Relevant bibliographies by topics / JAK

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'JAK'

Author: Grafiati
Published: 4 June 2021
Last updated: 24 August 2024

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Journal articles on the topic "JAK"

1

Danese, Silvio, Marjorie Argollo, Catherine Le Berre, and Laurent Peyrin-Biroulet. "JAK selectivity for inflammatory bowel disease treatment: does it clinically matter?" Gut 68, no. 10 (June 21, 2019): 1893–99. http://dx.doi.org/10.1136/gutjnl-2019-318448.

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The two major forms of inflammatory bowel disease (IBD), encompassing Crohn’s disease (CD) and ulcerative colitis (UC), are chronic immune-mediated conditions characterised by an increased production of pro-inflammatory cytokines that act as critical drivers of intestinal inflammation. Anti-cytokine therapy has been shown to improve clinical outcomes in IBD. Janus kinases (JAKs) are tyrosine kinases that bind different intracellular cytokine receptors, leading to phosphorylation of signal transducer and activation of transcription molecules implicated on targeted gene transcription. Four isoforms of JAKs have been described: JAK1, JAK2, JAK3 and TYK2. Oral JAK inhibitors (JAKi) have been developed as synergic anti-cytokine therapy in IBD, showing different selectivity towards JAK isoforms. Tofacitinib, a pan-JAK inhibitor, has been recently approved for the treatment of moderate-to-severe UC. With the aim of improving the benefit: risk ratio of this drug class, several second-generation subtype-selective JAKi are under development. However, whether selective inhibition of JAK isoforms is associated with an increased clinical efficacy and/or a better safety profile remains debatable. The aim of this review is to critically review the preclinical and clinical data for the differential selectivity of JAK inhibitors and to summarise the potential clinical implications of the selective JAK inhibitors under development for UC and CD.
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Constantinescu, Stefan N., Emilie Leroy, Vitalina Gryshkova, Christian Pecquet, and Alexandra Dusa. "Activating Janus kinase pseudokinase domain mutations in myeloproliferative and other blood cancers." Biochemical Society Transactions 41, no. 4 (July 18, 2013): 1048–54. http://dx.doi.org/10.1042/bst20130084.

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The discovery of the highly prevalent activating JAK (Janus kinase) 2 V617F mutation in myeloproliferative neoplasms, and of other pseudokinase domain-activating mutations in JAK2, JAK1 and JAK3 in blood cancers, prompted great interest in understanding how pseudokinase domains regulate kinase domains in JAKs. Recent functional and mutagenesis studies identified residues required for the V617F mutation to induce activation. Several X-ray crystal structures of either kinase or pseudokinase domains including the V617F mutant of JAK2 pseudokinase domains are now available, and a picture has emerged whereby the V617F mutation induces a defined conformational change around helix C of JH (JAK homology) 2. Effects of mutations on JAK2 can be extrapolated to JAK1 and TYK2 (tyrosine kinase 2), whereas JAK3 appears to be different. More structural information of the full-length JAK coupled to cytokine receptors might be required in order to define the structural basis of JH1 activation by JH2 mutants and eventually obtain mutant-specific inhibitors.
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Raivola, Juuli, Teemu Haikarainen, Bobin George Abraham, and Olli Silvennoinen. "Janus Kinases in Leukemia." Cancers 13, no. 4 (February 14, 2021): 800. http://dx.doi.org/10.3390/cancers13040800.

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Janus kinases (JAKs) transduce signals from dozens of extracellular cytokines and function as critical regulators of cell growth, differentiation, gene expression, and immune responses. Deregulation of JAK/STAT signaling is a central component in several human diseases including various types of leukemia and other malignancies and autoimmune diseases. Different types of leukemia harbor genomic aberrations in all four JAKs (JAK1, JAK2, JAK3, and TYK2), most of which are activating somatic mutations and less frequently translocations resulting in constitutively active JAK fusion proteins. JAKs have become important therapeutic targets and currently, six JAK inhibitors have been approved by the FDA for the treatment of both autoimmune diseases and hematological malignancies. However, the efficacy of the current drugs is not optimal and the full potential of JAK modulators in leukemia is yet to be harnessed. This review discusses the deregulation of JAK-STAT signaling that underlie the pathogenesis of leukemia, i.e., mutations and other mechanisms causing hyperactive cytokine signaling, as well as JAK inhibitors used in clinic and under clinical development.
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Taldaev, Amir, Vladimir R. Rudnev, Kirill S. Nikolsky, Liudmila I. Kulikova, and Anna L. Kaysheva. "Molecular Modeling Insights into Upadacitinib Selectivity upon Binding to JAK Protein Family." Pharmaceuticals 15, no. 1 (December 25, 2021): 30. http://dx.doi.org/10.3390/ph15010030.

