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Books on the topic 'Receptor tyrosine kinase family'

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Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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1

Wheeler, Deric L., and Yosef Yarden, eds. Receptor Tyrosine Kinases: Family and Subfamilies. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-11888-8.

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2

Germano, Serena. Receptor tyrosine kinases: Methods and protocols. New York: Humana Press, 2015.

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3

Shulman, Johanna. Biochemical analysis of activating mutations of the Kit receptor tyrosine kinase. Ottawa: National Library of Canada, 1998.

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4

Mustelin, Tomas. Src family tyrosine kinases in leukocytes. Austin: R.G. Landes, 1994.

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5

Ho, Jacqueline. A requirement for the receptor tyrosine kinase, Flk1, in hematopoiesis and vasculogenesis. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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6

Keane, Noeleen Emily. Nuclear magnetic resonance studies of the human insulin receptor tyrosine kinase autophosphorylation and activity. Birmingham: University of Birmingham, 1994.

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7

Gibson, Spencer Bruce. Role of the TEC family tyrosine kinase EMT in T cell activation. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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8

Viegas, Muriel. The intrinsic tyrosine kinase activity of the epidermal growth factor receptor is necessary for phospholipase A2 activation. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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9

Alaimo, Darrick James. Hepatic insulin receptor tyrosine kinase activity in diabetes: Modulation by assorted adenosine triphosphatases/phosphatases which copurify in partially purified preparations of the insulin receptor. [s.l: s.n.], 1992.

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10

1949-, Lichtner R. B., and Harkins R. N. 1947-, eds. EGF receptor in tumor growth and progression. Berlin: Springer, 1997.

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11

1952-, Drescher U., ed. Molecular bases of axonal growth and pathfinding. Berlin: Springer, 1997.

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12

Yarden, Yosef, and Deric L. Wheeler. Receptor Tyrosine Kinases: Family and Subfamilies. Springer, 2016.

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13

Yarden, Yosef, and Deric L. Wheeler. Receptor Tyrosine Kinases: Family and Subfamilies. Springer International Publishing AG, 2015.

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14

Yarden, Yosef, and Deric L. Wheeler. Receptor Tyrosine Kinases: Family and Subfamilies. Springer, 2015.

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15

Elowe, Sabine. Regulation of the ERK MAP kinase cascade by the Eph family of receptor tyrosine kinases. 2005.

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16

Wybenga-Groot, Leanne Elizabeth. Regulation of Eph receptor tyrosine kinase catalytic function. 2005.

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17

Germano, Serena. Receptor Tyrosine Kinases: Methods and Protocols. Springer New York, 2016.

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18

3BP-2: A novel substrate of the FLT3 receptor tyrosine kinase. Ottawa: National Library of Canada, 1996.

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19

Makowiecki, Mark Paul. Characterizing the role of EphB4 receptor tyrosine kinase during Xenopus gastrulation. 2005.

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20

Yarden, Yosef, and Deric L. Wheeler. Receptor Tyrosine Kinases: Structure, Functions and Role in Human Disease. Springer, 2014.

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21

Yarden, Yosef, and Deric L. Wheeler. Receptor Tyrosine Kinases: Structure, Functions and Role in Human Disease. Springer New York, 2016.

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22

Yarden, Yosef, and Deric L. Wheeler. Receptor Tyrosine Kinases: Structure, Functions and Role in Human Disease. Springer, 2014.

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23

Chohan, Manprit. Bidirectional co-signalling between the erythropoietin receptor and stem cell derived tyrosine kinase. 2006.

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24

Chen, Stephen Huang-Ting. Characterization of Dok-R-mediated cell migration downstream of the receptor tyrosine kinase, Tek/Tie2. 2004.

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25

Benson, Roseann M., and James W. Janetka. Extracellular Targeting of Cell Signaling in Cancer: Strategies Directed at MET and RON Receptor Tyrosine Kinase Pathways. Wiley & Sons, Incorporated, John, 2018.

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26

Benson, Roseann M., and James W. Janetka. Extracellular Targeting of Cell Signaling in Cancer: Strategies Directed at MET and RON Receptor Tyrosine Kinase Pathways. Wiley & Sons, Incorporated, John, 2018.

