Relevant bibliographies by topics / STK10

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Academic literature on the topic 'STK10'

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Published: 5 April 2025

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Journal articles on the topic "STK10"

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Ma, Jin-Xia, Dan-Dan Xu, Shun-Yuan Lu, Qian-Lan Wang, Lu Zhang, Rui Guo, Ling-Yun Tang, et al. "Stk10 Deficiency in Mice Promotes Tumor Growth by Dysregulating the Tumor Microenvironment." Biology 11, no. 11 (November 15, 2022): 1668. http://dx.doi.org/10.3390/biology11111668.

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Serine-threonine kinase 10 (STK10) is a member of the STE20/p21-activated kinase (PAK) family and is predominantly expressed in immune organs. Our previous reports suggested that STK10 participates in the growth and metastasis of prostate cancer via in vitro and in vivo data. However, the correlation between STK10 and the tumor microenvironment (TME) remains unclear. In this study, we assessed the relationship between STK10 and the immune cells in the tumor microenvironment of prostate cancer through bioinformatic analysis, and investigated the role of Stk10 in tumor growth using an Stk10 knockout mouse model. The results showed that STK10 is significantly associated with the tumor-infiltrating immune cells including lymphocytes, neutrophils, macrophages and dendritic cells. The target deletion of host Stk10 results in increased tumor growth, due to decreased activated/effector cytotoxic T lymphocytes (CTLs) and increased vessel density in the TME. In conclusion, we demonstrate that host Stk10 is involved in the host anti-tumor response by modulating the activated tumor-infiltrated CTLs and angiogenesis.
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Long, Zhangbiao, Jichun Yang, Xinyao Liu, Min Ruan, Danchen Meng, Junling Zhuang, Zhenqi Huang, Jian Ge, and Bing Han. "STK10 Mutation Block Erythropoiesis in Acquired Pure Red Cell Aplasia Via Down-Regulated the Ribosome Biosynthesis." Blood 142, Supplement 1 (November 28, 2023): 3825. http://dx.doi.org/10.1182/blood-2023-189722.

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Background: Acquired pure red cell aplasia (PRCA) is anemia associated with the absence of erythroblasts and characterized by persistent and easy recurrence. However, the underline mechanisms of acquired PRCA remain obscure, and the role of gene mutation in the pathogenesis of acquired PRCA was not elucidated yet. Aims: To identify gene mutations in acquired PRCA patients and their possible effects on the origin of the disease. Methods: Blood and buccal genome DNA extracted from thirty newly diagnosed patients with acquired PRCA were detected with whole exome sequencing. The candidate genes with high frequency in acquired PRCA but the low frequency in 1000 normal genomes which may affect protein function were selected. The pGreen-CMV-puro system was employed to generate lentivirus expressing short hairpin RNAs to target the candidate genes, and stable transfected K562 cell lines with silenced candidate genes were constructed. The erythroid and megakaryocytic differentiation was evaluated for the transfected K562 cell lines either by benzidine staining hemoglobin and CD235a expression or CD41 expression on the cell surface. STK10 gene was selected which affects the erythropoiesis. The influence of the STK10 gene on the expression of p53 mRNA/ protein was also detected. The RNA sequencing in STK10 silenced K562 cells was performed and KEGG enrichment was analyzed. Next, ribosome RNA synthesis was detected, and ribosome proteins and p53 signaling pathway were also detected by western blotting. Results: Through whole exome sequencing in patients with acquired PRCA, we confirmed that STK10 gene mutation is common in acquired PRCA patients, the mRNA/protein expression of STK10 was reduced and p53 increased in the bone marrow of the patients in which the gene mutated. Furthermore, the silence of the STK10 gene through the lentiviral vector harboring short hairpin RNAs in K562 cells could inhibit the erythropoiesis after being induced by Hemin. Whereas, CD41 expression was similar in STK10 silenced K562 cells to control K562 cells after being inducted by phorbol 12-myristate 13-acetate. We performed RNA sequencing in STK10 silenced K562 cells. KEGG enrichment analysis of differentially expressed ribosome biosynthesis pathway and p53 signaling pathway was affected. 28S and 18S in ribosome RNA synthesis impaired in these STK10 silenced K562 cells through RNA electrophoresis. Further, through the western blotting test in STK10 silenced K562 cells, we found ribosome proteins expression down-regulated and p53, phospho-p53 and p21 expression up-regulated due to STK10 mutated. Conclusion: STK10 gene mutation is common in patients with acquired PRCA and causes the reduction of mRNAs and protein expression in the mutated patients. The underlying research revealed STK10 gene mutation could affect the ribosome biosynthesis pathway and down-regulated the ribosome protein level, contributing to the abnormal erythropoiesis. This research elucidated the pathogenesis of PRCA, which may provide evidence for precise diagnosis and exploring potential therapeutic targets in patients with acquired PRCA. Keywords: pure red cell aplasia, mutation, erythropoiesis, STK10, ribosome biosynthesis
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FUKUMURA, KAZUTAKA, YOSHIHIRO YAMASHITA, MASAHITO KAWAZU, EIRIN SAI, SHIN-ICHIRO FUJIWARA, NAOYA NAKAMURA, KENGO TAKEUCHI, et al. "STK10 missense mutations associated with anti-apoptotic function." Oncology Reports 30, no. 4 (July 9, 2013): 1542–48. http://dx.doi.org/10.3892/or.2013.2605.

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Zhang, Lu, Shun-Yuan Lu, Rui Guo, Jin-Xia Ma, Ling-Yun Tang, Yan Shen, Chun-Ling Shen, et al. "Knockout of STK10 promotes the migration and invasion of cervical cancer cells." Translational Cancer Research 9, no. 11 (November 2020): 7079–90. http://dx.doi.org/10.21037/tcr-20-1601.

