Relevant bibliographies by topics / Nuak1

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  1. Journal articles
  2. Dissertations / Theses
  3. Conference papers

Academic literature on the topic 'Nuak1'

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Published: 25 January 2025

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Journal articles on the topic "Nuak1"

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Sun, Xianglan, Ling Gao, Hung-Yu Chien, Wan-Chun Li, and Jiajun Zhao. "The regulation and function of the NUAK family." Journal of Molecular Endocrinology 51, no. 2 (July 19, 2013): R15—R22. http://dx.doi.org/10.1530/jme-13-0063.

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AMP-activated protein kinase (AMPK) is a critical regulator of cellular and whole-body energy homeostasis. Twelve AMPK-related kinases (ARKs; BRSK1, BRSK2, NUAK1, NUAK2, QIK, QSK, SIK, MARK1, MARK2, MARK3, MARK4, and MELK) have been identified recently. These kinases show a similar structural organization, including an N-terminal catalytic domain, followed by a ubiquitin-associated domain and a C-terminal spacer sequence, which in some cases also contains a kinase-associated domain 1. Eleven of the ARKs are phosphorylated and activated by the master upstream kinase liver kinase B1. However, most of these ARKs are largely unknown, and the NUAK family seems to have different regulations and functions. This review contains a brief discussion of the NUAK family including the specific characteristics of NUAK1 and NUAK2.
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Banerjee, Sourav, Sara J. Buhrlage, Hai-Tsang Huang, Xianming Deng, Wenjun Zhou, Jinhua Wang, Ryan Traynor, Alan R. Prescott, Dario R. Alessi, and Nathanael S. Gray. "Characterization of WZ4003 and HTH-01-015 as selective inhibitors of the LKB1-tumour-suppressor-activated NUAK kinases." Biochemical Journal 457, no. 1 (December 10, 2013): 215–25. http://dx.doi.org/10.1042/bj20131152.

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We describe the discovery of structurally diverse kinase inhibitors to dissect the physiological roles of the NUAK isoforms. We recommend use of an inhibitor-resistant NUAK1[A195T] mutant to verify that the physiological effects of these compounds is indeed mediated through inhibition of NUAKs
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van de Vis, Reinofke A. J., Aristidis Moustakas, and Lars P. van der Heide. "NUAK1 and NUAK2 Fine-Tune TGF-β Signaling." Cancers 13, no. 13 (July 5, 2021): 3377. http://dx.doi.org/10.3390/cancers13133377.

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Transforming growth factor-β (TGF-β) signaling plays a key role in governing various cellular processes, extending from cell proliferation and apoptosis to differentiation and migration. Due to this extensive involvement in the regulation of cellular function, aberrant TGF-β signaling is frequently implicated in the formation and progression of tumors. Therefore, a full understanding of the mechanisms of TGF-β signaling and its key components will provide valuable insights into how this intricate signaling cascade can shift towards a detrimental course. In this review, we discuss the interplay between TGF-β signaling and the AMP-activated protein kinase (AMPK)-related NUAK kinase family. We highlight the function and regulation of these kinases with focus on the pivotal role NUAK1 and NUAK2 play in regulating TGF-β signaling. Specifically, TGF-β induces the expression of NUAK1 and NUAK2 that regulates TGF-β signaling output in an opposite manner. Besides the focus on the TGF-β pathway, we also present a broader perspective on the expression and signaling interactions of the NUAK kinases to outline the broader functions of these protein kinases.
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Banerjee, Sourav, Anna Zagórska, Maria Deak, David G. Campbell, Alan R. Prescott, and Dario R. Alessi. "Interplay between Polo kinase, LKB1-activated NUAK1 kinase, PP1βMYPT1 phosphatase complex and the SCFβTrCP E3 ubiquitin ligase." Biochemical Journal 461, no. 2 (June 26, 2014): 233–45. http://dx.doi.org/10.1042/bj20140408.

