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Books on the topic 'JAK/STAT'

Author: Grafiati

Published: 4 June 2021

Last updated: 24 August 2024

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1

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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2

Anastasis, Stephanou, ed. JAK-STAT pathway in disease. Austin, Tex: Landes Bioscience, 2009.

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3

Decker, Thomas, and Mathias Müller, eds. Jak-Stat Signaling : From Basics to Disease. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0891-8.

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4

Wilks, Andrew F., and Ailsa G. Harpur. Intracellular Signal Transduction: The JAK-STAT Pathway. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4.

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5

Wilks, Andrew F. Intracellular signal transduction: The JAK-STAT pathway. New York: Springer, 1996.

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6

Köberlein, Bernd. Interaktion von Hepatitis-B- und -C-Viren mit der inflammatorischen JAK-STAT-Signaltransduktion. Tübingen, Kastanienweg 5: B. Köberlein, 2008.

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7

Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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8

Goswami, Ritobrata. JAK-STAT Signaling in Diseases. CRC Press, 2020.

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9

Stephanou, Anastasis, and Bell Richard H. Jr. JAK-STAT Pathway in Disease. Taylor & Francis Group, 2009.

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10

Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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11

H, Bell Jr Richard. JAK-STAT Pathway in Disease. Taylor & Francis Group, 2009.

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12

Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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13

Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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14

Nicola, Nicos A., and Sandra E. Nicholson. JAK-STAT Signalling: Methods and Protocols. Humana Press, 2016.

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15

JAK-STAT Signalling: Methods and Protocols. Humana Press, 2013.

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16

Decker, Thomas, and Mathias Müller. Jak-Stat Signaling: From Basics to Disease. Springer, 2012.

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17

Harpur, Ailsa G., and Andrew F. Wilks. Intracellular Signal Transduction: The JAK-STAT Pathway. Springer, 2013.

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18

Decker, Thomas, and Mathias Müller. Jak-Stat Signaling: From Basics to Disease. Springer London, Limited, 2012.

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19

Decker, Thomas, and Mathias Müller. Jak-Stat Signaling: From Basics to Disease. Springer, 2012.

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20

Decker, Thomas, and Mathias Müller. Jak-Stat Signaling: From Basics to Disease. Springer Wien, 2014.

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21

Wilks, Andrew F. Intracellular Signal Transduction: The Jak-Stat Pathway. Springer, 2013.

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22

The Jak-Stat pathway in hematopoiesis and disease. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2002.

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23

Harpur, Ailsa G., and Andrew F. Wilks. The Jak-Stat Pathway (Molecular Biology Intelligence Unit). Springer, 1996.

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24

Jakstat Signalling Methods And Protocols. Humana Press, 2012.

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25

Ng, Sze-Ling. The Role of IKKepsilon in JAK/STAT Signaling During the Antiviral Immune Response. 2010.

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26

Ward, Alister C. The Jak-Stat Pathway in Hematopoiesis and Disease (Molecular Biology Intelligence Unit, 20). Springer, 2002.

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27

Mahdavi, Alborz. Analysis of transient JAK/STAT signaling kinetics predicts control modules of stem cell fate control. 2006.

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28

Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Abstract:

Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.

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