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Rheumatoid arthritis (RA) is a chronic disease characterized by bone joint damage and incapacitation. The mechanism underlying RA pathogenesis is autoimmunity in the connective tissue. Cytokines play an important role in the human immune system for signal transduction and in the development of inflammatory responses. Janus kinases (JAK) participate in the JAK/STAT pathway, which mediates cytokine effects, in particular interleukin 6 and IFNγ. The discovery of small molecule inhibitors of the JAK protein family has led to a revolution in RA therapy. The novel JAK inhibitor upadacitinib (RinvoqTM) has a higher selectivity for JAK1 compared to JAK2 and JAK3 in vivo. Currently, details on the molecular recognition of JAK1 by upadacitinib are not available. We found that characteristics of hydrogen bond formation with the glycine loop and hinge in JAKs define the selectivity. Our molecular modeling study could provide insight into the drug action mechanism and pharmacophore model differences in JAK isoforms.
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Montresor, Alessio, Matteo Bolomini-Vittori, Lara Toffali, Barbara Rossi, Gabriela Constantin, and Carlo Laudanna. "JAK tyrosine kinases promote hierarchical activation of Rho and Rap modules of integrin activation." Journal of Cell Biology 203, no. 6 (December 23, 2013): 1003–19. http://dx.doi.org/10.1083/jcb.201303067.

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Lymphocyte recruitment is regulated by signaling modules based on the activity of Rho and Rap small guanosine triphosphatases that control integrin activation by chemokines. We show that Janus kinase (JAK) protein tyrosine kinases control chemokine-induced LFA-1– and VLA-4–mediated adhesion as well as human T lymphocyte homing to secondary lymphoid organs. JAK2 and JAK3 isoforms, but not JAK1, mediate CXCL12-induced LFA-1 triggering to a high affinity state. Signal transduction analysis showed that chemokine-induced activation of the Rho module of LFA-1 affinity triggering is dependent on JAK activity, with VAV1 mediating Rho activation by JAKs in a Gαi-independent manner. Furthermore, activation of Rap1A by chemokines is also dependent on JAK2 and JAK3 activity. Importantly, activation of Rap1A by JAKs is mediated by RhoA and PLD1, thus establishing Rap1A as a downstream effector of the Rho module. Thus, JAK tyrosine kinases control integrin activation and dependent lymphocyte trafficking by bridging chemokine receptors to the concurrent and hierarchical activation of the Rho and Rap modules of integrin activation.
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Gonzalez-Traves, P., B. Murray, F. Campigotto, A. Meng, and J. A. DI Paolo. "THU0067 JAK SELECTIVITY AND THE IMPACT ON CYTOKINE SIGNALING INHIBITION AT CLINICAL RHEUMATOID ARTHRITIS DOSES." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 246.1–246. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2074.

