Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human JAK3 Antibodies:
anti-Mouse (Murine) JAK3 Antibodies:
anti-Rat (Rattus) JAK3 Antibodies:
Go to our pre-filtered search.
Human Monoclonal JAK3 Primary Antibody for ICC, FACS - ABIN969224
Lai, Jin, Graham, Witthuhn, Ihle, Liu: A kinase-deficient splice variant of the human JAK3 is expressed in hematopoietic and epithelial cancer cells. in The Journal of biological chemistry 1995
Show all 3 Pubmed References
Human Polyclonal JAK3 Primary Antibody for IF (p), IHC (p) - ABIN681013
Zhang, Liu, Li, Wang, Li, Sun: Jak3 is involved in CCR7-dependent migration and invasion in metastatic squamous cell carcinoma of the head and neck. in Oncology letters 2017
Human Polyclonal JAK3 Primary Antibody for WB - ABIN658182
Yu, Sun, Feng, Tan, Fang, Zhao, Zhao, Pu, Huang, Xiang, Cao, He: MSX3 Switches Microglia Polarization and Protects from Inflammation-Induced Demyelination. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2015
Human Monoclonal JAK3 Primary Antibody for ELISA, FACS - ABIN5581352
Sato, Okano, Tanaka-Kubota, Kimura, Miyamoto, Ono, Yamashita, Mitsuiki, Takagi, Imai, Kajiwara, Ebato, Ogata, Oda, Ohara, Kanegane, Morio: Novel compound heterozygous mutations in a Japanese girl with Janus kinase 3 deficiency. in Pediatrics international : official journal of the Japan Pediatric Society 2016
Human Monoclonal JAK3 Primary Antibody for ELISA, FACS - ABIN4327888
Oh, Hwang, Heo: Direct regulation of IL-2 by curcumin. in Biochemical and biophysical research communications 2017
Human Polyclonal JAK3 Primary Antibody for ELISA, ICC - ABIN6271486
Chen, Zhou, Liu, Huang, Liu, Kang, Chen, Guo, Zhu, Sun: Combination of gemcitabine and erlotinib inhibits recurrent pancreatic cancer growth in mice via the JAK-STAT pathway. in Oncology reports 2018
JAK3 mutations in Italian patients affected by SCID: New molecular aspects of a long-known gene.
identification of activating somatic mutations in JAK2 and germline mutations in JAK3 with clinical implications
we report the results of a screening for mutations in SETBP1 and JAK3 of a cohort of seventy Italian patients with juvenile myelomonocytic leukemia, identifying 11.4% of them harboring secondary mutations in these two genes and discovering two new mutations in the SKI domain of SETBP1
Jak3-mediated phosphorylation of beta-catenin suppressed EGF-mediated epithelial-mesenchymal transition and facilitated epithelial barrier functions by AJ localization of phosphorylated beta-catenin through its interactions with alpha-catenin.
frequency of JAK3 mutations in the JH2 domain was relatively low in extranodal natural killer/T-cell lymphoma, nasal type (NTCL) in contrast to a previous report; study identified novel JAK3H583Y- and JAK3G589D-activating mutations that were oncogenic and sensitive to a JAK3 inhibitor
In natural killer/T-cell lymphoma (NKTL) as a disease model, phosphorylation of EZH2 by JAK3 promotes the dissociation of the PRC2 complex leading to decreased global histone H3 lysine 27 methylation levels.
a causal relationship between MLH1-deficiency and incidence of oncogenic point mutations in tyrosine kinases driving cell transformation and acquired resistance to kinase-targeted cancer therapies, is reported.
JAK3 mediates smooth muscle cell proliferation and survival during injury-induced vascular remodeling.
Data indicate that phosphorylation of Janus kinase 3 (JAK3) and STAT3 transcription factor (STAT3) was inhibited by latent membrane protein 1 (LMP1)-IgG.
analysis of JAK3 kinetic mechanism and inhibition by tofacitinib
patient had a homozygote of the JAK3 mutation, and her parents were heterozygous carriers.
JAK3 up-regulates SGLT1 activity by increasing the carrier protein abundance in the cell membrane, an effect enforcing cellular glucose uptake into activated lymphocytes and thus contributing to the immune response.
