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Academic literature on the topic 'STAT'

Author: Grafiati

Published: 4 June 2021

Last updated: 24 August 2024

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Journal articles on the topic "STAT"

1

Ebersbach, Celina, Alicia-Marie K. Beier, Christian Thomas, and Holger H. H. Erb. "Impact of STAT Proteins in Tumor Progress and Therapy Resistance in Advanced and Metastasized Prostate Cancer." Cancers 13, no. 19 (September 28, 2021): 4854. http://dx.doi.org/10.3390/cancers13194854.

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Signal transducers and activators of transcription (STATs) are a family of transcription factors involved in several biological processes such as immune response, cell survival, and cell growth. However, they have also been implicated in the development and progression of several cancers, including prostate cancer (PCa). Although the members of the STAT protein family are structurally similar, they convey different functions in PCa. STAT1, STAT3, and STAT5 are associated with therapy resistance. STAT1 and STAT3 are involved in docetaxel resistance, while STAT3 and STAT5 are involved in antiandrogen resistance. Expression of STAT3 and STAT5 is increased in PCa metastases, and together with STAT6, they play a crucial role in PCa metastasis. Further, expression of STAT3, STAT5, and STAT6 was elevated in advanced and high-grade PCa. STAT2 and STAT4 are currently less researched in PCa. Since STATs are widely involved in PCa, they serve as potential therapeutic targets. Several inhibitors interfering with STATs signaling have been tested unsuccessfully in PCa clinical trials. This review focuses on the respective roles of the STAT family members in PCa, especially in metastatic disease and provides an overview of STAT-inhibitors evaluated in clinical trials.

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Konjevic, Gordana. "STAT proteins in cancerogenesis and therapy of malignancies." Srpski arhiv za celokupno lekarstvo 137, no. 1-2 (2009): 98–105. http://dx.doi.org/10.2298/sarh0902098k.

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Signal transducers and activators of transcription (STAT) proteins are a 7-member family of cytoplasmic transcription fators that participate in signal transduction by cytokines, hormones, and growth factors. STAT proteins control the most important cellular processes, including survival, proliferation and differentiation. A great number of cytokines and other factors in different cell types activate STAT1, STAT3 and STAT5 and in this manner regulate processes such as cellular proliferation, differentiation and survival. STATs such as STAT4 and STAT6 have a more specific effect and are engaged in the differentiation of T helper cell populations. Given the critical roles of STAT proteins it has been established in many studies that STAT3 and STAT5 are oncogenes that can contribute to cellular transformation by increasing proliferation and slowing-down apoptosis. On the other hand, STAT1 is a tumour suppressor gene and its inactivation contributes to malignant transformation. Initially STAT proteins were extensively studied in leukaemias, but later their role in the development of different solid tumours has been also shown. Aside from their role in the development of tumours, STAT1, STAT3 and STAT5 can be considered as molecular markers for early detection of certain types of tumours, as well as prognostic factors in the determination of tumour aggressiveness and predictors of response to various types of therapy. Evidence of the deregulation of STAT signalling pathway can serve as a basis for designing novel targeted molecular therapeutic strategies that carry a great potential in the therapy of solid tumours and leukaemias.

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de Haas, Nienke, Coco de Koning, Stefania di Blasio, Georgina Flórez-Grau, I. Jolanda M. de Vries, and Stanleyson V. Hato. "STAT Family Protein Expression and Phosphorylation State during moDC Development Is Altered by Platinum-Based Chemotherapeutics." Journal of Immunology Research 2019 (June 11, 2019): 1–12. http://dx.doi.org/10.1155/2019/7458238.