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Walter, Sarah A., Richard E. Cutler, Ricardo Martinez, Mikhail Gishizky, and Ronald J. Hill. "Stk10, a New Member of the Polo-like Kinase Kinase Family Highly Expressed in Hematopoietic Tissue." Journal of Biological Chemistry 278, no. 20 (March 13, 2003): 18221–28. http://dx.doi.org/10.1074/jbc.m212556200.

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Asquith, Christopher R. M., Tuomo Laitinen, James M. Bennett, Carrow I. Wells, Jonathan M. Elkins, William J. Zuercher, Graham J. Tizzard, and Antti Poso. "Design and Analysis of the 4‐Anilinoquin(az)oline Kinase Inhibition Profiles of GAK/SLK/STK10 Using Quantitative Structure‐Activity Relationships." ChemMedChem 15, no. 1 (November 26, 2019): 26–49. http://dx.doi.org/10.1002/cmdc.201900521.

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Kuramochi, Satomi, Yoichi Matsuda, Fujiko Kitamura, Mieko Okamoto, Hajime Karasuyama, and Hiromichi Yonekawa. "Molecular cloning of the human gene STK10 encoding lymphocyte-oriented kinase, and comparative chromosomal mapping of the human, mouse, and rat homologues." Immunogenetics 49, no. 5 (April 7, 1999): 369–75. http://dx.doi.org/10.1007/s002510050509.

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Asquith, Christopher R. M., Tuomo Laitinen, James M. Bennett, Carrow I. Wells, Jonathan M. Elkins, William J. Zuercher, Graham J. Tizzard, and Antti Poso. "Cover Feature: Design and Analysis of the 4‐Anilinoquin(az)oline Kinase Inhibition Profiles of GAK/SLK/STK10 Using Quantitative Structure‐Activity Relationships (ChemMedChem 1/2020)." ChemMedChem 15, no. 1 (January 7, 2020): 2. http://dx.doi.org/10.1002/cmdc.201900691.

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Sugawara, Yo, Hideharu Hagiya, Yukihiro Akeda, Dan Takeuchi, Noriko Sakamoto, Yuki Matsumoto, Daisuke Motooka, Isao Nishi, Kazunori Tomono, and Shigeyuki Hamada. "Community spread and acquisition of clinically relevant Escherichia coli harbouring blaNDM among healthy Japanese residents of Yangon, Myanmar." Journal of Antimicrobial Chemotherapy 76, no. 6 (March 24, 2021): 1448–54. http://dx.doi.org/10.1093/jac/dkab070.

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Abstract Background Carbapenemase-producing Enterobacterales (CPE) are spreading in hospitals, environment and retail foods in Yangon, Myanmar. Objectives To investigate whether CPE colonize healthy individuals living in Yangon and whether clinical-related strains are spreading in the community. Methods CPE was isolated from faecal samples obtained from healthy Japanese residents of Yangon with no history of hospitalization. Isolates were subjected to WGS using short- and long-read sequencers and compared with those previously isolated in Yangon. Results Six Escherichia coli strains harbouring blaNDM-1 or blaNDM-5 belonging to five different STs—ST10, ST38, ST48, ST410 and ST8453—were isolated from 69 volunteers. The ST38 isolates were related to those previously isolated from retail food in Yangon. The ST410 and ST8453 isolates were highly related to previous Yangon isolates including those of clinical and food origins. Conclusions The analysis suggested the acquisition of blaNDM-positive E. coli, which are disseminating in a clinical setting and through retail foods, by healthy residents in Yangon.
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Kaouass, M., M. Audette, D. Ramotar, S. Verma, D. De Montigny, I. Gamache, K. Torossian, and R. Poulin. "The STK2 gene, which encodes a putative Ser/Thr protein kinase, is required for high-affinity spermidine transport in Saccharomyces cerevisiae." Molecular and Cellular Biology 17, no. 6 (June 1997): 2994–3004. http://dx.doi.org/10.1128/mcb.17.6.2994.

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Eukaryotic polyamine transport systems have not yet been characterized at the molecular level. We have used transposon mutagenesis to identify genes controlling polyamine transport in Saccharomyces cerevisiae. A haploid yeast strain was transformed with a genomic minitransposon- and lacZ-tagged library, and positive clones were selected for growth resistance to methylglyoxal bis(guanylhydrazone) (MGBG), a toxic polyamine analog. A 747-bp DNA fragment adjacent to the lacZ fusion gene rescued from one MGBG-resistant clone mapped to chromosome X within the coding region of a putative Ser/Thr protein kinase gene of previously unknown function (YJR059w, or STK2). A 304-amino-acid stretch comprising 11 of the 12 catalytic subdomains of Stk2p is approximately 83% homologous to the putative Pot1p/Kkt8p (Stk1p) protein kinase, a recently described activator of low-affinity spermine uptake in yeast. Saturable spermidine transport in stk2::lacZ mutants had an approximately fivefold-lower affinity and twofold-lower Vmax than in the parental strain. Transformation of stk2::lacZ cells with the STK2 gene cloned into a single-copy expression vector restored spermidine transport to wild-type levels. Single mutants lacking the catalytic kinase subdomains of STK1 exhibited normal parameters for the initial rate of spermidine transport but showed a time-dependent decrease in total polyamine accumulation and a low-level resistance to toxic polyamine analogs. Spermidine transport was repressed by prior incubation with exogenous spermidine. Exogenous polyamine deprivation also derepressed residual spermidine transport in stk2::lacZ mutants, but simultaneous disruption of STK1 and STK2 virtually abolished high-affinity spermidine transport under both repressed and derepressed conditions. On the other hand, putrescine uptake was also deficient in stk2::lacZ mutants but was not repressed by exogenous spermidine. Interestingly, stk2::lacZ mutants showed increased growth resistance to Li+ and Na+, suggesting a regulatory relationship between polyamine and monovalent inorganic cation transport. These results indicate that the putative STK2 Ser/Thr kinase gene is an essential determinant of high-affinity polyamine transport in yeast whereas its close homolog STK1 mostly affects a lower-affinity, low-capacity polyamine transport activity.
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Dissertations / Theses on the topic "STK10"

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Falco, Marta. "Mechanistic insights into the EGFR-STK10 pathway in chronic kidney disease." Electronic Thesis or Diss., Université Paris Cité, 2024. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=6583&f=76942.