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Background:Janus kinase 1 (JAK1) inhibitors are efficacious in rheumatoid arthritis (RA). Despite having similar efficacy, in vitro studies have shown differences in JAK selectivity profiles for the small-molecule JAK inhibitors (JAKi) baricitinib (BARI), tofacitinib (TOFA), and upadacitinib (UPA).1For example, BARI and UPA are JAK1/JAK2 selective, while TOFA is JAK1/JAK3 selective, but each JAKi has some activity against other JAKs. As JAKs form signaling pairs, differences in selectivity could lead to distinct pharmacologic profiles that may impact clinical efficacy and safety.Objectives:As a first step to understand the basis of potential differences at therapeutic doses, we compared the selectivity and potency of filgotinib (FIL) and its major metabolite (MET) to those of BARI, TOFA, and UPA in cytokine-stimulated peripheral blood mononuclear cells (PBMCs) and whole blood (WB).Methods:PBMCs and WB from healthy donors were incubated in vitro with 8 doses of each JAKi, and levels of signal transducer and activator of transcription phosphorylation (pSTAT) were measured following cytokine stimulation. Half maximal inhibitory concentration (IC50) values were calculated in phenotypically sorted leukocyte populations by flow cytometry. Therapeutic dose relevance of the in vitro analyses was assessed using calculated mean concentration-time profiles from JAKi population pharmacokinetic data in RA subjects. For each JAKi, the time above IC50and average daily pSTAT inhibition were calculated for each cytokine/STAT pair in B cells, CD4+ T cells, CD8+ T cells, monocytes, and/or NK cells.Results:Cellular assays in PBMCs and WB showed dose-dependent inhibition of cytokine-induced pSTATs with all JAKi (correlation between the protein-adjusted IC50values from PBMCs and IC50values from WB, r2=0.98). Among the most potently inhibited pathways were JAK1/TYK2-dependent cytokine, interferon alpha (IFNα), and the JAK1/2-dependent cytokine, interleukin (IL)-6. FIL and MET had weaker potencies against JAK2/TYK2 (G-CSF/pSTAT3), JAK1/2 (IFNƴ/pSTAT1), and JAK2/2 (granulocyte-macrophage colony-stimulating factor [GM-CSF])-dependent pathways compared to JAK1/TYK2 (IFNα/pSTAT5). FIL and MET showed the greatest selectivity vs the JAK2/2 pathway (GM-CSF/pSTAT3) in monocytes.The mean concentration-time profiles and time above IC50over 24 hr for each cytokine/STAT pathway showed that JAK1/2 (IL-6/pSTAT1) and JAK1/TYK2 (IFNα/pSTAT1) pathways were strongly modulated with all tested JAKi. FIL (200 mg) showed similar activity in average target coverage and time above IC50to the approved low doses of TOFA (5 mg) and UPA (15 mg); conversely, FIL had reduced mean average inhibition and time above IC50levels against JAK1/2 (IFNƴ/pSTAT1), JAK1/3-dependent cytokines (IL-2, -4, and -15), JAK2/TYK2 (G-CSF/pSTAT3), and JAK2/2 (GM-CSF/pSTAT5)-dependent pathways compared to TOFA and UPA, and in certain cases to BARI (2 mg).Conclusion:Different JAKi modulate distinct cytokine pathways to varying degrees, and no agent potently and continuously inhibited an individual cytokine signaling pathway throughout the dosing interval. FIL (200 mg) showed a similar inhibition profile to TOFA, BARI, and UPA against the JAK1/TYK2- (IFNα/pSTAT1) or JAK1/2-dependent (IL-6/pSTAT1) responses, consistent with the role of these pathways in clinical efficacy.2However, FIL displayed a differentiated pharmacologic profile from the other JAKi, showing biologically reduced activity on the JAK1/2 (IFNγ)-, JAK1/3 (IL-2, -4 and -15)-, JAK2/TYK2 (G-CSF)-, and JAK2/2 (GM-CSF)-dependent pathways, which play important roles in hematopoiesis and immune function. These data suggest that FIL (200 mg) may have less impact on a subset of homeostatic immune functions signaling via JAK2 and JAK3 than those observed at the clinically approved doses of TOFA (5 mg and 10 mg), UPA (15 mg), and BARI (4 mg).References:[1]McInnes IB, et al. Arthritis Res Ther. 2019;21:183.[2]Banerjee S, et al. Drugs. 2017;77:521-546.Disclosure of Interests:Paqui Gonzalez-Traves Employee of: Gilead, Bernard Murray Employee of: Gilead, Federico Campigotto Employee of: Gilead, Amy Meng Shareholder of: Gilead Sciences, Employee of: Gilead, Julie A. Di Paolo Employee of: Gilead
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Conzelmann, Michael, Elena Rodionova, Michael Hess, Thomas Giese, Anthony D. Ho, Peter Dreger, and Thomas Luft. "Complementary JAK/STAT Signalling Is Required for the Pro-Inflammatory Effects of CD40 Ligation: Differential Effects in Human Myeloid and B Cells." Blood 110, no. 11 (November 16, 2007): 2413. http://dx.doi.org/10.1182/blood.v110.11.2413.2413.

