for the treatment of cancer. Here, we investigated the anticancer effects of KPNB1 blockage or in combination with ionizing radiation on human head and neck squamous cell carcinoma (HNSCC). HNSCC cell line SAS and Ca9-22 cells were used in this study. Importazole, an inhibitor of KPNB1, or knockdown of KPNB1 by siRNA

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Kodama, Michiko, Takahiro Kodama, Justin Y. Newberg, et al. "In vivo loss-of-function screens identify KPNB1 as a new druggable oncogene in epithelial ovarian cancer." Proceedings of the National Academy of Sciences 114, no. 35 (2017): E7301—E7310. http://dx.doi.org/10.1073/pnas.1705441114.

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Epithelial ovarian cancer (EOC) is a deadly cancer, and its prognosis has not been changed significantly during several decades. To seek new therapeutic targets for EOC, we performed an in vivo dropout screen in human tumor xenografts using a pooled shRNA library targeting thousands of druggable genes. Then, in follow-up studies, we performed a second screen using a genome-wide CRISPR/Cas9 library. These screens identified 10 high-confidence drug targets that included well-known oncogenes such as ERBB2 and RAF1, and novel oncogenes, notably KPNB1, which we investigated further. Genetic and pha

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Yoshino, Hironori, Yoshiaki Sato, and Manabu Nakano. "KPNB1 Inhibitor Importazole Reduces Ionizing Radiation-Increased Cell Surface PD-L1 Expression by Modulating Expression and Nuclear Import of IRF1." Current Issues in Molecular Biology 43, no. 1 (2021): 153–62. http://dx.doi.org/10.3390/cimb43010013.

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Programmed death-ligand 1 (PD-L1) is an immune checkpoint molecule that negatively regulates anti-tumor immunity. Recent reports indicate that anti-cancer treatments, such as radiation therapy, increase PD-L1 expression on the surface of tumor cells. We previously reported that the nuclear transport receptor karyopherin-β1 (KPNB1) is involved in radiation-increased PD-L1 expression on head-and-neck squamous cell carcinoma cells. However, the mechanisms underlying KPNB1-mediated, radiation-increased PD-L1 expression remain unknown. Thus, the mechanisms of radiation-increased, KPNB1-mediated PD-

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Park, Chanhee, Jiwon Oh, Won Mo Lee та ін. "Inhibition of NUPR1–Karyopherin β1 Binding Increases Anticancer Drug Sensitivity". International Journal of Molecular Sciences 22, № 6 (2021): 2794. http://dx.doi.org/10.3390/ijms22062794.

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Background: Nuclear protein-1 (NUPR1, also known as p8/Com-1) is a transcription factor involved in the regulation of cellular stress responses, including serum starvation and drug stimulation. Methods: We investigated the mechanism of NUPR1 nuclear translocation involving karyopherin β1 (KPNB1), using a single-molecule binding assay and confocal microscopy. The cellular effects associated with NUPR1–KPNB1 inhibition were investigated by gene expression profiling and cell cycle analysis. Results: The single-molecule binding assay revealed that KPNB1 bound to NUPR1 with a binding affinity of 0.

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Zeng, Yan, Yuna Wang, Zhiqin Wu, et al. "miR-9 enhances the transactivation of nuclear factor of activated T cells by targeting KPNB1 and DYRK1B." American Journal of Physiology-Cell Physiology 308, no. 9 (2015): C720—C728. http://dx.doi.org/10.1152/ajpcell.00299.2014.

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The fast response to stimuli and subsequent activation of the nuclear factor of activated T cells (NFAT) signaling pathway play an essential role in human T cell functions. MicroRNAs (miRNAs) are increasingly implicated in regulation of numerous biological and pathological processes. In this study we demonstrate a novel function of miRNA-9 (miR-9) in regulation of the NFAT signaling pathway. Upon PMA-ionomycin stimulation, miR-9 was markedly increased, consistent with NFAT activation. Overexpression of miR-9 significantly enhanced NFAT activity and accelerated NFAT dephosphorylation and its nu

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Kim, Yong-Hak, Siyoung Ha, Jungwon Kim, and Seung Wook Ham. "Identification of KPNB1 as a Cellular Target of Aminothiazole Derivatives with Anticancer Activity." ChemMedChem 11, no. 13 (2016): 1406–9. http://dx.doi.org/10.1002/cmdc.201600159.

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Zhu, Zhi-Chuan, Ji-Wei Liu, Kui Li, Jing Zheng, and Zhi-Qi Xiong. "KPNB1 inhibition disrupts proteostasis and triggers unfolded protein response-mediated apoptosis in glioblastoma cells." Oncogene 37, no. 22 (2018): 2936–52. http://dx.doi.org/10.1038/s41388-018-0180-9.

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Zeng, Renya, and Jixin Dong. "Abstract 5491: Targeting importin-YAP axis in pancreatic ductal adenocarcinoma." Cancer Research 82, no. 12_Supplement (2022): 5491. http://dx.doi.org/10.1158/1538-7445.am2022-5491.