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La maladie rénale chronique (MRC) représente un lourd fardeau pour la santé publique, et pourtant, les mécanismes moléculaires qui régissent la progression de la maladie restent mal compris. Parmi les voies de signalisation potentielles, la voie du récepteur du facteur de croissance épidermique (EGFR) joue un rôle crucial dans la progression de la MRC. Cependant, une inhibition prolongée de l'EGFR n'est pas une option envisageable pour les patients atteints de MRC en raison du risque d'effets indésirables importants. Une compréhension approfondie de la signalisation de l'EGFR est essentielle pour développer des stratégies thérapeutiques plus ciblées et plus sûres. Dans nos travaux antérieurs, nous avons identifié la kinase sérine-thréonine 10 (STK10) comme un partenaire clé de l'EGFR lors de l'activation médiée par un ligand. Ce projet vise à élucider les mécanismes moléculaires sous-jacents à la progression de la MRC, avec pour objectif d'identifier de nouvelles cibles thérapeutiques. Notre recherche se concentre sur la compréhension de la voie de signalisation EGFR-STK10 dans les cellules rénales. Nous avons employé une approche intégrée combinant la phosphoprotéomique impartiale et la biotinylation dépendante de la proximité (TurboID), suivie par la spectrométrie de masse, afin d'explorer l'activation de STK10, ses partenaires d'interaction et ses voies de signalisation lors de l'activation médiée par un ligand de l'EGFR. Grâce à l'analyse phosphoprotéomique, nous avons caractérisé les phosphorylations de STK10 suite à l'activation de l'EGFR par EGF et TGFa, Nous avons identifié deux sites de phosphorylation, S191 et T195, dans la boucle d'activation de STK10, qui sont spécifiquement régulés à la hausse suite à l'activation de l'EGFR par TGFa, mais pas par EGF. De plus, nous avons observé que la phosphorylation en aval d'ERM, une cible connue de STK10, est significativement augmentée uniquement lors de la stimulation par TGFa. L'inhibition pharmacologique ou la réduction génétique de STK10 a empêché l'augmentation de ces phosphosites et l'activation d'ERM, suggérant une activation spécifique au ligand de STK10 dans les cellules épithéliales tubulaires rénales. Mécaniquement, nos analyses ont identifié un enrichissement de protéines impliquées dans le trafic des récepteurs, suggérant que STK10 joue un rôle dans la régulation du tri de l'EGFR. Notamment, nous avons démontré que l'inhibition pharmacologique et la réduction génétique de STK10 n'affectent pas l'activation précoce de l'EGFR, mais entravent le trafic à long terme du récepteur suite à la stimulation par TGFa. Dans les cellules shSTK10, l'EGFR est significativement plus dégradé que dans les cellules contrôles, ce qui suggère que STK10 pourrait favoriser le recyclage du récepteur, conduisant à son activation soutenue. L'activation soutenue de l'EGFR a été impliquée dans plusieurs modèles de MRC, contribuant à des processus pathologiques. L'analyse ontologique des gènes a révélé que STK10 est impliqué dans différents processus pathologiques associés à la progression de la MRC et qui sont médiés par une activation constante de l'EGFR. L'inhibition de STK10 in vitro a effectivement bloqué certains de ces processus délétères tels que la migration cellulaire, la croissance et la prolifération dans les cellules épithéliales rénales. Ainsi, l'inhibition de STK10 pourrait bloquer ces processus et potentiellement ralentir la progression de la MRC. En conclusion, cette étude mène à de nouvelles perspectives sur la voie STK10 dans le contexte de la signalisation de l'EGFR dans les cellules rénales. Elle met en lumière un nouveau rôle potentiel pour cette kinase dans la régulation du trafic des récepteurs suite à la stimulation par TGFa, probablement en favorisant son recyclage et son activation soutenue, conduisant à des processus pathogéniques. L'inhibition de STK10 devrait être davantage testée pour évaluer son potentiel en tant que stratégie thérapeutique pour la MRC
Chronic Kidney Disease (CKD) is a major public health burden, yet the molecular mechanisms driving its progression remain poorly understood. Among the potential pathways, the Epidermal Growth Factor Receptor (EGFR) signaling axis plays a critical role in CKD progression. However, prolonged inhibition of EGFR is not a feasible option for CKD patients due to the risk of significant adverse effects. Therefore, a deeper understanding of EGFR signaling is essential for developing more targeted and safer therapeutic strategies. In our previous work, we identified Serine-Threonine Kinase 10 (STK10) as a key partner of EGFR during ligand-mediated activation. The project aims to unravel the molecular mechanisms underlying CKD progression, with the goal of identifying new therapeutic targets. Our research focuses on understanding the EGFR-STK10 signaling pathway in kidney cells. To investigate this, we employed an integrated approach combining unbiased phosphoproteomics and proximity-dependent biotinylation (TurboID), followed by mass spectrometry, to explore STK10 activation, its interacting partners, and its signaling pathways, upon EGFR mediated ligand activation. Through phosphoproteomic analysis, we characterized STK10 phosphorylations following EGFR activation by EGF and TGFa. We identified two phosphorylation sites, S191 and T195, in the STK10 activation loop, which are specifically upregulated following EGFR activation by TGFa, but not by EGF. Additionally, we observed that downstream phosphorylation of ERM, a known STK10 target, is significantly increased only upon TGFa treatment. Pharmacological inhibition or genetic knockdown of STK10 using shRNA successfully prevented the upregulation of these phosphosites and the activation of ERM, suggesting a ligand-specific activation of STK10 in kidney epithelial tubular cells. Mechanistically, our analyses identified an enrichment of proteins involved in receptor trafficking, suggesting that STK10 plays a role in regulating EGFR sorting. Notably, we demonstrated that pharmacological inhibition or genetic downregulation of STK10 does not affect early EGFR activation but does impair the long-term trafficking of the receptor following TGFa treatment. In shSTK10 cells, EGFR is significantly more degraded than in control cells, suggesting that STK10 might favor the recycling of the receptor, leading to its sustain activation. Sustained EGFR activation has been implicated in several CKD models, contributing to pathological processes. Importantly, gene ontology analysis revealed that STK10 is involved in different pathological processes associated with CKD progression mediated by constant EGFR activation. Inhibition of STK10 in vitro effectively blocked some of these deleterious processes such as cell migration, growth, and proliferation in kidney epithelial cells. Thus, inhibition of STK10 could block these processes and potentially slow down CKD progression. In conclusion, this study provides new insights into the STK10 pathway in the context of EGFR signaling in kidney cells. It highlights a potential novel role for this kinase in regulating receptor trafficking upon TGFa treatment, likely promoting its recycling and sustained activation, leading to pathogenic processes. STK10 inhibition should be further tested to evaluate its potential as a therapeutic strategy for CKD
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Cahill, Fiona. "The role of LKB1 (STK11) in non-small cell lung cancer." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:a3162d1b-96d3-4420-82eb-e261c9732f33.