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Abstract CD40L represents a strong endogenous danger signal that induces pro-inflammatory activation of CD40-expressing cells such as dendritic cells (DC), monocytes, and B cells. However, since CD40 activation alone is insufficient to induce pro-inflammatory cytokines such as IL-12p70, we studied whether CD40-mediated pro-inflammatory activity might be dependent on co-signalling pathways involving JAK/STAT. Using quantitative Western blotting, we demonstrate that JAK/STAT signalling is induced by cytokines such as IL-4, GM-CSF and IFNg, whereas CD40 activation mediates NFkB signalling. CD40L-induced IL-12p70 and IL-10 secretion in human DC, monocytes, B cells, and chronic lymphocytic leukemia (CLL) cells was measured upon complementary JAK/STAT activation by IL-4, GM-CSF and IFNg in the presence and absence of specific inhibitors of JAK2, JAK3, and pan-JAK. Whereas IL-12p70 could not be induced by CD40 ligation or by cytokines alone, IL-12p70 secretion and suppression of IL-10 was reproducibly observed after co-stimulation of CD40L with IL-4, GM-CSF, or IFNg. This effect could be completely reversed by pan-JAK inhibition. Persistence of IL-4/GM-CSF/IFNg-mediated JAK/STAT signalling as late as 12 hours following cellular activation via CD40 was required for IL-12p70 secretion as shown by the effects of delayed JAK inhibition. Similarly, persistence between 12 and 24 hours of IL-12p35 and p40 mRNA expression correlated best with the level of IL-12p70 secretion. Specific inhibition of JAK2 and JAK3 further revealed a context-dependent action of the distinct JAK family members: JAK2 showed a strong co-dominant effect in the setting of IL-4-induced JAK/STAT activity. Both, JAK2 and JAK3 were required for IL-12p70 secretion, whereas JAK2 alone was sufficient to modulate IL-10 secretion. However, in the context of IFNg-induced JAK/STAT signalling in DC, neither JAK2 nor JAK3 inhibition had effects on IL-12p70. Here, only inhibition by the pan-JAK inhibitor involving JAK1 abrogated IL-12p70 secretion, indicating that in IFNg-dependent signalling, JAK2 is apparently sub-dominant to JAK1 and had only a small enhancing effect on IL-10. This context dependence markedly differed in myeloid cells and B cells, as normal and malignant (CLL) B cells maintain a co-dominant JAK2 activity in the context of IFNg-induced JAK/STAT-signalling. In conclusion, complementary JAK/STAT signalling is required for the pro-inflammatory effects of CD40 ligation in humans, with different JAK subset predominance in myeloid and B cells. These results may open new ways of lineage-specific interfering with CD40 signals by modulating JAK/STAT activity using tyrosine kinase inhibitors.
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Rodriguez Moncivais, Omar J., Stephanie A. Chavez, Victor H. Estrada Jimenez, Shengjie Sun, Lin Li, Robert A. Kirken, and Georgialina Rodriguez. "Structural Analysis of Janus Tyrosine Kinase Variants in Hematological Malignancies: Implications for Drug Development and Opportunities for Novel Therapeutic Strategies." International Journal of Molecular Sciences 24, no. 19 (September 26, 2023): 14573. http://dx.doi.org/10.3390/ijms241914573.

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Janus tyrosine kinase (JAK) variants are known drivers for hematological disorders. With the full-length structure of mouse JAK1 being recently resolved, new observations on the localization of variants within closed, open, and dimerized JAK structures are possible. Full-length homology models of human wild-type JAK family members were developed using the Glassman et al. reported mouse JAK1 containing the V658F structure as a template. Many mutational sites related to proliferative hematological disorders reside in the JH2 pseudokinase domains facing the region important in dimerization of JAKs in both closed and open states. More than half of all JAK gain of function (GoF) variants are changes in polarity, while only 1.2% are associated with a change in charge. Within a JAK1-JAK3 homodimer model, IFNLR1 (PDB ID7T6F) and the IL-2 common gamma chain subunit (IL2Rγc) were aligned with the respective dimer implementing SWISS-MODEL coupled with ChimeraX. JAK3 variants were observed to encircle the catalytic site of the kinase domain, while mutations in the pseudokinase domain align along the JAK-JAK dimerization axis. FERM domains of JAK1 and JAK3 are identified as a hot spot for hematologic malignancies. Herein, we propose new allosteric surfaces for targeting hyperactive JAK dimers.
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Musumeci, Francesca, Chiara Greco, Ilaria Giacchello, Anna Lucia Fallacara, Munjed M. Ibrahim, Giancarlo Grossi, Chiara Brullo, and Silvia Schenone. "An Update on JAK Inhibitors." Current Medicinal Chemistry 26, no. 10 (June 20, 2019): 1806–32. http://dx.doi.org/10.2174/0929867325666180327093502.

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Janus kinases (JAKs) are a family of non-receptor tyrosine kinases, composed by four members, JAK1, JAK2, JAK3 and TYK2. JAKs are involved in different inflammatory and autoimmune diseases, as well as in malignancies, through the activation of the JAK/STAT signalling pathway. Furthermore, the V617F mutation in JAK2 was identified in patients affected by myeloproliferative neoplasms. This knowledge prompted researchers from academia and pharmaceutical companies to investigate this field in order to discover small molecule JAK inhibitors. These efforts recently afforded to the market approval of four JAK inhibitors. Despite the fact that all these drugs are pyrrolo[2,3-d]pyrimidine derivatives, many compounds endowed with different heterocyclic scaffolds have been reported in the literature as selective or multi-JAK inhibitors, and a number of them is currently being evaluated in clinical trials. In this review we will report many representative compounds that have been published in articles or patents in the last five years (period 2013-2017). The inhibitors will be classified on the basis of their chemical structure, focusing, when possible, on their structure activity relationships, selectivity and biological activity. For every class of derivatives, compounds disclosed before 2013 that have entered clinical trials will also be briefly reported, to underline the importance of a particular chemical scaffold in the search for new inhibitors.
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Raivola, Juuli, Teemu Haikarainen, and Olli Silvennoinen. "Characterization of JAK1 Pseudokinase Domain in Cytokine Signaling." Cancers 12, no. 1 (December 27, 2019): 78. http://dx.doi.org/10.3390/cancers12010078.