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The present study provides insights into the biological regulation of the NUAK isoforms and highlights the remarkable interplay that exists between Polo kinase, NUAK1, PP1βMYPT1 and SCFβTrCP signalling components. It demonstrates NUAK1 inhibitors suppress cell proliferation and PLK1.
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Yang, Jian, Jian Lu, Ni Yin, Jingyue Sun, Jianhong Pu, and Jin Zang. "miR-622 Counteracts the NUAK1-Induced Gastric Cancer Cell Proliferation and the Antioxidative Stress." Disease Markers 2022 (July 14, 2022): 1–21. http://dx.doi.org/10.1155/2022/9616764.

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Background. Gastric cancer (GC), a highly prevalent gastric cancer, has high-risk mortality. Thus, investigating strategies to counteract its growth is important to provide theoretical guidance for its prevention and treatment. It has been pointed out that abnormal expression of microRNAs (miRNAs) serves as noninvasive biomarkers for GC. This present study probed into the role of miR-622 and the NUAK family SNF1-like kinase 1 (NUAK1). Methods. Five mRNA datasets (GSE64916, GSE118916, GSE122401, GSE158662, and GSE159721) and one miRNA dataset (GSE128720) from the Gene Expression of Omnibus (GEO) database were used to analyze the differentially expressed miRNAs and mRNA in GC and noncancer samples. Further, western blot, real-time quantitative PCR (qRT-PCR), reactive oxygen species (ROS) assay kit experiments, and wound healing assay, together with in vivo experiments, were performed. Results. miR-622 was downregulated, and NUAK1 was upregulated in GC, and NUAK1 was a potential target of miR-622. Knocking down NUAK1 decreased GC cell proliferation and migration but increased oxidative stress in vitro and inhibited the development of tumor in vivo, while miR-622 acted to suppress the action of NUAK1 through the miR-622/NUAK1/p-protein kinase B (Akt) axis, thereby inhibiting the occurrence of GC. Conclusion. miR-622 and NUAK1 demonstrated potential for being targets and biomarkers for GC treatment.
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Ohmura, Tomomi, Go Shioi, Mariko Hirano, and Shinichi Aizawa. "Neural tube defects by NUAK1 and NUAK2 double mutation." Developmental Dynamics 241, no. 8 (June 22, 2012): 1350–64. http://dx.doi.org/10.1002/dvdy.23816.

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Yu, Yuhui, Yongsheng Wang, Xiangying Xiao, Wei Cheng, Liqiang Hu, Weiyun Yao, Zhangxuan Qian, and Wei Wu. "MiR-204 inhibits hepatocellular cancer drug resistance and metastasis through targeting NUAK1." Biochemistry and Cell Biology 97, no. 5 (October 2019): 563–70. http://dx.doi.org/10.1139/bcb-2018-0354.

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Liver cancer is a leading cause of cancer-related deaths globally. Tumor response rate of liver cancer patients towards systemic chemotherapy is low and chemoresistance can easily develop. Identifying novel molecules that can repress drug resistance and metastasis of liver cancer will facilitate the development of new therapeutic strategies. The aim of this study is to determine the roles of NUAK1 and miR-204 in the drug resistance and metastasis of liver cancer and to reveal their relationship. We found that NUAK1 was increased in the tumor of primary liver cancer. Knockdown of NUAK1 significantly inhibited cell growth and migration. Moreover, NUAK1 was the direct downstream target of miR-204, and there was clinical relevance between miR-204 down-regulation and NUAK1 up-regulation in liver cancer. Furthermore, we found that miR-204 increased drug sensitivity by down-regulating NUAK1 expression. Based on these results, we identified miR-204 as a tumor suppressor by inhibiting NUAK1 expression in liver cancer, indicating both miR-204 and NUAK1 may act as promising targets for liver cancer therapy.
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Navarrete, Daniel J., Chi Yong Kim, Mario Gonzalez, Barbara Baro, Christian Doerig, Shao-En Ong, Martin Golkowski, and Elizabeth S. Egan. "Investigating a Novel Erythrocyte Kinase and Its Impact on Plasmodium Falciparum Infection." Blood 144, Supplement 1 (November 5, 2024): 2456. https://doi.org/10.1182/blood-2024-211105.