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LKB1 is the second most commonly altered tumour suppressor gene in lung adenocarcinoma, the most prevalent form of lung cancer. LKB1 is a "master kinase" that has been shown to phosphorylate up to 13 downstream targets. We hypothesised that LKB1 loss is associated with an increased dependency on alternative, targetable pathways. The overall aims of this project were to better understand the role of LKB1 loss in lung cancer and to identify novel approaches to selectively target LKB1 mutated cells. We generated isogenic cells with or without LKB1 and used these to study the effect of LKB1 on cell proliferation. Importantly, we used a range of models including 2D culture, 3D spheroids and, sub-cutaneous and orthotopic xenograft models. To understand the role of LKB1 loss in lung cancer, the effect of LKB1 on mRNA expression was analysed using whole genome RNA Sequencing. To identify novel approaches to selectively target LKB1 mutated cells, we used biological screening methods and also investigated the effect of several metabolic inhibitors. We found that loss of LKB1 expression had no effect on cell proliferation in 2D culture, but was associated with increased growth in 3D spheroids, sub-cutaneous and orthotopic xenografts, as well as greater metastasis in a lung orthotopic model. Gene ontology analysis of the transcriptome identified that genes associated with cAMP signalling and cytoskeletal organisation were differentially expressed between LKB1 deficient and proficient cells. We confirmed that cAMP signalling was increased in LKB1 deficient cells, though there was no difference in sensitivity between LKB1 deficient and proficient cells to cAMP signalling modulators. The bioactive small molecule screen showed that LKB1 deficient cells underwent apoptosis more slowly and therefore, were less sensitive to many compounds, compared with LKB1 proficient cells. Screening in 3D spheroids was a novel approach that we used to identify microtubule inhibitors as potentially selective compounds acting in LKB1 deficient cells. Our RNASeq data suggests that there was a metabolic shift from oxidative phosphorylation to aerobic glycolysis in LKB1 deficient cells, although this did not affect sensitivity to complex I inhibitors. Importantly, LKB1 deficient cells were more sensitive to glucose and glutamine deprivation which suggests that targeting these metabolic pathways may hold the greatest promise to selectively inhibit proliferation in LKB1 mutated cells.
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Just, Pierre-Alexandre. "Etude du rôle de LKB1 dans le foie." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T085/document.