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The Janus kinase-signal transducer and activator of transcription protein (JAK-STAT) pathway mediates essential biological functions from immune responses to haematopoiesis. Deregulated JAK-STAT signaling causes myeloproliferative neoplasms, leukaemia, and lymphomas, as well as autoimmune diseases. Thereby JAKs have gained significant relevance as therapeutic targets. However, there is still a clinical need for better JAK inhibitors and novel strategies targeting regions outside the conserved kinase domain have gained interest. In-depth knowledge about the molecular details of JAK activation is required. For example, whether the function and regulation between receptors is conserved remains an open question. We used JAK-deficient cell-lines and structure-based mutagenesis to study the function of JAK1 and its pseudokinase domain (JH2) in cytokine signaling pathways that employ JAK1 with different JAK heterodimerization partner. In interleukin-2 (IL-2)-induced STAT5 activation JAK1 was dominant over JAK3 but in interferon-γ (IFNγ) and interferon-α (IFNα) signaling both JAK1 and heteromeric partner JAK2 or TYK2 were both indispensable for STAT1 activation. Moreover, IL-2 signaling was strictly dependent on both JAK1 JH1 and JH2 but in IFNγ signaling JAK1 JH2 rather than kinase activity was required for STAT1 activation. To investigate the regulatory function, we focused on two allosteric regions in JAK1 JH2, the ATP-binding pocket and the αC-helix. Mutating L633 at the αC reduced basal and cytokine induced activation of STAT in both JAK1 wild-type (WT) and constitutively activated mutant backgrounds. Moreover, biochemical characterization and comparison of JH2s let us depict differences in the JH2 ATP-binding and strengthen the hypothesis that de-stabilization of the domain disturbs the regulatory JH1-JH2 interaction. Collectively, our results bring mechanistic understanding about the function of JAK1 in different receptor complexes that likely have relevance for the design of specific JAK modulators.
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Dissertations / Theses on the topic "JAK"

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Berkovičová, Raušová Petra. "Film jako téma - jak vidí médium samo sebe." Master's thesis, Akademie múzických umění v Praze. Filmová a televizní fakulta AMU. Knihovna, 2006. http://www.nusl.cz/ntk/nusl-78781.

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Práce se zamýšlí nad tématem filmu ve filmu, procesem tvorby a iluzí skutečné reality, kterou filmy o filmu vytvářejí. Zobrazení filmu uvnitř filmu je metodou, která vytváří další rovinu - nový rozměr a nutí diváka uvažovat nejen o uměleckém záměru, ale i procesu, čímž přibližuje autora divákovi.
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Is'Harc, Hayaatun. "JAK/STAT signalling." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272414.

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Mráz, Jakub. "Jak si založit podnik." Master's thesis, Vysoká škola ekonomická v Praze, 2007. http://www.nusl.cz/ntk/nusl-1410.

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Práce se zaměřuje na popis teoretických oblastí souvisejících s charakteristikou osoby podnikatele, rozhodnutím podnikat, sestavením podnikatelského plánu, praktickými kroky vedoucími k založení společnosti s ručením omezeným. Teoretické poznatky jsou posléze aplikovány na příklad založení malého podniku ve formě s.r.o.
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Lošek, David. "Jak si založit podnik." Master's thesis, Vysoká škola ekonomická v Praze, 2009. http://www.nusl.cz/ntk/nusl-15710.

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This thesis aims to serve as a suitable material for future entrepreneurs who want to orientate quickly and reliably in the issue of starting a business in the legislative environment of the Czech Republic before making own decision to establish a company. The work is divided into two parts - first, theoretical and methodological, will explain all theoretical aspects regarding establishment of businesses in our country. The second part, analytical, will transfer these aspects into practice. On example of a fictional company the reader will be step by step acquainted with it's whole life cycle.
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Vít, Jan. "Jak si založit podnik." Master's thesis, Vysoká škola ekonomická v Praze, 2009. http://www.nusl.cz/ntk/nusl-16779.