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The STAT signaling pathway is important in dendritic cell (DC) development and function. Tumor cells can induce STAT signaling, thereby inhibiting DC maturation and immunostimulatory functions, leading to hampered efficacy of DC-based immunotherapies. Platinum-based chemotherapeutics can inhibit STAT signaling, thereby making them an interesting tool to improve DC development and function. In this study, we provide a comprehensive overview of STAT expression and phosphorylation during DC differentiation and maturation and investigate the effects of platinum drugs on STAT signaling during these processes. Monocytes were differentiated into monocyte-derived DCs (moDCs) with IL-4 and GM-CSF and matured with cytokines or TLR ligands. STAT expression and phosphorylation were analyzed by western blotting, and moDC viability and phenotype were analyzed by flow cytometry. Platinum drugs were added at day 3 of differentiation or at the start of maturation to investigate regulation of the STAT signaling pathway. All STAT proteins were expressed during moDC differentiation and STAT1, STAT5, and STAT6 were phosphorylated. No significant changes occurred in the expression and phosphorylation state of the STAT proteins during differentiation. After maturation with TLR ligands, the expression of STAT1 increased, but other STAT proteins were not affected. Phosphorylation of STAT1 and STAT3 increased during maturation, where TLR ligands induced significantly higher levels of phosphorylation than cytokines. Platinum drugs cisplatin and oxaliplatin significantly inhibited phosphorylation of STAT6 during differentiation and maturation. Treatment did not affect the phenotype or viability of the cells. As STAT6 is an important regulator of DC function, these findings suggest a role for platinum-based chemotherapeutics to enhance DC function via inhibition of STAT signaling, thereby potentially enhancing efficacy of DC-based immunotherapies.

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Lee, Hyun-Ku, Gita Singh, and Sujay Singh. "STAT reporter cell line systems as a tool for cancer therapeutic target screening." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 169.8. http://dx.doi.org/10.4049/jimmunol.200.supp.169.8.

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Abstract Signal transducer and activator of transcription (STAT) proteins as cytoplasmic transcription factors respond to cytokines and growth factors that mediate downstream signaling. STATs are closely related with cancers as they are frequently found to be dysregulated in primary tumors, leading to enhanced survival of tumors and increased angiogenesis. Among seven STAT family members, STAT3, STAT4 and STAT5 are considered to primarily promote cancer development and progression, while STAT1 may function either as a tumor suppressor or tumor promoter. STAT3, 4 and 5 are persistently activated in many human cancer cell lines, leading to increased cancer cell survival. Several studies demonstrate that inhibition of STAT3 or STAT5 signaling decreases cancer cell proliferation leading to apoptosis. Taken together, these indicate that STAT proteins can be ideal targets for anti-cancer therapy, and so it is crucial to develop assay systems that can identify inhibitors targeting those pro-tumorigenic STATs. Hence we developed the four reporter cell lines, each of which stably expresses STAT1-, STAT3-, STAT4-, or STAT5-response element that controls an optimized Renilla luciferase reporter gene upon stimulation. Functional activity of each cell line was evaluated through dose response of various cytokines such as IFNs, IL-3 and IL-6. One of the STAT inhibitors, curcumin as well as other putative STAT suppressors were utilized to characterize how each STAT can differentially respond to each test molecule and how its response can affect the host cells.

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Gorissen, Marnix, Erik de Vrieze, Gert Flik, and Mark O. Huising. "STAT genes display differential evolutionary rates that correlate with their roles in the endocrine and immune system." Journal of Endocrinology 209, no. 2 (February 17, 2011): 175–84. http://dx.doi.org/10.1530/joe-11-0033.

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We identified orthologues of all mammalian Janus kinase (JAK) and signal transducer and activator of transcription (STAT) genes in teleostean fishes, indicating that these protein families were already largely complete before the teleost tetrapod split, 450 million years ago. In mammals, the STAT repertoire consists of seven genes (STAT1, -2, -3, -4, -5a, -5b, and -6). Our phylogenetic analyses show that STAT proteins that are recruited downstream of endocrine hormones (STAT3 and STAT5a and -5b) show a markedly higher primary sequence conservation compared with STATs that convey immune signals (STAT1-2, STAT4, and STAT6). A similar dichotomy in evolutionary conservation is observed for the JAK family of protein kinases, which activate STATs. The ligands to activate the JAK/STAT-signalling pathway include hormones and cytokines such as GH, prolactin, interleukin 6 (IL6) and IL12. In this paper, we examine the evolutionary forces that have acted on JAK/STAT signalling in the endocrine and immune systems and discuss the reasons why the JAK/STAT cascade that conveys classical immune signals has diverged much faster compared with endocrine JAK/STAT paralogues.