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Les carcinomes hépatocellulaires (CHC) mutés CTNNB1 ont des caractéristiques phénotypiques propres en termes de polarité et de métabolisme (absence de stéatose). Nous avons émis l’hypothèse que ce phénotype pouvait être secondaire à l’activation du gène suppresseur de tumeurs LKB1 qui code une Ser/Thr kinase multitâches.Nous avons tout d’abord montré qu’il existait effectivement un dialogue complexe entre les voies Wnt/β-Caténine et LKB1 dans le foie. Les mutations de CTNNB1 sont en effet capables d’induire l’expression protéique de LKB1 dans des lignées hépatomateuses humaines, et les CHC mutés CTNNB1 présentent une expression protéique accrue de LKB1 et une signature transcriptionnelle d’activation de LKB1. De plus, dans deux modèles murins d’invalidation hépatospécifique de Lkb1, LKB1 est apparu comme requis pour l’activation complète du programme transcriptionnel de β-Caténine mais de façon dépendante du stade de développement et du contexte nutritionnel. Enfin, la signalisation LKB1 est apparue comme nécessaire à la survie des hépatocytes activés pour β-Caténine dans deux modèles murins différents.Nous avons aussi caractérisé les rôles métaboliques de LKB1 dans le foie. L’invalidation hépatospécifique de Lkb1 induisait une augmentation progressive de la masse grasse corporelle avec utilisation préférentielle des glucides comme substrat énergétique. Il existait une activation de la néoglucogenèse hépatique avec hyperglycémie et une lipogenèse accrue avec accumulation hépatocytaire de lipides. Enfin, nous avons mis en évidence une activation paradoxale de la signalisation AKT dans les hépatocytes, même à jeun, et une dépendance énergétique aux acides aminés. Enfin, nous avons identifié une nouvelle isoforme protéique de LKB1 délétée de son domaine N-Terminal et d’une partie de son domaine kinase. D’expression tissulaire préférentiellement musculaire et myocardique, cette isoforme catalytiquement inactive se comportait comme dominant positif sur l’activation de l’AMPK par la forme conventionnelle mais comme dominant négatif dans l’activité polarisation induite par LKB1. Enfin, elle était capable d’induire, en l’absence de la forme conventionnelle, la prolifération cellulaire et la tumorigenèse chez la souris nude. Elle pourrait exercer des rôles métaboliques particuliers dans les tissus fortement oxydatifs et des rôles oncogéniques dans certains contextes
CTNNB1-Mutated hepatocellular carcinomas (HCC) share a specific polarity and metabolic phenotype without steatosis. We hypothesized that such phenotype could imply the tumor suppressor gene LKB1 that encodes for a multi-Task Ser/Thr kinase.We first demonstrated that a complex crosstalk indeed exists in the liver between LKB1 and the Wnt/β-Catenin pathway. LKB1 proteic expression was controlled by mutant β-Catenin in hepatomatous cell line and CTNNB1-Mutated HCCs had an enhanced LKB1 proteic expression as well a transcriptomic signature of LKB1 activation. In two mouse model of liver-Specific invalidation of Lkb1, we showed that LKB1 was required for full activation of the β-Catenin transcriptomic program, but it depended on the developmental stage and nutritional context. At least, LKB1 appeared to be required for the survival of β-Catenin activated liver cells in two other mouse models.Then, we wanted to caracterize the metabolic roles of LKB1 in the liver. Liver-Specific invalidation of Lkb1 progressively raised the body fat mass and we observed that carbohydrates were preferred as whole-Body energetic fuel. In the liver, gluconeogenesis and lipogenesis were enhanced, resulting in mild hyperglycemia and lipid accumulation in the hepatocytes. At least, we identified an aberrant activation of the AKT signaling in the liver, even during fasting, and an energetic dependence towards amino acids.At least, we identified a novel LKB1 proteic isoform that is deleted of its N-Terminal domain and part of its kinase domain. Highly expressed in the muscle and in the heart, this catalytically inactive isoform however acted as a positive dominant towards AMPK activation by full length LKB1 but as a negative dominant towards LKB1-Induced cell polarization. This isoform is also able to enhance cell proliferation and to induce tumors in a xenograft model, even when expressed alone. It could play specific metabolic roles in oxidative tissues and could be oncogenic in some contexts
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Briassouli, Paraskevi. "Biochemical and functional studies of the STK15 kinase and its role in cancer development." Thesis, Institute of Cancer Research (University Of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417380.

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Tanaka, Eiji. "The clinical significance of aurora-A/STK15/BTAK expression in human esophageal squamous cell carcinoma." Kyoto University, 2007. http://hdl.handle.net/2433/135748.

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Cluzel, Marie-Ève. "Caractérisation de nouveaux substrats de la sérine/thréonine kinase Stk1 de Staphylococcus aureus." Thesis, Lyon 1, 2012. http://www.theses.fr/2012LYO10144.

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La phosphorylation de protéines correspond à l’addition covalente d’un groupement phosphate (PO4 3-) par une protéine kinase sur un substrat. Cette réaction est réversible : la déphosphorylation est catalysée par des protéines phosphatases. Chez S. aureus, la sérine/thréonine kinase Stk1 phosphoryle des acides aminés sérines et thréonines et a été montrée impliquée dans la régulation de la virulence du pathogène : nous avons approfondi les connaissances sur ce mécanisme en identifiant trois nouveaux substrats et en étudiant les effets de la phosphorylation sur leur activité : - l’enzyme LuxS, responsable de la synthèse de l’AI-2 impliqué dans la communication intra bactérienne, voit son activité enzymatique drastiquement diminuée en étant phosphorylée par Stk1 sur un site thréonine unique (T14) ; - le régulateur CcpA, dont la fixation sur l’ADN module l’expression de nombreux gènes de virulence, est phosphorylée par Stk1 sur deux sites (T18 et T33) et cette phosphorylation diminue l’affinité de la protéine régulatrice CcpA pour l’ADN de ses gènes cibles ; - l’élément réponse du système à deux composants SaeR est phosphorylé sur deux sites thréonines (T87 et T192) de la région impliquée dans l’affinité de SaeR pour l’ADN. Les rôles de la kinase Stk1 sont donc multiples et liés à la régulation de la virulence de S. aureus. Les autres voies mettant en jeu la phosphorylation de protéines bactériennes, comme les systèmes à deux composants ou le système CcpA/HPr, sont couplées à cette phosphorylation par la sérine/thréonine kinase : ces résultats soulignent à la fois la diversité et la complexité de la régulation des mécanismes responsables de la virulence de S. aureus
Protein phosphorylation consists in the catalyzed addition of a phosphate group on a substrate. This reversible reaction is ensured by both kinase and phosphatase proteins. S. aureus is a human prokaryote pathogen and a part of its virulence is known to be regulated by the serine/threonine kinase Stk1, which phosphorylates serine or threonine residues of its substrates. We investigated the mechanisms of this virulence regulation and newly identified three substrates of Stk1: the quorumsensing LuxS protein, the catabolite carbon protein CcpA and the two components system response element SaeR. LuxS is phosphorylated on a unique threonine residue in position 14 and phosphorylation dramatically influences its enzymatic activity on AI-2 production. CcpA phosphorylation on two threonine residues in the DNA-binding region of the protein (T18 and T33) decreases the affinity of the protein for its targeted DNA sequences. Besides, Stk1 also phosphorylates the response element SaeR on two threonine residues (T87 and T192) in the DNAbinding region. Therefore Stk1 kinase plays numerous roles in S. aureus virulence regulation and the complexity of this regulation pattern increases when considering that three of the phosphorylation pathways in prokaryotes are crossed over: the two components system phosphorylation, the HPr/HPrK system and the serine/threonine kinase proteins phosphorylation. These results highlight the need to focus on Stk1 as a key element in the complexity of virulence regulation in S. aureus
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Ellingson, William John. "The Effects of 3-Phosphoglycerate and Other Metabolites on the Activation of AMP-Activated Protein Kinase by LKB1/STRAD/MO25." BYU ScholarsArchive, 2006. https://scholarsarchive.byu.edu/etd/485.