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The first part of this thesis on "How to Establish a Company" describes the basic terms such as entrepreneurship, entrepreneur, enterprise and its surroundings. It lists the possible legal forms, highlights their differences, sums up relevant regulations, explains the basics of accounting and shows the common structure of business plans. The second part focuses on setting up an actual company specializing in "Repeated purchases". In the form of a business plan it discusses its organizational, marketing and financial aspects as well as describes actual steps leading to founding the company legally.
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Kokešová, Tereza. "Jak si založit podnik." Master's thesis, Vysoká škola ekonomická v Praze, 2010. http://www.nusl.cz/ntk/nusl-74134.

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The goal of this diploma thesis is to provide a comprehensive overview of main activities that precede creation of an enterprise and to verify viability of a specific business plan. The theoretical part focuses on the definition of basic terms, analysis of legal environment concerning undertakings in the Czech Republic, business plan and event management itself. The practical part contains description of a specific business case for establishing an enterprise focused on event management. It also includes a company name choice, legal form of newly established enterprise and a thorough business plan.
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Konečný, Viktor. "Jak si založit podnik." Master's thesis, Vysoká škola ekonomická v Praze, 2010. http://www.nusl.cz/ntk/nusl-75536.

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This diploma thesis is focused on a franchising business establishment, particularly on the business establishment of a fictive coffe house which could become a well known franchising concept on the Czech market. Primary advantage of franchise compared to the other types of business cooperation is mainly risk reduction for the investor (franchisee) who obtains proven model of the business. For the franchisor the franchise means an easier way how to widen his business without taking higher lability. The main reason for choosing this topic is an attractivity of this field. Correct preparation and serving of a cup of coffee is not an easy process and there is not a big number of coffee houses and restaurants which can offer such a coffee. By offering high-quality and delicious coffee at user acceptable price our company would like to achieve its objectives and be a successful. The primary objective of this diploma thesis is to analyse and define strategy, mission, vision, marketing activities, product strategy and price policy of a new coffee house. These factors should be used for successful enter to the market. Secondary objective is to determine necessary initial capital, planned costs analysis and investment rate of return.
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Jiřincová, Jana. "Jak si založit podnik." Master's thesis, Vysoká škola ekonomická v Praze, 2011. http://www.nusl.cz/ntk/nusl-113641.

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The diploma thesis "How to establish a company" focuses on pre-school education. Specifically, on the establishment of a fictitious company day care at a planned business center comprised of office buildings and an ambulance station. Primary purpose of this study is to summarize the activities and difficulties that are associated with the foundation of a successful project. The study describes business strategy, competitive advantage, business vision and mission and legislative issues relating to operation of a company day care. The thesis is divided into two parts, theoretical and practical. In the first, theoretical part, we focus on description of terms associated with starting a business, entrepreneurs, and legal environment in the Czech Republic. The second, practical and analytical, part consists of detailed project of establishment of a company day care and also outlines problems arising in this area. These are hidden discrimination against women and the lack of capacity in public nurseries. The final financial plan evaluates feasibility of the project and assesses whether the investment is the right choice.
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Kolda, Michal. "Jak vyučovat společenský tanec." Master's thesis, Akademie múzických umění v Praze.Hudební a taneční fakulta. Knihovna, 2014. http://www.nusl.cz/ntk/nusl-177755.

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The Master thesis follows up on the previous Bachelor thesis title Methodology of traching of the ballroom dancing and it focuses on the second phase of teaching. The thesis engages in describes methodological techniques in teaching individual dances and dance figures within the advanced ballroom dancing courses. Commentaries are included, dealing with potencial problems in teaching and frequent faults.
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Dawson, M. A. F. "JAK-STAT signalling at chromatin." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598423.