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Plasmodium falciparum has the proclivity to develop drug resistance, raising a need for novel malaria treatments. Host-directed therapeutics are emerging as a new approach to the treatment of several infectious diseases, but their potential utility in malaria infection remains largely unexplored, in part because of our limited understanding of erythrocyte host determinants of malaria infection. To begin to elucidate erythrocyte signaling pathways important for P. falciparum invasion, we performed phospho-antibody microarray experiments using cultured red blood cells (cRBCs) derived ex-vivo from hematopoietic stem cells (HSPCs), enabling the interrogation of both wildtype cells and those with deletion of a critical invasion factor, CD44. Stimulation of these cells with the P. falciparum invasion ligand EBA175 revealed altered phosphorylation of several host kinases, including NUAK1. Using immunoblotting, we confirmed that NUAK1 phosphorylation is increased in EBA175-stimulated cRBCs and in P. falciparum-infected donor RBCs. Together, these data suggest that NUAK1 plays an important role during P. falciparum infection. In other cells, NUAK1 is associated with tumor suppression, proliferation, and oxidative stress, but its function in RBCs is unknown. To determine if NUAK1 controls P. falciparum proliferation in erythrocytes, we performed parasite proliferation assays using two highly selective NUAK1 inhibitors, HTH-01-015 and WZ4003. We found that they inhibited the growth of multiple P. falciparum strains in a dose-dependent manner (IC50 <3 µM), with activity throughout the blood stage. Using egress assays and live microscopy, we found that HTH-01-015 does not inhibit merozoite egress but instead specifically blocks invasion. Importantly, discharge of the P. falciparum microneme organelles was not affected, suggesting that the observed phenotypes were due to an effect of the inhibitor on the host cell. Studies using the immortalized erythroblast cell line BEL-A revealed that the inhibitors disrupted erythroid cell growth (IC50 2.6 µM), consistent with a host cell target. To further examine specificity, we performed kinobead competition assays with HTH-01-015 and WZ4003 in human cell lysates, which identified only NUAK1 and two other human kinases as possible targets. In contrast, our kinobead experiments using P. falciparum lysates revealed that none of the 60 Plasmodium kinases interacted with the inhibitors, underscoring their selectivity for human kinases. Furthermore, we have demonstrated that treatment with HTH-01-015 inhibits phosphorylation of a well-characterized NUAK1 substrate, Myosin phosphatase target subunit 1 (MYPT1), in BEL-A cells. Since myosin is a component of the RBC cytoskeleton, it is tempting to speculate that EBA binding results in NUAK activation, which in turn triggers the mobilization of regulators of RBC cytoskeleton dynamics to promote invasion. In ongoing work to validate this hypothesis, we are using phosphoproteomics to interrogate the system-wide effect of these inhibitors on signaling networks in P. falciparum-infected RBCs, as well as genome editing to generate inhibitor-resistant cRBCs for use in P. falciparum growth assays. We propose that a better understanding of these intricate host-parasite interactions offers opportunities for more effective, resistance-refractory antimalarial therapies, highlighting the crucial role of hematological insights in advancing malaria treatment strategies.
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Fritz, Jamie Lee, Olga Collins, Parima Saxena, Adrian Buensuceso, Yudith Ramos Valdes, Kyle E. Francis, Kevin R. Brown, et al. "A Novel Role for NUAK1 in Promoting Ovarian Cancer Metastasis through Regulation of Fibronectin Production in Spheroids." Cancers 12, no. 5 (May 15, 2020): 1250. http://dx.doi.org/10.3390/cancers12051250.