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Skeletal muscle contraction results in the phosphorylation and activation of the AMP-activated protein kinase (AMPK) by an upstream kinase, AMPKK. The LKB1-STRAD-MO25 complex is the major AMPKK in skeletal muscle; however, LKB1-STRAD-MO25 activity is not increased by muscle contraction. This relationship suggests that phosphorylation of AMPK by LKB1-STRAD-MO25 during skeletal muscle contraction may be regulated by allosteric mechanisms. In this study we tested an array of metabolites including glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), fructose 1,6-bisphosphate (F1,6-P2), 3-phosphoglycerate (3PG), glucose-1-phosphate (G1P), glucose-1,6-bisphosphate (G1,6-P2), adenosine diphosphate (ADP), carnitine (Carn), acetyl-carnitine (Acarn), inosine monophosphate (IMP), inosine, and ammonia for allosteric regulation. We found that 3PG stimulated LKB1-STRAD-MO25 activity and allowed for increased AMPK phosphorylation. 3PG did not stimulate LKB1-STRAD-MO25 activity toward the peptide substrate LKB1tide. These results have identified 3PG as an AMPK-specific regulator of AMPK phosphorylation and activation by LKB1-STRAD-MO25.
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Engel, Brienne E. "Mechanisms and Molecular Biology of Major Tumor Suppressors." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5357.

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This dissertation is devoted to the study of the molecular biology of major tumor suppressors, defined as those that prevent the cellular processes identified as the hallmarks of cancer. Specifically, the major tumor suppressors pRb and STK11 are explored in the context of osteosarcoma and lung cancer, respectively. RB1 was the first tumor suppressor gene discovered. Over four decades of work have revealed that the Rb protein (pRb) is a master regulator of biological pathways influencing virtually every aspect of intrinsic cell fate including cell growth, cell-cycle checkpoints, differentiation, senescence, self-renewal, replication, genomic stability and apoptosis. While these many processes may account for a significant portion of RB1's potency as a tumor suppressor, a small, but growing stream of evidence suggests that RB1 also significantly influences how a cell interacts with its environment, including cell-to-cell and cell-to-extracellular matrix interactions. Chapter 2 highlights pRb's role in the control of cell adhesion and how alterations in the adhesive properties of tumor cells may drive the deadly process of metastasis. Chapter 3 defines a role for pRb as a suppressor of the progression to metastasis by upregulating integrin α10. Transcription of this integrin subunit is herein found to be pRb-dependent in mouse osteoblasts. Classic pRb partners in cell cycle control, E2F1 and E2F3, do not repress transcription of integrin α10 and phosphorylation of pRb is not necessary for activation of the integrin α10 promoter. Promoter deletion revealed a pRb responsive region between -108bp to -55bp upstream of the start of the site of transcription. pRb activation of transcription also leads to increased levels of integrin α10 protein and a greater concentration of the integrin α10 protein at the cell membrane of mouse osteoblasts. These higher levels of integrin α10 correspond to increased binding to collagen substrate. Consistent with our findings in mouse osteoblasts, we found that integrin α10 is significantly underexpressed in multiple solid tumors that have frequent inactivation of the pRb pathway. Bioinformatically, we identified data consistent with an 'integrin switch' that occurs in multiple solid tumors consisting of underexpression of integrins α7, α8, and α10 with concurrent overexpression of integrin β4. pRb promotes cell adhesion by inducing expression of integrins necessary for cell adhesion to a substrate. We propose that pRb loss in solid tumors exacerbates aggressiveness by debilitating cellular adhesion, which in turn facilitates tumor cell detachment and metastasis. Lung cancer is the leading cause of cancer-related death in the U.S. and additional targeted therapies are desperately needed to treat these patients. STK11 is the third most frequently mutated gene in lung adenocarcinoma following only KRAS and TP53, yet its mutational status is not currently clinically evaluated and no therapies have been approved to specifically target its pathway. A deep understanding of the complex pathways controlled by STK11 and their alterations in cancer are required to develop effective therapies for patients with loss-of-function mutations. In Chapter 4 we present the current understanding of STK11, focusing on its molecular biology and therapeutic implications, including a compilation of studies evaluating STK11 somatic mutations in human lung cancer tissue and how the frequency of these mutations varies across histological subtypes and patient populations. Finally, we review the strategies being used to target STK11-deficient cancers at the clinical trial, pre-clinical, and basic science levels as well as proposing potential new therapies that might benefit this patient population. STK11 is a tumor-suppressor commonly mutated in lung adenocarcinoma (LuAd). There are a number of agents that may selectively target the deregulated pathways in STK11 mutated tumors, and thus, identifying the subset of adenocarcinomas that harbor these mutations could have significant clinical benefit. In Chapter 5, we characterized a cohort of 442 adenocarcinoma patients with respect to STK11 mutation status and subset of this cohort using immunochemistry, gene expression, and western blotting. We found that measuring STK11 mutation status is complicated by the fact that many STK11 mutations lead to expression of a stable protein that is indistinguishable from wild type (WT) via immunohistochemistry. To circumvent this, we used published cell line mutation and gene expression data to derive a signature correlating with STK11 mutation status. This signature was validated in the cohort of 442 lung adenocarcinomas and strongly correlates with mutation status (ROC curve AUC = 85.29). These data suggest that STK11; mutation status may be best assessed by measuring the downstream targets included in our signature.
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Motschmann, Martin Gerhard [Verfasser], and Axel [Akademischer Betreuer] Walch. "Bedeutung von EGFR, Her2/neu, STK15 und Cyclin D1 für Therapieresistenz und Prognose am neoadjuvant therapierten Adenokarzinom des gastroösophagealen Überganges Typ I (Barrettkarzinom)." Freiburg : Universität, 2013. http://d-nb.info/112347527X/34.