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Tian, SS, P. Tapley, C. Sincich, RB Stein, J. Rosen, and P. Lamb. "Multiple signaling pathways induced by granulocyte colony-stimulating factor involving activation of JAKs, STAT5, and/or STAT3 are required for regulation of three distinct classes of immediate early genes." Blood 88, no. 12 (December 15, 1996): 4435–44. http://dx.doi.org/10.1182/blood.v88.12.4435.bloodjournal88124435.

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Granulocyte colony-stimulating factor (G-CSF) is the major regulator of proliferation and differentiation of neutrophilic granulocyte precursor cells. G-CSF activates multiple signaling molecules, including the JAK1 and JAK2 kinases and the STAT transcription factors. To investigate G-CSF signaling events regulated by the JAK-STAT pathway, we have generated UT7-epo cells stably expressing either wild-type (wt) G-CSF receptor or a series of C-terminal deletion mutants. Gel mobility shift and immunoprecipitation/Western analysis showed that STAT5 is rapidly activated by G-CSF in cells expressing the wt G-CSF receptor, in addition to the previously reported STAT3 and STAT1. Mutants lacking any tyrosine residues in the cytoplasmic domain maintain their ability to activate STAT5 and STAT1 but cannot activate STAT3, implying that STAT5 and STAT1 activation does not require receptor tyrosine phosphorylation. We also observed significant changes in the ratio of STAT1:STAT3:STAT5 activated by various G-CSF receptor C-terminal deletion mutants. These mutant receptors were further used to investigate the role of JAKs and STATs in G-CSF-mediated responses in these cells. We found that JAK activation correlates with G-CSF-induced cell proliferation, whereas STAT activation is not required. We have also identified three classes of G-CSF immediate early genes, whose activation correlates with the activation of distinct JAK-STAT pathways. Our data show that, whereas c-fos is regulated through a pathway independent of STAT activation, oncostatin M, IRF-1, and egr-1 are regulated by an STAT5-dependent pathway and fibrinogen is regulated by an STAT3-dependent pathway. In conclusion, our results suggest that G-CSF regulates its complex biologic activities by selectively activating distinct early response genes through different JAK-STAT signaling molecules.

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Chen, Honglin, Lindsey Hutt-Fletcher, Liang Cao, and S. Diane Hayward. "A Positive Autoregulatory Loop of LMP1 Expression and STAT Activation in Epithelial Cells Latently Infected with Epstein-Barr Virus." Journal of Virology 77, no. 7 (April 1, 2003): 4139–48. http://dx.doi.org/10.1128/jvi.77.7.4139-4148.2003.

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ABSTRACT STAT3 and STAT5 are constitutively activated and nuclear in nasopharyngeal carcinoma (NPC) cells. In normal signaling, STATs are only transiently activated. To investigate whether Epstein-Barr virus (EBV), and in particular the protein LMP1, contributes to sustained STAT phosphorylation and activation in epithelial cells, we examined STAT activity in two sets of paired cell lines, HeLa, an EBV-converted HeLa cell line, HeLa-Bx1, the NPC-derived cell line CNE2-LNSX, and an LMP1-expressing derivative, CNE2-LMP1. EBV infection was associated with a significant increase in the tyrosine-phosphorylated forms of STAT3 and STAT5 in HeLa-Bx1 cells. This effect correlated with LMP1 expression, since phosphorylated STAT3 and STAT5 levels were also increased in CNE2-LMP1 cells relative to the control CNE2-LNSX cells. No change was observed in STAT1 or STAT6 phosphorylation in these cell lines, nor was there a significant change in the levels of total STAT3, STAT5, STAT1, or STAT6 protein. Tyrosine phosphorylation allows the normally cytoplasmic STAT proteins to enter the nucleus and bind to their recognition sequences in responsive promoters. The ability of LMP1 to activate STAT3 was further established by immunofluorescence assays in which coexpression of LMP1 in transfected cells was sufficient to mediate nuclear relocalization of Flag-STAT3 and by an electrophoretic mobility shift assay which showed that LMP1 expression in CNE2-LNSX cells was associated with increased endogenous STAT3 DNA binding activity. In addition, the activity of a downstream target of STAT3, c-Myc, was upregulated in HeLa-Bx1 and CNE2-LMP1 cells. A linkage was established between interleukin-6 (IL-6)- and LMP1-mediated STAT3 activation. Treatment with IL-6 increased phosphorylated STAT3 levels in CNE2-LNSX cells, and conversely, treatment of CNE2-LMP1 cells with IL-6 neutralizing antibody ablated STAT3 activation and c-Myc upregulation. The previous observation that STAT3 activated the LMP1 terminal repeat promoter in reporter assays was extended to show upregulated expression of endogenous LMP1 mRNA and protein in HeLa-Bx1 cells transfected with a constitutively activated STAT3. A model is proposed in which EBV infection of an epithelial cell containing activated STATs would permit LMP1 expression. This in turn would establish a positive feedback loop of IL-6-induced STAT activation, LMP1 and Qp-EBNA1 expression, and viral genome persistence.

