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The production of recombinant human JAK2 protein, featuring a 6xHis tag at the N-terminus, begins with cloning the JAK2 gene fragment (752-1132aa) into an expression vector. The N-terminal 6xHis tag gene is also co-inserted into the vector at the suitable site. After the transformation of the recombinant vector into competent E. coli cells, IPTG is used to induce high-level expression of the target protein. Following cell lysis, the JAK2 protein is purified via affinity chromatography. The purification process is followed by SDS-PAGE analysis, which consistently demonstrates a purity of over 90% of the recombinant JAK2 protein. Human Tyrosine-protein kinase JAK2, a member of the Janus kinase family, plays a pivotal role in various cellular processes, particularly in hematopoiesis and immune response. Discovered in 1992, JAK2 is essential for signaling pathways initiated by several cytokines, including erythropoietin and thrombopoietin, which are crucial for red blood cell and platelet production, respectively [1][2]. JAK2 facilitates the phosphorylation of STAT proteins, thereby propagating signals from the cell surface to the nucleus, which is vital for gene expression regulation [1][2]. In addition to its role in hematopoiesis, JAK2 is implicated in various cancers, where its signaling pathways can promote cell survival and proliferation. Studies have shown that JAK2 interacts with oncogenic proteins like Bcr-Abl, enhancing the survival of leukemic cells [3][4]. Its mutations and aberrant activation are central to the pathogenesis of several hematological disorders, making it a key target for therapeutic intervention. References:[1] J. Ihle and D. Gilliland, Jak2: normal function and role in hematopoietic disorders, Current Opinion in Genetics & Development, vol. 17, no. 1, p. 8-14, 2007. https://doi.org/10.1016/j.gde.2006.12.009[2] S. Verstovsek, Therapeutic potential of jak2 inhibitors, The Journal of Oncopathology, vol. 1, no. 1, p. 76-79, 2013. https://doi.org/10.13032/tjop.2052-5931.100024[3] A. Samanta, S. Chakraborty, Y. Wang, E. Schlette, E. Reddy, & R. Arlinghaus, Destabilization of bcr-abl/jak2 network by a jak2/abl kinase inhibitor on044580 overcomes drug resistance in blast crisis chronic myelogenous leukemia (cml), Genes & Cancer, vol. 1, no. 4, p. 346-359, 2010. https://doi.org/10.1177/1947601910372232[4] S. Chakraborty, X. Leng, B. Perazzona, X. Sun, Y. Lin, & R. Arlinghaus, Combination of jak2 and hsp90 inhibitors: an effective therapeutic option in drug-resistant chronic myelogenous leukemia, Genes & Cancer, vol. 7, no. 5-6, p. 201-208, 2016. https://doi.org/10.18632/genesandcancer.111
The production of recombinant human JAK2 protein, featuring a 6xHis tag at the N-terminus, begins with cloning the JAK2 gene fragment (752-1132aa) into an expression vector. The N-terminal 6xHis tag gene is also co-inserted into the vector at the suitable site. After the transformation of the recombinant vector into competent E. coli cells, IPTG is used to induce high-level expression of the target protein. Following cell lysis, the JAK2 protein is purified via affinity chromatography. The purification process is followed by SDS-PAGE analysis, which consistently demonstrates a purity of over 90% of the recombinant JAK2 protein.
Human Tyrosine-protein kinase JAK2, a member of the Janus kinase family, plays a pivotal role in various cellular processes, particularly in hematopoiesis and immune response. Discovered in 1992, JAK2 is essential for signaling pathways initiated by several cytokines, including erythropoietin and thrombopoietin, which are crucial for red blood cell and platelet production, respectively [1][2]. JAK2 facilitates the phosphorylation of STAT proteins, thereby propagating signals from the cell surface to the nucleus, which is vital for gene expression regulation [1][2].
In addition to its role in hematopoiesis, JAK2 is implicated in various cancers, where its signaling pathways can promote cell survival and proliferation. Studies have shown that JAK2 interacts with oncogenic proteins like Bcr-Abl, enhancing the survival of leukemic cells [3][4]. Its mutations and aberrant activation are central to the pathogenesis of several hematological disorders, making it a key target for therapeutic intervention.