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The aim of my work was to explore the possibility that the mammalian JAK2 signalling pathway influences the structure and function of chromatin. I have demonstrated that JAK2 is present in the nucleus of both human haematopoietic cell lines and primary cells. My results suggest that JAK2 functions as a histone tyrosine kinase and phosphorylates histone H3 at tyrosine-41 (H3Y41). This novel histone modification, the first described tyrosine phosphorylation on any of the non-variant histones, regulates the binding of heterochromatin protein 1-alpha (HP1α) at a new binding site on chromatin. HP1α uses its chromo-shadow domain to bind the H3Y41 region. Phosphorylation of H3Y41 by JAK2 reduces its affinity for chromatin. This reciprocal relationship was given a functional context by demonstrating its relationship to the expression of a key haematopoietic oncogene Imo2. Genome-wide studies demonstrate that H3Y41ph is present at the 5’ end of genes and is highly correlated with active transcription. This is the first comprehensive genome wide mapping of a histone phosphorylation mark and potentially highlights a role for this novel modification in the regulation of transcription. H3Y41ph was also present at specific cis-regulatory elements on JAK2-STAT5 target genes and genome-wide mapping of STAT5 binding confirmed that STAT5 binding and H3Y41ph was coincident at a significant number of sites within the human genome. This interesting observation suggests that canonical JAK2-STAT5 signalling is not confined to the cytoplasma but also occurs at chromatin. These findings extend the existing paradigm of JAK-STAT signalling and provide a platform for a better understanding of this critical signalling pathway, which is important in both normal development and oncogenesis.
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Books on the topic "JAK"

1

Bock, Robert. Jak-7, Jak-9. Gdan sk: AJ-Press, 1999.

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Marek, Drogosz, ed. Jak Polacy przegrywają? Jak Polacy wygrywają? Gdańsk: Gdańskie Wydawn. Psychologiczne, 2005.

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Panek, Wacław. Jan Kiepura: Życie jak z bajki. 2nd ed. Poznań: Wydawn. Kurpisz, 2002.

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Fischerová, Viola. Jak pápěří. Praha: Artforum - Jazzová sekce, 1995.

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Warda, Małgorzata. Jak Oddech. Warszawa: Prószyński S-ka, 2013.

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Wildstein, Bronisław. Jak woda. [S.l.]: Oficyna Literacka, 1989.

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Bieńkowska, Katarzyna (1972- ). Tł, ed. Jak powieść. Warszawa: Warszawskie Wydawnictwo Literackie Muza, 2007.

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Latkowski, Sylwester. Pamiętam jak--. Gdańsk: Słowo/Obraz Terytoria, 2001.

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Ostaszewski, Tadeusz. Jak kot. Olsztyn: Pojerzieze, 1988.

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Szozda, Łukasz. Jak sen. Gdynia: Novae Res, 2012.

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Book chapters on the topic "JAK"

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Caldow, Marissa K., and David Cameron-Smith. "JAK." In Encyclopedia of Exercise Medicine in Health and Disease, 495. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2575.

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Caldow, Marissa K., and David Cameron-Smith. "JAK/STAT Pathway." In Encyclopedia of Exercise Medicine in Health and Disease, 495–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_242.

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Caldow, Marissa K., and David Cameron-Smith. "Janus Kinases (JAK)." In Encyclopedia of Exercise Medicine in Health and Disease, 497. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4306.

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Meyer, Thomas, and Uwe Vinkemeier. "JAK-STAT Pathway." In Encyclopedia of Molecular Pharmacology, 1–5. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_157-1.

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Meyer, Thomas, and Uwe Vinkemeier. "JAK-STAT Pathway." In Encyclopedia of Molecular Pharmacology, 889–93. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_157.

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Leonard, Warren J. "The JAK-STAT Pathway." In Hormone Signaling, 103–20. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3600-7_6.

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Levine, Ross L. "JAK-Mutant Myeloproliferative Neoplasms." In Therapeutic Kinase Inhibitors, 119–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/82_2011_170.

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Oates, Andrew C., and Leonard I. Zon. "JAK/STATS in Zebrafish." In Signal Transducers and Activators of Transcription (STATs), 123–34. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-3000-6_9.

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Heron, Courtney E., Lindsay C. Strowd, and Steven R. Feldman. "Janus Kinase (JAK) Inhibitors." In Handbook of Systemic Drug Treatment in Dermatology, 170–76. 3rd ed. London: CRC Press, 2022. http://dx.doi.org/10.1201/9781003016786-25.

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Kozlowski, Nina, and Anna Hinc. "Korczak, Janusz: Jak kochać dziecko." In Kindlers Literatur Lexikon (KLL), 1–2. Stuttgart: J.B. Metzler, 2020. http://dx.doi.org/10.1007/978-3-476-05728-0_703-1.

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Conference papers on the topic "JAK"

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Marková, Hana. "DANĚ A VEŘEJNÉ PODPORY." In V. SLOVENSKO-ČESKÉ DNI DAŇOVÉHO PRÁVA: Daňové právo a nové javy v ekonomike. Vydavateľstvo ŠafárikPress, Univerzita Pavla Jozefa Šafárika v Košiciach, 2023. http://dx.doi.org/10.33542/vscd-0269-5-13.