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Murphy, Theresa L., Erik D. Geissal, J. David Farrar, and Kenneth M. Murphy. "Role of the Stat4 N Domain in Receptor Proximal Tyrosine Phosphorylation." Molecular and Cellular Biology 20, no. 19 (October 1, 2000): 7121–31. http://dx.doi.org/10.1128/mcb.20.19.7121-7131.2000.

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ABSTRACT Stat4 is activated by the cytokines interleukin 12 and alpha interferon (IFN-α) and plays a significant role in directing development of naı̈ve CD4+ T cells to the Th1 phenotype. Signal transducers and activators of transcription (STAT) proteins undergo phosphorylation on a conserved tyrosine residue, resulting in homo- and heterodimerization, nuclear translocation, and DNA binding. Stat4 can bind to single IFN-γ-activated sites (GASs) as a dimer or bind two tandem GASs as a pair of STAT dimers, or tetramer, stabilized through N-terminal domain (N domain) interactions between dimers. We uncovered an unexpected effect of the Stat4 N domain in controlling the proximal activation of Stat4 by tyrosine phosphorylation at activated receptor complexes. Mutation of the N domain at tryptophan residue W37, predicted to interrupt N domain dimer formation, unexpectedly prevented IFN-α-induced tyrosine phosphorylation of the Stat4 monomer, blocking dimer formation and nuclear translocation. Furthermore, N domains appear to exert private STAT functions, since interchanging the N domains between Stat1 and Stat4 prevented receptor-mediated tyrosine phosphorylation in one case and interrupted STAT-specific gene activation in another. Finally, replacement of the N domain of Stat1 with that of Stat4 abrogated the normal Stat2 dependence of Stat1 phosphorylation, again suggesting the domains are not equivalent. Thus, in addition to its role in STAT tetramerization, the conserved STAT N domain appears to participate in very proximal steps of receptor-mediated ligand-induced tyrosine phosphorylation.

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Guo, DanQun, James D. Dunbar, Chuan He Yang, Lawrence M. Pfeffer, and David B. Donner. "Induction of Jak/STAT Signaling by Activation of the Type 1 TNF Receptor." Journal of Immunology 160, no. 6 (March 15, 1998): 2742–50. http://dx.doi.org/10.4049/jimmunol.160.6.2742.

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Abstract Cellular responses to TNF are initiated by either of two cell surface receptors, the type 1 TNF receptor (TNFR1) and the type 2 TNF receptor (TNFR2). Although neither receptor contains an intrinsic protein tyrosine kinase, such activity has been implicated in TNF action. In this study, we show that murine TNF induces the tyrosine phosphorylation and activation of the intracellular Janus tyrosine kinases Jak1, Jak2, and Tyk2 in murine 3T3-L1 adipocytes. Activation of Jak kinases by TNF was associated with tyrosine phosphorylation of STAT1, STAT3, STAT5, and STAT6, but not STAT2 or STAT4, showing that TNF acts on a specific subset of these latent cytoplasmic transcription factors in 3T3-L1 adipocytes. Agonist antiserum to TNFR1 induced Jak kinase and STAT protein phosphorylation. Phosphorylation of Jak proteins was also induced by human TNF, which selectively binds to TNFR1 on murine cells. 35S-labeled Jak kinases were precipitated from a cell-free system and from lysates of 3T3-L1 adipocytes by a glutathione S-transferase fusion protein containing the cytoplasmic domain of TNFR1. These results suggest that the cytoplasmic domain of TNFR1 can directly interact with and form signaling complexes with Jak kinases. Jak2 was precipitated from HeLa cells by antiserum to TNFR1, directly demonstrating their association in vivo. Thus, TNF activates a Jak/STAT signal-transduction cascade by acting through TNFR1.