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Giacomazzi, Juliana. "Fatores de risco para câncer de mama e polimorfismos nos genes ER, PR e STK15 em mulheres participantes de um programa de rastreamento mamográfico em Porto Alegre." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2008. http://hdl.handle.net/10183/14043.

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O câncer de mama é uma doença multifatorial causada pela combinação de fatores de risco genéticos e ambientais. Polimorfismos genéticos de baixa penetrância têm sido associados a esta doença, porém existem poucos estudos publicados sobre a prevalência destes na população brasileira. No presente estudo, determinamos a freqüência alélica e genotípica dos polimorfismos ER)-397 PvuII C/T, ER)-351 XbaI A/G, PR PROGINS e STK15 F31I e investigamos a relação destes com fatores de risco estabelecidos para câncer de mama. Foram estudadas 750 mulheres sem câncer de mama, envolvidas em um programa de rastreamento mamográfico no Sul do Brasil, uma região com altos índices de incidência da doença. As freqüências genotípicas do polimorfismo PROGINS não foram significativamente diferentes das encontradas em populações brasileiras e nãobrasileiras. A distribuição dos genótipos de ER)-397 PvuII C/T, ER)-351 XbaI A/G e STK15 F31I, no entanto, foram significativamente diferentes da maioria dos estudos previamente publicados, enfatizando a necessidade de análises de populações específicas para avaliação do impacto de polimorfismos de baixa penetrância no risco para câncer de mama. Adicionalmente, a distribuição dos haplótipos de ER) (ER)-397 PvuII - ER)-351 XbaI) foram significativamente diferentes das descritas em outras populações. A média estimada do risco de desenvolver câncer de mama ao longo da vida na amostra estudada foi de 7.8%, a maioria (97.5%) das mulheres apresentavam achados normais ao exame de mamografia (BIRADS 1 e 2), e nenhum fator de ri sco reprodutivo para câncer de mama foi identificado na amostra. No entanto, a média do índice de massa corporal foi 29.6 e 41.1% das mulheres apresentavam índice de massa corporal a 30. Ao analisamos a relação entre os três polimorfismos e fatores de risco já estabelecidos, as seguintes associações estatisticamente significativas foram encontradas: (a) genótipo GG de ER)-351 e menarca a 14 anos, (b) genótipos A2A2 e A1A2 de PR PROGINS e maior estimativa de risco de desenvolver câncer de mama em 5-anos em mulheres pósmenopáusicas; (c) genótipos A2A2 e A1A2 PR PROGINS e maior índice de massa corporal em mulheres pós-menopáusicas; (d) genótipo AT e AA de STK15 F31I e densidade mamográfica moderadamente densa (tecido fibroglandular em 50-75% do tecido mamário) em mulheres pré-menopáusicas; (e) genótipo TT de STK15 F31I e mamas menos densas (tecido fibroglandular em 0-50% do tecido mamário) em mulheres pré-menopáusicas e (f) genótipo TT de STK15 F31I e idade da menarca a 12 anos. Estudos de caso-controle adicionais são necessários para melhor compreensão da relação entre estes e outros polimorfismos e risco para câncer de mama na população brasileira.
Breast cancer is a multifactorial disease caused by a combination of genetic and environmental risk factors. Highly prevalent low-penetrance genetic polymorphisms have been associated with an increased risk of developing the disease. Only a few studies have been published about the prevalence of such polymorphisms in the highly heterogeneous Brazilian population. In the present study, we have determined the allelic and genotypic frequencies of the ER)-397 PvuII C/T, ER)-351 XbaI A/G, PR PROGINS and STK15 F31I polymorphisms and investigated their relationship with established breast cancer risk factors. We studied 750 breast cancer-unaffected women enrolled in a mammographic screening program in Southern Brazil, a region with particularly high breast cancer incidence rates. Genotypic frequencies for PROGINS were not significantly different from previous studies in Brazilian and non-Brazilian individuals. The distribution of ER)- 397 PvuII C/T, ER)-351 XbaI A/G and STK15 F31I genotypes, however, was significantly different from most of the previously published reports, emphasizing the need for population-specific analyses in evaluating the impact of low-penetrance gene polymorphisms on breast cancer risk. Furthermore, the distribution of ER) haplotypes using the ER)-397 PvuII C/T and ER)-351 XbaI A/G polymorphic markers was also distinct from that described in other populations. The mean estimated lifetime risk of developing breast cancer in the sample was 7.8%, most of the women (97.5%) had normal mammographic image results (BIRADS 1 and 2) and no significant reproductive risk factors for breast cancer were identified in the sample. However, mean body mass index was 29.6 and 41.1% of the women had a body mass index a 30. When analyzing the relationship between the three polymorphisms and other established breast cancer risk factors the following significant associations were found between: (a) ER)-351 GG genotype and menarche a 14 years; (b) PROGINS A2 allele and higher mean estimated 5-year risk of developing breast cancer in postmenopausal women; (c) A1A2 and A2A2 genotypes and higher mean body mass index in postmenopausal women; (d) STK15 F31I AT and AA genotypes and moderately dense (50-75% of the breast with fibroglandular tissue) in premenopausal women; (e) STK15 F31I TT genotype and less dense (0-50% of the breast with fibroglandular tissue) in premenopausal women and (f) STK15 F31I TT genotype and later age at menarche (a 12 years). Additional case-control studies are necessary to clarify the relationship between this and other polymorphisms and breast cancer risk in the Brazilian population.
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Books on the topic "STK10"

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Solid Edge St10 for Designers. Cadcim Technologies, 2017.