References:[1] J. Ihle and D. Gilliland, Jak2: normal function and role in hematopoietic disorders, Current Opinion in Genetics & Development, vol. 17, no. 1, p. 8-14, 2007. https://doi.org/10.1016/j.gde.2006.12.009[2] S. Verstovsek, Therapeutic potential of jak2 inhibitors, The Journal of Oncopathology, vol. 1, no. 1, p. 76-79, 2013. https://doi.org/10.13032/tjop.2052-5931.100024[3] A. Samanta, S. Chakraborty, Y. Wang, E. Schlette, E. Reddy, & R. Arlinghaus, Destabilization of bcr-abl/jak2 network by a jak2/abl kinase inhibitor on044580 overcomes drug resistance in blast crisis chronic myelogenous leukemia (cml), Genes & Cancer, vol. 1, no. 4, p. 346-359, 2010. https://doi.org/10.1177/1947601910372232[4] S. Chakraborty, X. Leng, B. Perazzona, X. Sun, Y. Lin, & R. Arlinghaus, Combination of jak2 and hsp90 inhibitors: an effective therapeutic option in drug-resistant chronic myelogenous leukemia, Genes & Cancer, vol. 7, no. 5-6, p. 201-208, 2016. https://doi.org/10.18632/genesandcancer.111
| Cat.No | ACP04298 | Target Name | JAK2 |
|---|---|---|---|
| Form | Liquid or Lyophilized powder | Expression System | E.coli |
| Expression Range | 752-1132aa | Mol Weight | 48.6kDa |
| Protein Length | Partial | Purity | Greater than 90% as determined by SDS-PAGE. |
| Storage Buffer | 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, Liquid form: default storage buffer is Tris/PBS-based buffer, pH 8.0. |
| Target Species | Human | Uniprot ID | O60674 |
|---|
Uniprot Id
O60674
Target Species
Human
Target Name
JAK2
Target Full Name
Tyrosine-protein kinase JAK2
Target Function
Non-receptor tyrosine kinase involved in various processes such as cell growth, development, differentiation or histone modifications. Mediates essential signaling events in both innate and adaptive immunity. In the cytoplasm, plays a pivotal role in signal transduction via its association with type I receptors such as growth hormone (GHR), prolactin (PRLR), leptin (LEPR), erythropoietin (EPOR), thrombopoietin (THPO); or type II receptors including IFN-alpha, IFN-beta, IFN-gamma and multiple interleukins. Following ligand-binding to cell surface receptors, phosphorylates specific tyrosine residues on the cytoplasmic tails of the receptor, creating docking sites for STATs proteins. Subsequently, phosphorylates the STATs proteins once they are recruited to the receptor. Phosphorylated STATs then form homodimer or heterodimers and translocate to the nucleus to activate gene transcription. For example, cell stimulation with erythropoietin (EPO) during erythropoiesis leads to JAK2 autophosphorylation, activation, and its association with erythropoietin receptor (EPOR) that becomes phosphorylated in its cytoplasmic domain. Then, STAT5 (STAT5A or STAT5B) is recruited, phosphorylated and activated by JAK2. Once activated, dimerized STAT5 translocates into the nucleus and promotes the transcription of several essential genes involved in the modulation of erythropoiesis. Part of a signaling cascade that is activated by increased cellular retinol and that leads to the activation of STAT5 (STAT5A or STAT5B). In addition, JAK2 mediates angiotensin-2-induced ARHGEF1 phosphorylation. Plays a role in cell cycle by phosphorylating CDKN1B. Cooperates with TEC through reciprocal phosphorylation to mediate cytokine-driven activation of FOS transcription. In the nucleus, plays a key role in chromatin by specifically mediating phosphorylation of 'Tyr-41' of histone H3 (H3Y41ph), a specific tag that promotes exclusion of CBX5 (HP1 alpha) from chromatin.
Target Involvement
Budd-Chiari syndrome (BDCHS); Polycythemia vera (PV); Thrombocythemia 3 (THCYT3); Myelofibrosis (MYELOF); Leukemia, acute myelogenous (AML)
Target Subcellular Location
Endomembrane system; Peripheral membrane protein. Cytoplasm. Nucleus.
Target Protein Families
Protein kinase superfamily, Tyr protein kinase family, JAK subfamily
Target Tissue Specificity
Ubiquitously expressed throughout most tissues.
Target Research Area
Immunology
Target Synonyms
JAK 2; JAK-2; JAK2; JAK2_HUMAN; Janus Activating Kinase 2; Janus kinase 2 (a protein tyrosine kinase); Janus kinase 2; JTK 10; JTK10; kinase Jak2; OTTHUMP00000043260; THCYT3; Tyrosine protein kinase JAK2; Tyrosine-protein kinase JAK2
Target Background
This gene encodes a non-receptor tyrosine kinase that plays a central role in cytokine and growth factor signalling. The primary isoform of this protein has an N-terminal FERM domain that is required for erythropoietin receptor association, an SH2 domain that binds STAT transcription factors, a pseudokinase domain and a C-terminal tyrosine kinase domain. Cytokine binding induces autophosphorylation and activation of this kinase. This kinase then recruits and phosphorylates signal transducer and activator of transcription (STAT) proteins. Growth factors like TGF-beta 1 also induce phosphorylation and activation of this kinase and translocation of downstream STAT proteins to the nucleus where they influence gene transcription. Mutations in this gene are associated with numerous inflammatory diseases and malignancies. This gene is a downstream target of the pleiotropic cytokine IL6 that is produced by B cells, T cells, dendritic cells and macrophages to produce an immune response or inflammation. Disregulation of the IL6/JAK2/STAT3 signalling pathways produces increased cellular proliferation and myeloproliferative neoplasms of hematopoietic stem cells. A nonsynonymous mutation in the pseudokinase domain of this gene disrupts the domains inhibitory effect and results in constitutive tyrosine phosphorylation activity and hypersensitivity to cytokine signalling. This gene and the IL6/JAK2/STAT3 signalling pathway is a therapeutic target for the treatment of excessive inflammatory responses to viral infections. Alternative splicing results in multiple transcript variants encoding distinct isoforms.
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