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Epithelial ovarian cancer (EOC) has a unique mode of metastasis, where cells shed from the primary tumour, form aggregates called spheroids to evade anoikis, spread through the peritoneal cavity, and adhere to secondary sites. We previously showed that the master kinase Liver kinase B1 (LKB1) is required for EOC spheroid viability and metastasis. We have identified novel (nua) kinase 1 (NUAK1) as a top candidate LKB1 substrate in EOC cells and spheroids using a multiplex inhibitor beads-mass spectrometry approach. We confirmed that LKB1 maintains NUAK1 phosphorylation and promotes its stabilization. We next investigated NUAK1 function in EOC cells. Ectopic NUAK1-overexpressing EOC cell lines had increased adhesion, whereas the reverse was seen in OVCAR8-NUAK1KO cells. In fact, cells with NUAK1 loss generate spheroids with reduced integrity, leading to increased cell death after long-term culture. Following transcriptome analysis, we identified reduced enrichment for cell interaction gene expression pathways in OVCAR8-NUAK1KO spheroids. In fact, the FN1 gene, encoding fibronectin, exhibited a 745-fold decreased expression in NUAK1KO spheroids. Fibronectin expression was induced during native spheroid formation, yet this was completely lost in NUAK1KO spheroids. Co-incubation with soluble fibronectin restored the compact spheroid phenotype to OVCAR8-NUAK1KO cells. In a xenograft model of intraperitoneal metastasis, NUAK1 loss extended survival and reduced fibronectin expression in tumours. Thus, we have identified a new mechanism controlling EOC metastasis, through which LKB1-NUAK1 activity promotes spheroid formation and secondary tumours via fibronectin production.
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Al-Hakim, Abdallah K., Anna Zagorska, Louise Chapman, Maria Deak, Mark Peggie, and Dario R. Alessi. "Control of AMPK-related kinases by USP9X and atypical Lys29/Lys33-linked polyubiquitin chains." Biochemical Journal 411, no. 2 (March 27, 2008): 249–60. http://dx.doi.org/10.1042/bj20080067.

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AMPK (AMP-activated protein kinase)-related kinases regulate cell polarity as well as proliferation and are activated by the LKB1-tumour suppressor kinase. In the present study we demonstrate that the AMPK-related kinases, NUAK1 (AMPK-related kinase 5) and MARK4 (microtubule-affinity-regulating kinase 4), are polyubiquitinated in vivo and interact with the deubiquitinating enzyme USP9X (ubiquitin specific protease-9). Knockdown of USP9X increased polyubiquitination of NUAK1 and MARK4, whereas overexpression of USP9X inhibited ubiquitination. USP9X, catalysed the removal of polyubiquitin chains from wild-type NUAK1, but not from a non-USP9X-binding mutant. Topological analysis revealed that ubiquitin monomers attached to NUAK1 and MARK4 are linked by Lys29 and/or Lys33 rather than the more common Lys48/Lys63. We find that AMPK and other AMPK-related kinases are also polyubiquitinated in cells. We identified non-USP9X-binding mutants of NUAK1 and MARK4 and find that these are hyper-ubiquitinated and not phosphorylated at their T-loop residue targeted by LKB1 when expressed in cells, suggesting that polyubiquitination may inhibit these enzymes. The results of the present study demonstrate that NUAK1 and MARK4 are substrates of USP9X and provide the first evidence that AMPK family kinases are regulated by unusual Lys29/Lys33-linked polyubiquitin chains.
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Dissertations / Theses on the topic "Nuak1"

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Bull, Duncan. "Investigating the role and regulation of the AMPK-related kinase NUAK1." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/23995.