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27

Benson, Roseann M., and James W. Janetka. Extracellular Targeting of Cell Signaling in Cancer: Strategies Directed at MET and RON Receptor Tyrosine Kinase Pathways. Wiley & Sons, Incorporated, John, 2018.

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28

Klüppel, Michael. Analysis of regulatory W mutations and the function of the kit receptor tyrosine kinase in the intestine. 1998.

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29

Jones, Nina. Identification and characterization of downstream signaling partners of the endothelial cell-specific receptor tyrosine kinase, Tek/Tie-2. 2000.

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30

Abl family kinases in development and disease. New York, NY: Landes bioscience/Springer Science+Business Media, 2007.

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31

Koleske, Anthony. Abl Family Kinases in Development and Disease. Springer, 2007.

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32

Koleske, Anthony. Abl Family Kinases in Development and Disease. Springer New York, 2014.

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33

Koleske, Anthony. Abl Family Kinases in Development and Disease. Springer London, Limited, 2006.

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34

Zhao, Zhiying. Investigation of the Arabidopsis Thaliana proline-rich extensin-like receptor kinase family and plant defense responses. 2003, 2003.

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35

Stafstrom, Carl E., and Thomas P. Sutula. 2-Deoxyglucose. Edited by Dominic P. D’Agostino. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0036.

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Abstract:
Metabolic regulation of excitability is increasingly appreciated as a strategy to control seizures and reduce pathogenesis. Inhibiting or bypassing glycolysis may be one way in which the ketogenic diet suppresses seizures. 2-deoxy-D-glucose (2DG) is a glucose analog that partially inhibits glycolysis and has antiseizure effects in several acute and chronic seizure models. The mechanisms underlying the acute and chronic effects of 2DG are being investigated. Preliminary studies provide evidence that the acute anticonvulsant actions of 2DG involve activity-dependent presynaptic suppression of excitatory synaptic transmission during network synchronization. The chronic effects of 2DG entail reduction of the expression of brain-derived neurotrophic factor and its receptor, tyrosine kinase B. Preclinical toxicology studies demonstrate that 2DG has a favorable toxicity profile at doses effective for seizure protection. Currently available preclinical studies support 2DG as a novel first-in-class metabolic treatment for epilepsy with an antiglycolytic mechanism distinct from all other anticonvulsants.
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36

Reddy, Ugan, and Nicholas Hirsch. Diagnosis, assessment, and management of myasthenia gravis and paramyasthenic syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0244.

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Abstract:
Diseases that affect the neuromuscular junction (NMJ) interfere with normal nerve transmission and cause weakness of voluntary muscles. The two most commonly encountered are acquired myasthenia gravis (MG) and the Lambert–Eaton myasthenic syndrome (LEMS). Acquired MG is an autoimmune disease in which antibodies are directed towards receptors at the NMJ. In 85% of patients, IgG antibodies against the postsynaptic acetylcholine receptor (AChR) are found (seropositive MG). The thymus gland appears to be involved in the production of these which cause an increase rate of degradation of AChR resulting in a decreased receptor density resulting in a reduced postsynaptic end-plate potential following motor nerve stimulation and leading to muscle weakness. Although all voluntary muscles can be affected, ocular, bulbar, respiratory, and proximal limb weakness predominates. In the majority of seronegative patients, an antibody directed towards a NMJ protein called muscle specific tyrosine kinase (MUSK) is found. Anti-MUSK MG is characterized by severe bulbar and respiratory muscle weakness. Diagnosis of MG requires a high degree of clinical suspicion coupled with pharmacological and electrophysiological testing, and detection of the various causative antibodies. Treatment of MG involves enhancing neuromuscular transmission with long-acting anticholinesterase agents and immunosuppression. Acute exacerbations are treated with either plasma exchange or intravenous immunoglobulin. Myasthenic crisis is associated with severe muscle weakness that necessitates tracheal intubation and mechanical ventilation. LEMS is an autoimmune disease in which IgG antibodies are directed towards the pre-synaptic voltage-gated calcium channels at the NMJ. It is often associated with malignant disease (usually small cell carcinoma of the lung). Autonomic dysfunction is prominent and patients show abnormal responses to neuromuscular blocking drugs.
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