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Morgan, Ethan L., and Andrew Macdonald. "Manipulation of JAK/STAT Signalling by High-Risk HPVs: Potential Therapeutic Targets for HPV-Associated Malignancies." Viruses 12, no. 9 (September 3, 2020): 977. http://dx.doi.org/10.3390/v12090977.

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Human papillomaviruses (HPVs) are small, DNA viruses that cause around 5% of all cancers in humans, including almost all cervical cancer cases and a significant proportion of anogenital and oral cancers. The HPV oncoproteins E5, E6 and E7 manipulate cellular signalling pathways to evade the immune response and promote virus persistence. The Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathway has emerged as a key mediator in a wide range of important biological signalling pathways, including cell proliferation, cell survival and the immune response. While STAT1 and STAT2 primarily drive immune signalling initiated by interferons, STAT3 and STAT5 have widely been linked to the survival and proliferative potential of a number of cancers. As such, the inhibition of STAT3 and STAT5 may offer a therapeutic benefit in HPV-associated cancers. In this review, we will discuss how HPV manipulates JAK/STAT signalling to evade the immune system and promote cell proliferation, enabling viral persistence and driving cancer development. We also discuss approaches to inhibit the JAK/STAT pathway and how these could potentially be used in the treatment of HPV-associated disease.

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Dissertations / Theses on the topic "STAT"

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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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Strickland, Janae. "The Role of STAT and the Jak/STAT Pathway In Mediating the Effects of Interleukin-6 on StAR Expression." Diss., CLICK HERE for online access, 2007. http://contentdm.lib.byu.edu/ETD/image/etd1781.pdf.

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Une-Larsson, Martin. "Verkställighet mot främmande stat." Thesis, Stockholms universitet, Juridiska institutionen, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-129856.

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Lif, Zophie. "Stat i världen : En studie av Islamiska staten i förhållande till begreppet stat." Thesis, Mittuniversitetet, Avdelningen för samhällsvetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:miun:diva-26888.

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Titel: Stat i världen – En studie av Islamiska staten i förhållande till begreppet stat Kurs: Statsvetenskap C, Mittuniversitetet, vårterminen 2015 Författare: Zophie Lif Nyckelord: Statsvetenskap, Islamiska staten, stat, begreppsdefinition, kvalitativ metod Bakgrund Islamiska staten är en av flera islamistiska rörelser som på senare tid vunnit stora politiska och territoriella framgångar. Organisationen utmärker sig genom att göra anspråk på ett världsomspännande kalifat som ska omfatta hela världens muslimska befolkning.I västvärlden har Islamiska staten främst uppmärksammat för sitt extrema våld, medan de i Mellanöstern av många grupper uppfattas som möjliga makthavare. Syfte Uppsatsens syfte är undersöka om och i vilken utsträckning Islamiska staten teoretiskt kan definieras som en stat. Undersökningen har gjorts med utgångspunkt i frågeställningen "Om och i vilken utsträckning kan Islamiska staten i teoretisk mening definieras som en stat?" Metod Undersökningen är en kvalitativ textanalys, där Islamiska staten prövas mot begreppet stat såsom det definieras av Max Weber. Det empiriska materialet analyseras utifrån en kategorisering av Webers teori. Resultatet har visat att Islamiska staten delvis, om än inte fullt ut, uppfyller Webers kriterier för en stat. Slutsats Studien visar att Islamiska staten, helt eller delvis, uppfyller vissa av de preciserade kriterier som definierar en stat. Utifrån studiens resultat dras slutsatsen att Islamiska staten av idag inte i tillräcklig utsträckning uppfyller villkoren för en stat, men samtidigt att det inte går att utesluta att organisationen en dag kommer att uppnå det målet.

2015-06-03

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Lindström, Dag. "Skrå, stad och stat : Stockholm, Malmö och Bergen ca. 1350-1622 /." Stockholm : Almqvist och Wiksell, 1991. http://catalogue.bnf.fr/ark:/12148/cb35512925f.

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Laurén, Pär. "Sekt, stat och apokalyptiskt våld." Thesis, University of Gävle, Ämnesavdelningen för religionsvetenskap, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-3776.