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AMP-activated protein kinase (AMPK) is a well characterised central regulator of energy homeostasis with many downstream substrates and potential therapeutic targets. Recently several kinases related to AMPK have been identified which are activated by the same upstream kinase, LKB1, and share significant sequence homology with the catalytic α subunit of AMPK. Previous studies have implicated NUAK1, one of these related kinases, in cell cycle regulation and other studies have identified various partner proteins but as yet there is no consensus model of its regulation or physiological role. This aim of this study was to investigate the regulation and interactions of NUAK1 using an in vitro system and also use an in vivo tissue specific mouse knockout system to investigate its function in two different tissues. The results of these studies reveal new insights into the regulation of NUAK1 in vitro and suggest that the kinase is capable of activation by autophosphorylation, in the absence of LKB1. NUAK1 is shown to interact with 14-3-3 proteins and evidence that this interaction may be important for the function of the kinase is presented. Cell based studies in mouse embryonic fibroblasts (MEFs) lacking NUAK1 show that it is involved in proliferation and there are suggestions of pathways involved in regulating this effect. NUAK1 liver-specific knockout mice were generated and extensive metabolic phenotyping analyses were carried out. In young animals deletion of NUAK1 in liver did not lead to any obvious changes in whole body metabolism. However, preliminary studies revealed a possible role for NUAK1 in metabolic regulation in older mice and in response to liver damage. Mice with heart-specific deletion of NUAK1 were generated and these mice were found to have a cardiac hypertrophy phenotype in response to angiotensin II treatment. Potential signalling pathways downstream of NUAK1 in the heart were then investigated in this model.
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Port, Jennifer Lynne Forbes. "Investigating the therapeutic potential of NUAK1 for the treatment of colorectal cancer." Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/9125/.

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Banerjee, Sourav. "Phosphorylation, ubiquitylation and characterisation of specific inhibitors of AMPK-related kinase NUAK1/ARK5." Thesis, University of Dundee, 2013. https://discovery.dundee.ac.uk/en/studentTheses/56802fcc-a203-40fb-a73b-2390d50af0a8.

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Monteverde, Tiziana. "Investigating the function and regulation of NUAK1 and its role in non-small cell lung cancer." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8701/.

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Lý, Hà My. "Characterization of a novel molecular pathway linking metabolic regulation and muscle stem cell fate." Electronic Thesis or Diss., Lyon 1, 2024. http://www.theses.fr/2024LYO10193.

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Le muscle strié squelettique possède une capacité de régénération grâce à une population de cellules souches musculaires (CSM ou cellules satellites) qui gardent une capacité à exprimer un programme myogénique lors d'une lésion musculaire. Une perte de la capacité myogénique des CSM est associée à la perte musculaire avec l'âge, mais aussi à des maladies invalidantes telles que les myopathies. Une des caractéristiques de la fonction des CSMs est leur plasticité métabolique qui supporte le programme myogénique. Sur la base de travaux antérieurs du laboratoire mettant en évidence le rôle central du régulateur métabolique AMPK dans la myogenèse adulte, j'ai identifié que NUAK1, une kinase liée à l'AMPK dont la fonction est associée à la régulation métabolique dans les neurones en développement, est un nouvel acteur dans la régulation du programme des CSMs et de la myogenèse adulte. L'activité de NUAK1 est nécessaire à la capacité de régénération musculaire et NUAK1 contrôle les aspects séquentiels du programme myogénique, c'est-à-dire l’engagement, la différenciation et la fusion des CSMs pour produire des myofibres matures et le renouvellement des CSMs. A l’échelle moléculaire, mes données préliminaires suggèrent que NUAK1 agit par la régulation du métabolisme des acides gras et de la biogenèse du cholestérol. Pendant ma doctorat, je confirme ce lien et décrypterai comment le facteur de transcription SREBP1, qui contrôle les voies métaboliques des lipides, intervient dans les fonctions de NUAK1 lors de la myogenèse adulte. Cette approche-candidat complétes par une approche non biaisée visant à identifier les changements du protéome et du fonctionnement mitochondrial. Par conséquent, mon travail de doctorat démontres un lien original entre le métabolisme des lipides et le devenir des CSMs, ce qui permettra d’identifier des cibles thérapeutiques potentielles dans les maladies du muscle
Muscle stem cells (MuSCs) provide a constant regenerative capacity to the skeletal muscle owing to their capacity to recapitulate a myogenic program upon muscle lesion. Alterations of MuSC myogenic capacity are associated to muscle loss with age, but also debilitating diseases such as myopathies. Metabolic plasticity is a hallmark of MuSC fate program. Based on previous work from the lab highlighting a central role for the metabolic regulator kinase AMPK in adult myogenesis, I adopted a candidate-based study that identified NUAK1, an AMPK-related kinase whose function is associated to metabolic regulation in developing neurons, as a novel player in the regulation of MuSC fate and adult myogenesis. NUAK1 expression is required for muscle regeneration capacity and NUAK1 controls sequential aspects of the myogenic program, ie. MuSC commitment and differentiation into myoblast, myoblast fusion to produce mature myofibers, and MuSC renewal. On a molecular level, I obtained exciting preliminary data suggesting that NUAK1 acts through the regulation of fatty acids and cholesterol biogenesis. During my PhD, I confirm this link and decipher how the transcription factor SREBP1, which controls lipid metabolic pathways, mediates the functions of NUAK1 during adult myogenesis. This candidate-based study completes by an unbiased approach aiming at identifying changes in mitochondrial metabolism. Overall, my PhD work demonstrate an original link between lipids metabolism and MuSC fate, which will give hints toward putative targets of therapeutic value
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Conference papers on the topic "Nuak1"