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Abstract Background: To date, pancreatic ductal adenocarcinoma (PDAC) remains to have a dismal prognosis, with a 5-year survival rate of only 10%, which brings out an imperative to develop new therapeutic strategies to improve patient outcome. Recently, aberrant nucleocytoplasmic transport machinery in cancer cells has emerged as a rational therapeutic target. We aim to validate the nuclear importin complex involved in the import of macromolecules across the nuclear membrane as a potential therapeutic target in PDAC. Methods: Tet-inducible shRNA and FDA-approved agent (Ivermectin) were used fo

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Більше джерел

Дисертації з теми "Kpnb1"

Stelma, Tamara. "The effect of inhibiting KPNB1-mediated nuclear import on cancer cell biology and inflammatory transcription factor signalling." Doctoral thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/27888.

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Cancer remains one of the major causes of morbidity and mortality globally. Many novel and innovative approaches have been employed to develop new chemotherapeutic strategies, of which targeted therapies aim to identify a molecular lesion or dysregulated pathway that cancer cells are dependent on. Research in our laboratory and others identified the nuclear import protein, Karyopherin β1 (KPNB1), to be overexpressed in various cancers and that inhibiting its expression blocks the proliferation of cancer cells. However, little is known about the potential role of KPNB1 in other cancer cell phen

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Queron, Brenda. "Étude du mode d'action du DV188 dans l'inhibition des propriétés souches et tumorigéniques des cellules souches cancéreuses de gliome." Electronic Thesis or Diss., Université Côte d'Azur, 2024. http://www.theses.fr/2024COAZ6050.

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Les glioblastomes se classent parmi les tumeurs cérébrales les plus agressives, caractérisées par une hétérogénéité intratumorale, une faible espérance de vie et une résistance prononcée aux traitements par radio-chimiothérapie. La complexité de ces tumeurs réside notamment dans la présence de cellules souches de gliomes (CSG), impliquées dans la prolifération clonale, l'invasivité et la récidive tumorale. Les CSG expriment divers marqueurs de cellules souches et de pluripotence tels que NANOG et SOX2. Ces facteurs de transcription doivent être transloqués dans le noyau cellulaire pour active

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Van, der Watt Pauline Janet. "Expression and regulation of the nuclear transport proteins, Crm1 and Kpnß1, in cervical cancer and transformed cells." Doctoral thesis, University of Cape Town, 2009. http://hdl.handle.net/11427/3152.

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Pradezynski, Fabrine. "Modulation du système interféron de type I par les virus : en particulier par le virus de l'hépatite C et le virus influenza." Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10252.

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Afin de se répliquer et de se propager efficacement, les virus ont développé de multiples stratégies leur permettant d’échapper au système de défense innée : le système IFN de type I. Ce travail de thèse a alors consisté à étudier les interactions entre protéines virales et protéines de ce système de défense afin de mieux comprendre les mécanismes de subversion virale et d’identifier d’éventuelles cibles cellulaires thérapeutiques. La reconstruction d’un réseau d’interactions entre ces protéines nous a permis d’identifier des stratégies différentielles de subversion pour 4 familles virales et

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Тези доповідей конференцій з теми "Kpnb1"

Park, Chan Hee, Seung Wook Ham, HyeKyoung Shin, and Kyung Soo Oh. "Abstract 5138: Inhibition of kPNB1 and NUPR1 binding increase the anti-cancer drug sensitivity." 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.sabcs18-5138.

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Chi, Ru-pin, Wei Wei, Michael Birrer, and Virna D. Leaner. "Abstract 1069: Inhibition of the nuclear import receptor, KpnB1 synergizes with cisplatin toxicity in cervical cancer cells." In 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.am2017-1069.

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Kodama, Michiko, Takahiro Kodama, Kosuke Yoshihara, et al. "Abstract 411:In vivopooled shRNA library identifies KPNB1 as a new drug target for epithelial ovarian cancer." In 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.am2017-411.

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Stelma, Tamara, Alicia Chi, Anwar Mall, Dhiren Govender, and Virna D. Leaner. "Abstract B09: KPNB1-mediated nuclear import is required for inflammatory cytokine expression, invasion and survival of cancer cells." In Abstracts: AACR International Conference: New Frontiers in Cancer Research; January 18-22, 2017; Cape Town, South Africa. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.newfront17-b09.

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Du, Wenwen, Jianjie Zhu, Yuanyuan Zeng, Yang Zhang, Zeyi Liu, and Jian-An Huang. "KPNB1-mediated PD-L1 nuclear translocation promotes non-small cell lung cancer cell proliferation via the Gas6/MerTK signalling pathway." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1753.

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Fielhaber, Jill A., Jason Tan, Ortal Attais, Ying Shan Han, Kwang Bo Joung, and Arnold S. Kristof. "MTOR Regulates STAT1 Nuclear Trafficking Via KPNA1 In Lung Epithelial Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5112.

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Carden, Sarah, Pauline van der Watt, Patrizia Lavia та Virna Leaner. "Abstract B12: Investigating the specificity of the small molecule inhibitor INI-43 for Kpnβ1 in cancer cells". У Abstracts: AACR International Conference: New Frontiers in Cancer Research; January 18-22, 2017; Cape Town, South Africa. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.newfront17-b12.

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