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Denna uppsats behandlar det fenomen som uppstår när en, mer eller mindre isolerad, grupp religiöst hängivna människor, hamnar i en så pass allvarlig konflikt med staten och dess instutitioner att våldsamheter uppstår. Fenomenet brukar gå under beteckningen fanatiskt religiöst våld, och är i dess västerländska tappning mer eller mindre synonymt med sekter och sekterism.

P.g.a. ämnets digra karaktär är en kraftig begränsning nödvändig för att kunna behandla ämnet i en C-uppsats. Jag har därför gjort valet att koncentrera mig på de två mest extrema och medialt uppmärksammade fallen av religiöst sektvåld. Då ett av syftena med uppsatsen är att undersöka orsakerna till hur och varför väpnade konflikter uppstår mellan stat och sekt har jag valt att utesluta de fall där enbart kollektivt själmord av och med sektmedlemmarna utförts, utan inblandning av staten. Exempel på dylika är Heavens Gate (Hale-Bopp sekten) och allra senast den Ugandiska neo-katolska domedagssekten ”Restoration of the ten commandments of God”, där över tusen människor begick kollektivt självmord. Dessa och liknande händelser är onekligen mycket intressanta, men faller tyvärr utanför ramen för detta arbete.

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Hagberg, Axel. "Bankkrishantering : aktörer, marknad och stat." Doctoral thesis, Handelshögskolan i Stockholm, EHFF - Stiftelsen för Ekonomisk-historisk och Företagshistorisk Forskning, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:hhs:diva-1264.

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I likhet med i andra länder har det i Sverige under vissa högkonjunkturer uppstått ett så betydande kapitalöverskott, att den finansiella marknaden fått problem att bemästra flödena. Konsekvensen har blivit att den aggregerade risknivån ökat i takt med stigande tillgångspriser. När väl en kontraktion uppstått, har det saknats kapital för att i ordnade former bemästra de nya ekonomiska förutsättningarna. Det är den utvecklingen som föregått kriserna 1878/79, 1921/22 och 1991/92. Temporära insatser har då måst ske vid sidan av det befintliga institutionella systemet. Forskningen ger för Sveriges del en kriskronologi för det finansiella området med krisåren 1763, 1817/18, 1857/58, 1878/79, 1907/08, 1921/22, 1932/33 och 1991/92. Det har vid kriserna 1878/79, 1921/22 och 1991/92 förelegat ett betydande hot om kollaps av det finansiella systemet. Vid dessa tre tillfällen har det efter förhandlingar mellan bankerna och staten kommit att skapas temporära krishanteringsorganisationer – Järnvägshypoteksfonden 1879, AB Kreditkassan 1922 samt Securum AB 1992 – vid sidan om den svenska Riksbanken. Kriserna har hävts med hjälp av de temporärt skapade krisorganisationerna, vilka samtliga har haft en Lender of Last Resort-funktion. Krishanteringstekniken vid krisen 1921/22 kan ses som en vidareutveckling av den som kommit till användning 1878/79. Även om bakgrunden till krisen 1991/92 skiljer sig åt från de två här tidigare nämnda tillfällena, kom tekniken med överflyttandet av tyngande engagemang till ett nytt bolag att likna den teknik som användes redan av AB Kreditkassan. Trots detta betydde tidigare svenska erfarenheter mindre för krisen 1991/92 i detta fall. Idéerna till Securum hämtades istället från senare tids bankkrishantering i USA med inrättandet av så kallade ”bad banks”. Syftet med denna avhandling är att med en institutionell ansats klarlägga och analysera hur de två första av dessa tre finansiella kriser har hanterats. Avhandlingen belyser i detalj det förhandlingsdrama mellan statens och marknadens aktörer som föregått inrättandet av respektive krisorganisation.

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Hagberg, Axel. "Bankkrishantering : aktörer, marknad och stat /." Stockholm : Handelshögskolan i Stockholm : Ekonomiska forskningsinstitutet vid Handelshögskolan i Stockholm (EFI) [distributör], 2007. http://www2.hhs.se/EFI/summary/725.htm.

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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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Hjelmqvist, Ingvar. "Relationer mellan stat och kommun." [Stockholm] : Stockholms universitet, Statsvetenskapliga institutionen, 1994. http://books.google.com/books?id=yi0FAQAAIAAJ.