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Státy se musí rozhodnout, jak budou řešit schodek veřejných rozpočtů. Tato otázka je klíčovou pro všechny státy, které se potýkají s rostoucí inflací a dalšími krizovými jevy. Jak situaci řešit a zároveň nenarušit rámec veřejné podpory stanovené v evropských smlouvách se řeší z politického a ekonomického hlediska. Je otázkou, zda to může být i daňové právo, které vnáší do veřejné podpory určité odchylky a jak se s touto situací vyrovnávají nejen státy jako celek, ale i jednotlivé články územní samosprávy.
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Šmajs, Josef. "Jak skončí prométheovský mýtus?" In Budoucnost strojové civilizace. Brno: Vysoké učení technické v Brně, Institut celoživotního vzdělávání, 2014. http://dx.doi.org/10.13164/conf.bsc.2014.4.

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Kotyza, Vojtěch. "Jak jsem potkal Františka Hezoučkého." In Seminář uspořádaný při příležitosti 80. narozenin Františka Hezoučkého. Západočeská univerzita v Plzni, 2022. http://dx.doi.org/10.24132/zcu.2022.11047.106.

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Kammerer, Susanne. "JAK inhibitors: A risk assessment." In 2022 American Academy of Dermatology Annual Meeting, edited by Peter van de Kerkhof. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/95bd51dd.

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Kammerer, Susanne. "JAK inhibitors: A risk assessment." In 2022 American Academy of Dermatology Annual Meeting, edited by Peter van de Kerkhof. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/b82d0ac3.

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Denk, Dagmar, Klaus Fortschegger, and Sabine Strehl. "Abstract 2171: The fusion protein PAX5-JAK2 constitutively activates JAK-STAT signaling." 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.am2011-2171.

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Hussain, H., S. Faryad, and D. Taneja. "Questioning the Janus Kinase (JAK) Inhibitors!" In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a4480.

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De Velasco, Marco A., Yurie Kura, Naomi Ando, Emiko Fukushima, Yuji Hatanaka, Yutaka Yamamoto, Nobutaka Shimizu, et al. "Abstract 906: Therapeutic potential of JAK/STAT signal inhibition in prostate cancer by the JAK inhibitor AZD1480." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-906.

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Otryaskin, Ya S., A. V. Yurtova, and S. I. Pinyaev. "CELL RECEPTORS AND SIGNALING PATHWAYS INVOLVED IN THE REGENERATION OF INJURED PERIPHERAL NERVES." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-353.

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The paper considers the process of injury to peripheral nerve fibers and the possibility of influencing their regeneration through reactions mediated by interaction with receptors that activate signaling pathways. Pathways such as RAS/ERK, PI3K, PLC-γ, JAK-STAT, MAPK/ERK, JNK and p38MAPK are key in signal transduction through biochemical cascade reactions, and modulating them can speed up the process of repair of damaged nerve fibers.
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Mentlík, Roman. "AI a její využití nejen v bankovním sektoru." In Lidský kapitál a investice do vzdělání. Vysoká škola finanční a správní, 2024. http://dx.doi.org/10.37355/lk-2023-08.

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Umělá inteligence (AI) není jen módní slovo - je to transformační síla, která přetváří náš svět způsoby, které jsme si před několika desítkami let nedokázali představit. Jak se posouváme dále do 21. století, umělá inteligence se stává nedílnou součástí našeho každodenního života, podniků, průmyslových odvětví, zdravotnictví, služeb bankovního a finančního sektoru apod. V tomto příspěvku prozkoumáme základy umělé inteligence, její aplikace, její dopad na společnost, budeme hledat odpověď na otázky typu: Jak ovlivní budoucnost bankovnictví? Jak mohou banky využívat umělou inteligenci (AI)? Jak by mohla vypadat digitální banka budoucnosti? Součástí bude i vhled do výsledků výzkumu AI ve finančních službách. Lze očekávat, že banky v Česku využívají umělou inteligenci stále častěji a investují do jejího rozvoje nemalé zdroje.
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Reports on the topic "JAK"

1

Brooks-Kayal, Amy, and Bret Smith. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada612534.

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Smith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada613987.

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Brooks-Kayal, Amy, Lauren Frey, and Bret N. Smith. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada614126.

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Smith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada568150.

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Brooks-Kayal, Amy. Jak/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada568663.

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Smith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada586062.

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Neilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada485255.

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Neilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada472476.

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Clevenger, Charles V., and Anthony A. Kossiakoff. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2011. http://dx.doi.org/10.21236/ada543162.

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Clevenger, Charles. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2010. http://dx.doi.org/10.21236/ada551381.

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