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Janus kinase 3

JAK3, Janus Kinase 3
The protein encoded by this gene is a member of the Janus kinase (JAK) family of tyrosine kinases involved in cytokine receptor-mediated intracellular signal transduction. It is predominantly expressed in immune cells and transduces a signal in response to its activation via tyrosine phosphorylation by interleukin receptors. Mutations in this gene are associated with autosomal SCID (severe combined immunodeficiency disease). [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Janus kinase, JAK2, STAT5, Interleukin-2, STAT3
Papers using JAK3 antibodies
Induction by antigen of intrathymic apoptosis of CD4+CD8+TCRlo thymocytes in vivo
Mascaró Cristina et al., In Molecular Therapy. Nucleic Acids, 1989
... Jak1 primary antibody (Chemicon, Temecula, CA) was used at 1/500 dilution, while human Jak3 (Cell Signaling, Danvers, MA) and mouse ...
Papers on JAK3
Deep intronic mis-splicing mutation in JAK3 gene underlies T-B+NK- severe combined immunodeficiency phenotype.
Barak et al., Jerusalem, Israel. In Clin Immunol, Feb 2016
In this study we describe three patients with a novel deep intronic mis-splicing mutation in JAK3 as a cause of T-B+NK- SCID highlighting the need for careful evaluation of intronic regulatory elements of known genes associated with clearly defined clinical phenotypes.
Staphylococcus aureus enterotoxin A (SEA) stimulates STAT3 activation and IL-17 expression in cutaneous T-cell lymphoma.
Odum et al., Copenhagen, Denmark. In Blood, Feb 2016
The response is induced via IL-2Rg cytokines and a Janus kinase 3 (JAK3) - dependent pathway in malignant T cells and blocked by Tofacitinib, a clinical-grade JAK3 inhibitor.
Enhancing specificity in the Janus kinases: a study on the thienopyridine JAK2 selective mechanism combined molecular dynamics simulation.
Zhang et al., Lanzhou, China. In Mol Biosyst, Jan 2016
UNASSIGNED: The selective inhibition for JAK2 over the other JAK family kinases (JAK1, JAK3 and TYK2) has shared an immense challenge due to high conservatism.
IL-4 orchestrates STAT6-mediated DNA demethylation leading to dendritic cell differentiation.
Ballestar et al., Barcelona, Spain. In Genome Biol, Dec 2015
Most importantly, activation of the JAK3-STAT6 pathway, downstream of IL-4, is required for the acquisition of the dendritic-cell-specific demethylation and expression signature, following STAT6 binding.
Future perspectives in target-specific immunotherapies of myasthenia gravis.
Dalakas, Philadelphia, United States. In Ther Adv Neurol Disord, Nov 2015
Novel biological agents currently on the market, directed against the following molecular pathways, are relevant and specific therapeutic targets that can be tested in MG: (a) T cell intracellular signaling molecules, such as anti-CD52, anti-interleukin (IL) 2 receptors, anti- costimulatory molecules, and anti-Janus tyrosine kinases (JAK1, JAK3) that block the intracellular cascade associated with T-cell activation; (b) B cells and their trophic factors, directed against key B-cell molecules; (c) complement C3 or C5, intercepting the destructive effect of complement-fixing antibodies; (d) cytokines and cytokine receptors, such as those targeting IL-6 which promotes antibody production and IL-17, or the p40 subunit of IL-12/1L-23 that affect regulatory T cells; and (e) T and B cell transmigration molecules associated with lymphocyte egress from the lymphoid organs.
Recent progress and perspective in JAK inhibitors for rheumatoid arthritis: from bench to bedside.
Tanaka, Kitakyūshū, Japan. In J Biochem, Sep 2015
Tofacitinib, a small product targeting JAK, inhibits phosphorylation of JAK1 and JAK3, subsequent Stat1 and expression of Stat1-inducible genes, which contribute to efficient propagation of its anti-inflammatory effects for the treatment of RA.
Mechanisms and pathophysiological significance of eryptosis, the suicidal erythrocyte death.
Lang et al., Tübingen, Germany. In Semin Cell Dev Biol, Mar 2015
AMPK, GK, PAK2, CK1α, JAK3, PKC, p38-MAPK).
Activity of JAK/STAT and NF-kB in patients with axial spondyloarthritis.