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Books on the topic "STAT"

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Johnson, Robert Russell. Stat. 2nd ed. Belmont, CA: Brooks/Cole Cengage Learning, 2010.

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Messmer, Craig M. Stat One. New York: McGraw-Hill, 2008.

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Brett, Hudson, ed. Stat man. Edinburgh: Barrington Stoke, 2007.

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SAS Institute. SAS Stat Studio 3.1 for SAS/STAT users. Cary, N.C: SAS Institute, 2008.

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SAS Institute. SAS Stat Studio 3.11 for SAS/STAT Users. Cary, NC: SAS, 2009.

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SAS Institute. SAS Stat Studio 3.1 for SAS/STAT users. Cary, N.C: SAS Institute, 2008.

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Christensen, Jørgen Grønnegård. Den usynlige stat. Copenhagen: Gyldendal, 1991.

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Nicholson, Sandra E., and Nicos A. Nicola, eds. JAK-STAT Signalling. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-242-1.

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Kotov, A. Kak stat' grossmeĭsterom. Moskva: Russian Chess House, 2007.

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Min'jar-Belorucev, R. K. Kak stat' perevodcikom? Moskva: Gotica, 1999.

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Book chapters on the topic "STAT"

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Lim, Su Jun, and Willis X. Li. "STAT." In Encyclopedia of Signaling Molecules, 5170–75. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_636.

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Vidal, C., and W. R. Külpmann. "STAT." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_2896-1.

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Vidal, C., and W. R. Külpmann. "STAT." In Springer Reference Medizin, 2210. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_2896.

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Lim, Su Jun, and Willis X. Li. "STAT." In Encyclopedia of Signaling Molecules, 1–5. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_636-1.

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Lynch, Gordon S., David G. Harrison, Hanjoong Jo, Charles Searles, Philippe Connes, Christopher E. Kline, C. Castagna, et al. "STAT." In Encyclopedia of Exercise Medicine in Health and Disease, 810. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_3071.

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Dempsey, Brian R., Anne C. Rintala-Dempsey, Gary S. Shaw, Yuan Xiao Zhu, A. Keith Stewart, Jaime O. Claudio, Constance E. Runyan, et al. "SSI (STAT-Induced STAT Inhibitor)." In Encyclopedia of Signaling Molecules, 1787. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101283.

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Gressner, A. M., and O. A. Gressner. "STAT-Labor." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_2903-1.

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Gressner, A. M., and O. A. Gressner. "STAT-Labor." In Springer Reference Medizin, 2213. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_2903.

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Gooch, Jan W. "Anti-Stat." In Encyclopedic Dictionary of Polymers, 44. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_725.

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Johannessen, Janne Bondi, Kristin Hagen, André Lynum, and Anders Nøklestad. "OBT+stat." In Exploring Newspaper Language, 51–66. Amsterdam: John Benjamins Publishing Company, 2012. http://dx.doi.org/10.1075/scl.49.03joh.

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Conference papers on the topic "STAT"

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Barnett, Mike, Badrish Chandramouli, Robert DeLine, Steven Drucker, Danyel Fisher, Jonathan Goldstein, Patrick Morrison, and John Platt. "Stat!" In the 2013 international conference. New York, New York, USA: ACM Press, 2013. http://dx.doi.org/10.1145/2463676.2463683.

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Zhang, Baogang, Necati Uysal, and Rickard Ewetz. "STAT." In GLSVLSI '19: Great Lakes Symposium on VLSI 2019. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3299874.3318032.

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Kunath, Stephen A., and Steven H. Weinberger. "STAT." In Human Language Technologies: The 2009 Annual Conference of the North American Chapter of the Association for Computational Linguistics, Companion Volume: Demonstration Session. Morristown, NJ, USA: Association for Computational Linguistics, 2009. http://dx.doi.org/10.3115/1620959.1620962.

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Perry, MIke. "Stat-Maps." In Proceedings of the First Scientific Meeting of the IASE. International Association for Statistical Education, 1993. http://dx.doi.org/10.52041/srap.93106.