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Book chapters on the topic "STK10"

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Iturrate, Mikel, Xabier Amezua, Xabier Garikano, Jose Antonio Oriozabala, Iñaki Martin, and Eneko Solaberrieta. "Generative Design in the Transmission System of a Skateboard." In Lecture Notes in Mechanical Engineering, 169–74. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-70566-4_27.

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AbstractGenerative design (GD) is a new way of designing products that respond to the current characteristics of the 4.0 industry era. It allows the customization of designs and helps to minimize process times and material quantities. In the case study, two parts of the transmission system of a skateboard have been designed using GD of Solid Edge ST10. The design has been customized for 67 kg users who will use the skateboard for riding and not for jumping or doing tricks. On the other hand, the aim was to minimize the weight and the use of material for its manufacture. Once the initial solid is defined, the software generates specific designs for different levels of mass reduction or product quality. An axle with a mass reduction of 70% from the initial solid and a base with reduction of 60% have been proposed. The GD more than an alternative is a requirement to respond to the demands of the 4.0 industry in which customization and cost reduction are one of the fundamental pillars. This type of design, at the same time, forces to adapt the manufacturing processes so that it is necessary to manufacture in additive manufacturing (AM) machines.
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Saurin, Jean-Christophe, and Sylviane Olschwang. "Hamartomatoses digestives chez l’enfant: Polypose adénomateuse familiale (APC), polypose juvénile (SMAD4, BMPR1A), maladie de Peutz-Jeghers (STK11)." In Épidémiologie des cancers de l’enfant, 149–60. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-78337-1_15.

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Edwards, John. "STK190-010/STK190-020." In Television IC Data Files, 91. Elsevier, 2000. https://doi.org/10.1016/b978-0-7506-4581-2.50087-6.

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"STK12." In Encyclopedia of Cancer, 4368. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_102187.

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"STK13." In Encyclopedia of Cancer, 4368. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_102188.

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"STK15." In Encyclopedia of Cancer, 4368. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_102189.

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"STK12." In Encyclopedia of Cancer, 3534. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_5517.

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"STK13." In Encyclopedia of Cancer, 3534. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_5518.

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"STK15." In Encyclopedia of Cancer, 3534. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_5519.

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"STK11." In Encyclopedia of Cancer, 3534. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_6624.

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Conference papers on the topic "STK10"

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Moll, Santiago E., José A. Moraño, and Luis M. Sánchez Ruiz. "Aprender Mecánica de Vuelo Orbital mediante problemas y simulaciones con STK10." In In-Red 2015 - Congreso Nacional de Innovación Educativa y Docencia en Red. Editorial Universitat Politècnica de València, 2015. http://dx.doi.org/10.4995/inred2015.2015.1595.

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Arora, Shilpi, Irma M. Gonzales, Chao Sima, Javed Khan, Spyro Mousses, and David O. Azorsa. "Abstract 3408: RNAi screening identifies STK10 as a novel therapeutic target for Ewing's sarcoma." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3408.

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Guo, Sujuan, Kevin Pridham, and Zhi Sheng. "Abstract A04: LINC00467 regulates the autophagy signaling pathway STK11/AMPK." In Abstracts: AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines; December 4-7, 2015; Boston, MA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.nonrna15-a04.

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Gauthier, Lovic, and Ahmed Amine Jerraya. "Cycle-true simulation of the ST10 microcontroller (poster paper)." In the conference. New York, New York, USA: ACM Press, 2000. http://dx.doi.org/10.1145/343647.344125.

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Engel, Brienne E., Matthew B. Schabath, Zachary J. Thompson, Steven A. Eschrich, Stephen G. Brantley, Anastasia R. Belock, Anders Berglund, et al. "Abstract 4159: Characterization of three recurring STK11/LKB1 mutants in lung adenocarcinoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4159.

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Li, Rui, Tonya C. Walser, Kostyantyn Krysan, David Shackelford, Jill E. Larsen, John D. Minna, and Steven M. Dubinett. "Abstract C296: The contribution of LKB1/STK11-mediated CXCL8 dysregulation to lung carcinogenesis." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c296.

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Pagano, Flavia, Flurina Anna-Carina Maria Saner, Solass Wiebke, Sara Imboden, and Michael David Mueller. "2022-RA-915-ESGO STK11 adnexal tumors: challenge of a new tumor entity." In ESGO 2022 Congress. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/ijgc-2022-esgo.877.

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Li, X., and T. Nyunoya. "Cigarette Smoke Augments Human Airway Epithelial Cell Death via FBXL19 Mediated STK11 Protein Degradation." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4279.

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Wohlhieter, Corrin A., Allison L. Richards, John T. Poirier, Fathema Uddin, Christopher Hulton, Elisa De Stanchina, Thales Papagiannakopoulos, Triparna Sen, and Charles M. Rudin. "Abstract 1800A: STK11 and KEAP1 co-mutation cooperatively promotes rapid tumor growth in lung adenocarcinoma." 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.am2020-1800a.

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Cai, Ling, Thomas J. Rogers, Huiyu Li, Jiyeon Kim, Yang Xie, Guanghua Xiao, John Minna, and Ralph J. DeBerardinis. "Abstract 871: KYNU expression is a prognostic factor in KEAP1/STK11 co-mutated lung adenocarcinoma." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-871.

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Reports on the topic "STK10"

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Sen, Subrata. STK15/BTAK and Centrosome Anomaly in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada424645.

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