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Escalona, Emilia, Marcelo Muñoz, Roxana Pincheira, Alvaro A. Elorza, and Ariel F. Castro. "Abstract B083: NUAK1 regulates breast cancer cell bioenergetics." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-b083.

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Saxena, Parima, Olga Collins, Yudith Ramos Valdes, Adrian Buensuceso, Kyle Francis, Kevin Brown, Karen Colwill, et al. "Abstract A17: NUAK1 acts as a growth suppressor in epithelial ovarian cancer." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-a17.

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Titov, I. Yu, V. S. Stroylov, O. V. Stroganov, F. N. Novikov, I. V. Svitanko, and G. G. Chilov. "NOVEL 5,6,7,8-TETRAHYDROPYRAZINO[2,3-c]PYRIDAZINE3-CARBOXAMIDE DERIVATIVES AS DUAL ALK/NUAK1 INHIBITORS." In MedChem-Russia 2021. Издательство Волгоградского государственного медицинского университета, 2022. http://dx.doi.org/10.19163/medchemrussia2021-2022-25.

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Palma, Mario, Daniela Peña, Katherine Venturelli, and Ariel F. Castro. "Abstract A36: Nuclear NUAK1 function on cancer cell survival, independently of LKB1 and p53." In Abstracts: Fourth AACR International Conference on Frontiers in Basic Cancer Research; October 23-26, 2015; Philadelphia, PA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.fbcr15-a36.

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Sejd, Josilyn, and Smita Yadav. "Elucidating the Molecular Function of the Autism-Associated Kinase Nuak1 in Neurodevelopment and Disease." In ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.356.973290.

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Phippen, Neil T., Nicholas W. Bateman, Guisong Wang, Chad A. Hamilton, George L. Maxwell, Kathleen M. Darcy, and Thomas P. Conrads. "Abstract 4632: Poor survival associated with NUAK1 overexpression in serous ovarian cancer may be explained by chemotherapy resistance." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4632.

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Fu, Weiwei, Megan Zhao, Amelia Schirmer, Erick J. Maravilla, Junhee Yoon, Sungyong You, Stephen J. Freedland, and Everardo Macias. "Abstract B07: NUAK2 inhibition for prostate cancer." In Abstracts: AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; May 8-11, 2019; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-b07.

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Jia, Wang, XUE Jingyan, Hou Jianjing, Xiu Bingqiu, Li Lun, Chi Yayun, and Wu Jiong. "Abstract P3-01-21: Functional duality of NUAK2 in breast cancer metastases." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p3-01-21.

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Chen, Li, Oscar Gee-Wan Wong, Ivy Tsz-Lo Wong, and Annie Nga-Yin Cheung. "Abstract 5906: NUAK2 is highly overexpressed in ovarian cancer and the overexpression of its nuclear form correlates with tumor aggressiveness." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5906.

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Emmanuel, Catherine, Natalie Gava, Georgia Chenevix-Trench, Rosemary L. Balleine, Joshy George, David DL Bowtell, Christine L. Clarke, and Anna deFazio. "Abstract 3875: NUAK2, a gene with a putative driver mutation in ovarian cancer, is regulated through the murine estrus cycle and loss is associated with worse outcome in ovarian cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3875.

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