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STAT-MAPS, "Statistics-Materials and Activities for Problem Solving", is a four year project (1991-94) in the Department of mathematical Sciences, Appalachian State University, USA. Funded by the National Science Foundation, The STAT-MAPS project is developing curriculum and materials for students in grades 9-12 (ages 15-17), The STAT-MAPS curriculum is giving attention to students with a broad range of abilities and interests, not just the college bound one or the advanced students who have a special interest in science or mathematics.

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"Authors Stat." In 2022 11th International Conference on Modern Circuits and Systems Technologies (MOCAST). IEEE, 2022. http://dx.doi.org/10.1109/mocast54814.2022.9837528.

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Liu, Xuan, Songhua Xing, Murali Uppala, and Arun Hampapur. "STAT: Spatio-Temporal Analytics Toolkit." In SPIE Defense, Security, and Sensing, edited by Matthew F. Pellechia, Richard Sorensen, Shiloh L. Dockstader, Rudy G. Benz II, and Bernard V. Brower. SPIE, 2011. http://dx.doi.org/10.1117/12.886677.

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Schield, Milo. "Offering stat 102: social statistics for decision makers." In Promoting Understanding of Statistics about Society. International Association for Statistical Education, 2016. http://dx.doi.org/10.52041/srap.16605.

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Statistical educators should support offering three introductory statistics courses: STAT 100 (Statistical Literacy for non-quantitative majors), STAT 101 (Traditional inferential statistics) and STAT 102 (Social statistics for decision makers). The support for the STAT 102 claim includes the needs of most students taking introductory statistics, the different kinds of decisions being made, the growing importance of big data, the limited amount of free time in the current STAT 101 course, the 2016 update to the GAISE guidelines, the importance of confounding in influencing statistical associations and the ability of confounding to influence statistical significance. This paper provides student-tested ways of showing and explaining confounding, statistical significance and the influence of confounding on statistical significance. Indeed 100% of the IASE respondents agreed that students should be shown how confounding can influence statistical significance, 84% agreed that failure to illustrate this confounder-significance connection constituted "professional negligence" and 69% agreed that statistical educators should support offering STAT 102 along with STAT 100 and STAT 101. In a separate survey of the Augsburg students taking this STAT 102 type course, 61% agreed or strongly agreed that a STAT 102 course should be required by all students for graduation. With most of these statistical educators supporting the existence of a STAT 102 course and most Augsburg students seeing significant value in such a course, the door is now open for a new generation of courses, textbooks and teachers.

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Shah, Dharambhai, and Tanish Zaveri. "A Novel Geo-Stat Endmember Extraction Algorithm." In TENCON 2019 - 2019 IEEE Region 10 Conference (TENCON). IEEE, 2019. http://dx.doi.org/10.1109/tencon.2019.8929562.

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Marr, James C. "SIM-Planetquest Mission: Overview and Current Stat..." In 56th International Astronautical Congress of the International Astronautical Federation, the International Academy of Astronautics, and the International Institute of Space Law. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2005. http://dx.doi.org/10.2514/6.iac-05-a3.1.04.

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Ismail, Iman, Walaa Gad, Mohamed Hamdy, and Khaled Bahnsy. "Text document annotation methods: Stat of art." In 2015 IEEE Seventh International Conference on Intelligent Computing and Information Systems (ICICIS). IEEE, 2015. http://dx.doi.org/10.1109/intelcis.2015.7397289.

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Reports on the topic "STAT"

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Indset, Marthe, Jan Erling Klausen, Geir Møller, Eivind Smith, and Hilde Hatleskog Zeiner. Likeverdighet mellom stat og kommunesektor. Oslo: By- og regionforskningsinstituttet NIBR, 2012. http://dx.doi.org/10.7577/nibr/samarbeidsrapport/2012/3.

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Liu, Xiaoyue Cathy, Qian Zuo, Shenruoyang Na, Ran Wei, Aaron Golub, Liming Wang, and Jake Davis. Social-Transportation Analytic Toolbox (STAT) for Transit Networks. Transportation Research and Education Center (TREC), 2019. http://dx.doi.org/10.15760/trec.229.

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Brazaitis, Michael P. Wireless Communication of STAT Radiology Reporting Pilot Study. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada612166.

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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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Reddy, Premkumar. Role of STAT-3 in ER- Breast Tumors. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada390722.

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