JAK3 Antibodies

Structure of JAK3

JAK3 is a tyrosine kinase with a molecular weight of approximately 125 kDa. Its precise molecular weight may vary slightly due to different transcript splicing methods and post-translational modifications such as phosphorylation.

This protein is composed of 1,124 amino acids, and its polypeptide chain folds into a typical kinase globular structure. The tertiary structural feature of JAK3 lies in its C-terminal dual-kinase domain: JH1 (true kinase domain) is responsible for catalytic activity, while the adjacent JH2 (pseudo-kinase domain) plays a crucial role in self-inhibitory regulation. Within the JH1 domain, the phosphorylation status of specific tyrosine residues on the activation loop (such as Y980 and Y981) directly determines its kinase activity. This sophisticated molecular switch composed of JH2 and JH1 is the structural basis for regulating the JAK-STAT signaling pathway and maintaining immune homeostasis.

Fig. 1 JAK3 mutations associated with immune cell diseases.¹

Key structural properties of JAK3:

• Modular JH domain assembly
• Mechanism of allosteric inhibition of the JH1 catalytic center by the JH2 domain
• The tyrosine phosphorylation regulatory node of the kinase active center

Functions of JAK3

The core function of JAK3 is to transduct cytokine signals to regulate the development of immune cells. However, it is also deeply involved in various pathophysiological processes such as the maintenance of immune homeostasis and the balance between cell proliferation and apoptosis.

Unlike the widespread expression of JAK1/2, the expression of JAK3 is strictly confined to the hematopoietic system. The loss of its function can lead to severe combined immune deficiency, a feature that highlights its non-redundancy in the immune system.

Applications of JAK3 and JAK3 Antibody in Literature

1. Velatooru, Loka Reddy, et al. "New JAK3-INSL3 fusion transcript—an oncogenic event in cutaneous T-cell lymphoma." Cells 12.19 (2023): 2381. https://doi.org/10.3390/cells12192381

The article indicates that in the study of mycosis fungoides, the newly discovered JAK3-INSL3 fusion transcript has been confirmed to be carcinogenic. The five-year survival rate of patients with high expression of this fusion gene was significantly reduced. Gene knockout experiments confirmed that it could promote the proliferation and tumorigenesis ability of tumor cells.

2. Kumar, Narendra, et al. "Mucosal implications of oral Jak3-targeted drugs in COVID patients." Molecular Medicine 31.1 (2025): 203. https://doi.org/10.1186/s10020-025-01260-z

The article indicates that in COVID-19 infection, the overactivation of the JAK3 signaling pathway can exacerbate inflammation and tissue damage, making JAK3 inhibitors a potential therapeutic option. However, its oral preparations carry the risk of side effects such as immunosuppression, and it is necessary to explore optimization strategies to balance efficacy and safety.

3. Liongue, Clifford, et al. "Janus kinase 3 (JAK3): a critical conserved node in immunity disrupted in immune cell cancer and immunodeficiency." International Journal of Molecular Sciences 25.5 (2024): 2977. https://doi.org/10.3390/ijms25052977

The article indicates that JAK3 is the core medium for cytokine signal transduction and is crucial for the development and function of immune cells. Its gain-of-function mutations can cause malignant diseases such as leukemia, while loss-of-function mutations lead to severe combined immunodeficiency.

4. Yuan, Shengnan, et al. "PHF6 and JAK3 mutations cooperate to drive T-cell acute lymphoblastic leukemia progression." Leukemia 36.2 (2022): 370-382. https://doi.org/10.1038/s41375-021-01392-1

The article indicates that in T-cell acute lymphoblastic leukemia, JAK3 mutations often coexist with PHF6 deletion. Research has found that the deletion of PHF6 aggravates the JAK3-driven leukemia process by inhibiting the Bai1-Mdm2-P53 pathway. The combined use of JAK3 inhibitors and MDM2 inhibitors can effectively alleviate the condition.

5. Smedley, William, and Amiya Patra. "JAK3 Inhibition Regulates Stemness and Thereby Controls Glioblastoma Pathogenesis." Cells 12.21 (2023): 2547. https://doi.org/10.3390/cells12212547

The article indicates that JAK3 inhibitors can significantly inhibit the cell proliferation and tumor sphere formation of glioblastoma, weaken its stem cell characteristics, and induce cell differentiation, providing a potential new treatment strategy for this fatal brain tumor.

Creative Biolabs: JAK3 Antibodies for Research

Creative Biolabs specializes in the production of high-quality JAK3 antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom JAK3 Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our JAK3 antibodies, custom preparations, or technical support, contact us at email.