Wiland et al., Wrocław, Poland. In Postepy Hig Med Dosw (online), 2014
OBJECTIVES: The aim of this study was to evaluate the expression of transcription factors STAT (signal transducer and activator of transcription) and NF-κB (nuclear factor kappa B) as well as Janus kinase3 (JAK3) in the peripheral blood leukocytes.
ALK-mediated post-transcriptional regulation: focus on RNA-binding proteins.
Espinos et al., Toulouse, France. In Front Biosci, 2014
These studies led to the concept that NPM-ALK acts at the transcriptional level through the activation of several transcription factors downstream of many different signaling pathways including JAK3/STAT3, PI3K/AKT and RAS/ERK.
Selective JAK inhibitors.
Yao et al., Singapore, Singapore. In Future Med Chem, 2013
Consisting of four members, JAK1, JAK2, JAK3 and TYK2, the JAK kinases have emerged as important targets for proliferative and immune-inflammatory disorders.
Exome sequencing identifies secondary mutations of SETBP1 and JAK3 in juvenile myelomonocytic leukemia.
Kojima et al., Nagoya, Japan. In Nat Genet, 2013
The SETBP1 and JAK3 genes were among common targets for secondary mutations.
Newly described activating JAK3 mutations in T-cell acute lymphoblastic leukemia.
Fan et al., In Leukemia, 2012
JAK3 mutations are associated with response to therapy in T-cell acute lymphoblastic leukemia.
Inborn errors of human JAKs and STATs.
Notarangelo et al., New York City, United States. In Immunity, 2012
Inborn errors of the genes encoding two of the four human JAKs (JAK3 and TYK2) and three of the six human STATs (STAT1, STAT3, and STAT5B) have been described.
Outcome modeling with CRLF2, IKZF1, JAK, and minimal residual disease in pediatric acute lymphoblastic leukemia: a Children's Oncology Group study.
Willman et al., Albuquerque, United States. In Blood, 2012
Outcome modeling with CRLF2, IKZF1, JAK, and minimal residual disease in pediatric acute lymphoblastic leukemia.
Suppression of cytokine signaling by SOCS3: characterization of the mode of inhibition and the basis of its specificity.
Nicola et al., Australia. In Immunity, 2012
We found that SOCS3 bound and directly inhibited the catalytic domains of JAK1, JAK2, and TYK2 but not JAK3 via an evolutionarily conserved motif unique to JAKs.
The genetic basis of early T-cell precursor acute lymphoblastic leukaemia.
Mullighan et al., Memphis, United States. In Nature, 2012
ETP ALL was characterized by activating mutations in genes regulating cytokine receptor and RAS signalling (67% of cases; NRAS, KRAS, FLT3, IL7R, JAK3, JAK1, SH2B3 and BRAF), inactivating lesions disrupting haematopoietic development (58%; GATA3, ETV6, RUNX1, IKZF1 and EP300) and histone-modifying genes (48%; EZH2, EED, SUZ12, SETD2 and EP300).
JAK3, STAT3 and CD3-zeta signaling proteins status in regard to the lymphocytes function in patients with ovarian cancer.
Sulowska et al., Łódź, Poland. In Immunol Invest, 2011
peripheral blood lymphocytes (PBLs) of ovarian cancer patients showed lower JAK3, CD3-zeta molecules expression levels, as well as lower STAT3 and CD3-zeta phosphorylation levels than cells of control.
Hemagglutinin from the H5N1 virus activates Janus kinase 3 to dysregulate innate immunity.
Xu et al., Guangzhou, China. In Plos One, 2011
hemagglutinin of H5N1 avian influenza triggered an abnormal innate immune signalling in the pulmonary epithelial cells, through an unusual process involving activation of Janus kinase 3
An N-ethyl-N-nitrosourea (ENU)-induced dominant negative mutation in the JAK3 kinase protects against cerebral malaria.
Gros et al., Montréal, Canada. In Plos One, 2011
These findings highlight the pathological role of CD8(+) T cells and Jak3-dependent IFN-gamma-mediated Th1 responses in cerebral malaria pathogenesis.
Oncogenic IL7R gain-of-function mutations in childhood T-cell acute lymphoblastic leukemia.
Barata et al., Campinas, Brazil. In Nat Genet, 2011
In most cases, these IL7R mutations introduce an unpaired cysteine in the extracellular juxtamembrane-transmembrane region and promote de novo formation of intermolecular disulfide bonds between mutant IL-7Rα subunits, thereby driving constitutive signaling via JAK1 and independently of IL-7, γc or JAK3.
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