Raivola et al. Front Oncol. 2018: Hyperactivation of Oncogenic JAK3 Mutants Depend on ATP Binding to the Pseudokinase Domain Hammarén, Virtanen, Raivola, Silvennoinen, Cytokine, 2018: The regulation of JAKs in cytokine signaling and its breakdown in disease
Janus kinase 3 (JAK3) tyrosine kinase has a central role in the control of lymphopoiesis, and mutations in JAK3 can lead to either severe combined immunodeficiency or leukemia and lymphomas. JAK3 associates with the common gamma chain (γc) receptor and functions in a heteromeric signaling pair with JAK1. In IL-2 signaling JAK1 is the effector kinase for STAT5 phosphorylation but the precise
Although JAK3 SCID-associated mutations are found in all JAK domains, the majority is located either in JH2 or the FERM domain . identified in JAK3, which cause severe combined immune deficiency (SCID); a disease resulting a depletion of B-cells and complete loss of T- and NK-cells [11,12]. A majority of the pathogenic mutants clusters in JH2 highlighting the regulative role of the domain [10]. The most common mutation, JAK2 V617F also resides in JH2. Raivola, J, Hammarén, HM, Virtanen, AT, Bulleeraz, V, Ward, AC, Silvennoinen, O et al.. Hyperactivation of Oncogenic JAK3 Mutants Depend on ATP Binding to the Pseudokinase Domain.
Advanced Search Genetic deficiency of Jak3 leads to abrogation of signal transduction through the common gamma chain (γc) and thus to immunodeficiency suggesting that specific inhibition of Jak3 kinase may result in immunosuppression. Jak1 cooperates with Jak3 in signaling through γc-containing receptors. Unexpectedly, a Jak3-selective inhibitor was less efficient in abolishing STAT5 phosphorylation than Loop is the open research network that increases the discoverability and impact of researchers and their work. Loop enables you to stay up-to-date with the latest discoveries and news, connect with researchers and form new collaborations.
Acute myeloid leukemia (AML) is thought to be the consequence of two broad complementation classes of mutations: those that confer a proliferative and/or survival advantage to hem Raivola et al. Front Oncol. 2018: Hyperactivation of Oncogenic JAK3 Mutants Depend on ATP Binding to the Pseudokinase Domain Hammarén, Virtanen, Raivola, Silvennoinen, Cytokine, 2018: The regulation of JAKs in cytokine signaling and its breakdown in disease 2021-02-14 Optimization of this chemical series led to the identification of VX-509 (decernotinib), a novel, potent, and selective JAK3 inhibitor, which demonstrates good efficacy in vivo in the rat host versus graft model (HvG).
Loop is the open research network that increases the discoverability and impact of researchers and their work. Loop enables you to stay up-to-date with the latest discoveries and news, connect with researchers and form new collaborations.
The JAK-STAT signal transduction pathway is responsible for mediating signals of over fifty cytokines, growth factors and hormones. Signaling through the JAK-STAT pathway is regulated on multiple levels, including intramolecular regulation by the JAK pseudokinase domain, and intermolecular regulatio … Raivola on tunnettu Lintulan lehtikuusimetsästä, joka aikanaan oli Suomen suurin lehtikuusikko.
The pseudokinase JH2 domain of JAK2 is a negative regulator of JAK2 activity, but the mechanism for this is unclear. Now it is shown that JH2 is actually an active kinase that phosphorylates
Juuli Raivola, Teemu Haikarainen, Bobin George Abraham The JAK-STAT pathway plays a central role in IBD, such as UC 1. In UC, the activity of pro- and anti-inflammatory mediators is dysregulated, provoking an exaggerated immune response and initiating a chronic cycle of inflammation.
O. Selective JAKinibs: prospects in inflammatory and autoimmune diseases. Cytokine-independent Jak3 activation upon T cell receptor
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. …
2002-09-25 · The JH2 domain has been implicated in regulation of Jak activity, but its function remains poorly understood. Here, we found that the JH2 domain negatively regulates the activity of Jak2 and Jak3. Deletion of JH2 resulted in increased tyrosine phosphorylation of the Jak2- and Jak3-JH2 deletion mutants as well as of coexpressed STAT5.
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A majority of the pathogenic mutants clusters in JH2 highlighting the regulative role of the domain [10].
Several Virtanen A; Haikarainen T; Raivola J; Silvennoinen O. Selective
Hyperactivation of oncogenic JAK3 mutants depend on ATP binding to the pseudokinase domain. J Raivola, HM Hammarén, AT Virtanen, V Bulleeraz, AC Ward,
Selective JAK Pairings That Mediate Cytokine Signalling, JAK1 and JAK3 Virtanen AT, Haikarainen T, Raivola J, Silvennoinen O. Bio Drugs. 2019;33(1):15 -32
6 Aug 2020 inhibitor); I-41, JAK3 (Janis kinase 3) Inhibitor II; I-44, LCK JAK3 Inhibitor II Hammarén HM, Virtanen AT, Raivola J, Silvennoinen O. The
1 Apr 2021 JAK1/JAK3 participate in the proliferation and survival of T cells and memory T A.T. Virtanen, T. Haikarainen, J. Raivola, O. Silvennoinen.
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15 Sep 2020 notopterol directly binds Janus kinase (JAK)2 and JAK3 kinase Virtanen, A.T., Haikarainen, T., Raivola, J., and Silvennoinen, O. (2019).
Molekyylitason ymmärrys JAK-kinaasien toiminnasta edesauttaa muun muassa JAK-kinaaseihin kohdistuvien lääkemolekyylien kehitystä. Juuli Raivola 1, Teemu Haikarainen 1 and Olli Silvennoinen 1,2,3,* over JAK3 but in interferon-γ (IFNγ) and interferon-α (IFNα) signaling both JAK1 and heteromeric Hyperactivation of Oncogenic JAK3 Mutants Depend on ATP Binding to the Pseudokinase Domain Raivola, Juuli; Hammaren, Henrik M; Virtanen, Anniina T; Bulleraz, Vilasha; Ward, Alister C; Silvennoinen, Olli (2018) JAK3 R657Q was chosen as a representative activating JAK3 JH2 mutation because JAK3 lacks the residue homologous to JAK2 V617 that is present in other JAK JH2s (see Table 1). Furthermore, JAK3 has a leucine in the JH2 αC that in all other JAKs is occupied by a phenylalanine (Phe) . Hyperactivation of Oncogenic JAK3 Mutants Depend on ATP Binding to the Pseudokinase Domain By Juuli Raivola, Henrik M. Hammarén, Anniina T. Virtanen, Vilasha Bulleeraz, Alister C. Ward and Olli Silvennoinen Hyperactivation of Oncogenic JAK3 Mutants Depend on ATP Binding to the Pseudokinase Domain. Raivola, Juuli: dc.contributor.author: Hammaren, Henrik M. Wang et al.