JAK3 and MCL-1 were down-regulated in patient CD8(+) T cells versus their normal counterparts, likely due to defective suppressor activity of miR-29b and miR-198 in RCC CD8(+) T cells.
N225K and A550V PTPN6 mutations cause loss-of-function leading to JAK3 mediated deregulation of STAT3 pathway and uncover a mechanism that tumor cells can use to control PTPN6 substrate specificity.
Study shows JAK3 mutations in 16% of patients with T-cell prolymphocytic leukemia which might be an important prognostic marker.
This study showed that JAK3 is a powerful negative regulator of the creatine transporter SLC6A8.
Letter/Case Report: ersistent rotavirus diarrhea post-transplant in a novel JAK3-SCID patient after vaccination.
interleukin-4 regulates hematopoietic lineage choice by activating the JAK3-STAT6 pathway, which causes dendritic-cell-specific DNA demethylation.
Foxp3 has a rapid turn over in Treg partly controlled at the transcriptional level by the JAK/STAT pathway
Results confirm that JAK3 is mutated in T-PLL and underscore the potential therapeutical relevance of epigenetic regulator.
Blockade of JAK1-JAK3 accelerated, and selective inactivation of STAT3 decelerated differentiation of progenitor cells.
Study investigated the effect of Jak3 signaling on differentiation from nestin progenitor cells using E13.5 spinal progenitor cell cultures. Results indicated that neuronal and microglial cell differentiation was regulated primarily by Jak3 signaling and the developing neurons and neurite outgrowth might also be regulated by Jak3-dependent microglial activity.
Small-scale in vivo screening identified several genes, including Cd109, that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 as a critical, pharmacologically targetable effector of CD109-driven lung cancer metastasis
JAK1, JAK2, and JAK3 are involved in stimulation of functional activity of mesenchymal progenitor cells by fibroblast growth factor.
JAK mediated signaling is involved in the differentiation and proliferation of mesenchymal progenitor cells.
This study evaluated a chemical genetic toolkit that evaluated a biphasic requirement for JAK3 kinase activity in IL-2-driven T cell proliferation.
Experiments implicate JAK1/3 signaling in cancer- and myocardial infarction-mediated diaphragm weakness in mice.
JAK3 contributes to the regulation of membrane Kv1.5 protein abundance and activity, an effect sensitive to ouabain and thus possibly involving Na(+)/K(+) ATPase activity.
JAK3 deficiency is followed by down-regulation of cytosolic Ca(2+) release, receptor and store operated Ca(2+) entry and Na(+)/Ca(2+) exchanger activity in dendritic cells.
Jak3 has a role in promoting mucosal tolerance through suppressed expression and limiting activation of TLRs thereby preventing intestinal and systemic chronic low-grade inflammation and associated obesity and MetS
Our results demonstrate that JAK3/STAT6 has an important role in bone marrow-derived fibroblast activation, extracellular matrix production, and interstitial fibrosis development.
results showed that different JAK3 mutations induce constitutive activation through distinct mechanisms, pointing to specific therapeutic perspectives
JAK3 down-regulates Na(+)/K(+)-ATPase activity, an effect involving gene expression and profoundly curtailing ATP consumption.
In conclusion, JAK3 deficiency leads to increased formation of calcitriol, which contributes to or even accounts for increased release of FGF23 and enhanced intestinal phosphate absorption.
JAK1 and JAK3 mutants cooperate in T-cell transformation
Jak3 pseudokinase mutants require JAK1 for their transforming potential causing T-cell acute lymphoblastic leukemia in a mouse model.
JAK3 deficiency leads to intestinal sodium (Na+) loss, decrease of blood pressure, increased aldosterone release and subsequent stimulation of renal tubular Na(+) reabsorption.
Data show that IL-4 induces upregulation of the junction protein claudin-5 in endothelial cells (ECs) through activation of Jak/STAT6 and phosphorylation and translocation of FoxO1 from the nucleus to the cytoplasm.
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).
Janus kinase 3 (a protein tyrosine kinase, leukocyte)
, leukocyte Janus kinase
, tyrosine-protein kinase JAK3
, Janus kinase 3 protein-tyrosine kinase
, Janus kinase 3, protein-tyrosine kinase
, Janus tyrosine kinase