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Panoply™ Human JAK2 Over-expressing Stable Cell Line

For research use only. Not intended for any clinical use.

Cat. No. :   CSC-SC007850

Host Cell :   HEK293 (CHO and other cell types are also available) Size :   >1x106 frozen cells/vial

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Cell Line Information

Cell Culture Information

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Gene Information

Cat. No. CSC-SC007850
Description Using Creative Biogene's proprietary lentiviral vectors, we subclone the target gene into lentivector, generate the lentivirus particles, sequentially infect the cell line HEK293 (other cell types are also available according to your requirements), and select the clones constantly expressing target gene at high level.
Target Gene JAK2
Gene Species Homo sapiens (Human)
Host Cell HEK293 (CHO and other cell types are also available)
Host Cell Species Species varies
Applications

1. Gene expression studies

2. Signaling pathway research

3. Drug screening and toxicology

4. Disease research

Size 2 × 10^6 cells / vial
Stability Validated for at least 10 passages
Quality Control Negative for bacteria, yeast, fungi and mycoplasma.
Storage Liquid nitrogen
Shipping Dry Ice
Revival Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media.
Mycoplasma Negative
Format One frozen vial containing millions of cells
Storage Liquid nitrogen
Safety Considerations The following safety precautions should be observed.
1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum.
2. No eating, drinking or smoking while handling the stable line.
3. Wash hands after handling the stable line and before leaving the lab.
4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells.
5. All waste should be considered hazardous.
6. Dispose of all liquid waste after each experiment and treat with bleach.
Ship Dry ice
Gene Name JAK2 Janus kinase 2 [ Homo sapiens ]
Gene Symbol JAK2
Synonyms JTK10; THCYT3
Gene ID 3717
Uni Prot ID O60674
m RNA Refseq NM_004972.3
Protein Refseq NP_004963.1
Chromosome Location 9p24
Function ATP binding; SH2 domain binding; acetylcholine receptor binding; growth hormone receptor binding; heme binding; histone binding; histone kinase activity (H3-Y41 specific); insulin receptor substrate binding; interleukin-12 receptor binding; non-membrane spanning protein tyrosine kinase activity; peptide hormone receptor binding; phosphatidylinositol 3-kinase binding; protein binding; protein kinase activity; protein kinase binding; protein tyrosine kinase activity; protein tyrosine kinase activity; receptor binding;
Pathway Adipocytokine signaling pathway, organism-specific biosystem; Adipocytokine signaling pathway, conserved biosystem; CXCR4-mediated signaling events, organism-specific biosystem; Chemokine signaling pathway, organism-specific biosystem; Chemokine signaling pathway, conserved biosystem; Cholinergic synapse, organism-specific biosystem; Cytokine Signaling in Immune system, organism-specific biosystem;
MIM 147796
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JAK2 has been confirmed to be a key player in various biological processes and is frequently aberrantly expressed in multiple cancers. Furthermore, JAK2 may play an important role in the pathogenesis of lung cancer. Here, researchers found that JAK2 mRNA expression was upregulated in lung adenocarcinoma tissues compared to adjacent non-tumor tissues and was associated with lymph node metastasis. JAK2V617F and N30S mutations, as well as JAK2 gene amplification, were detected in plasmid samples from lung adenocarcinoma patients using next-generation sequencing (NGS). Downregulation of JAK2 expression inhibited the proliferation, migration, and invasion of lung adenocarcinoma A549 cells. Conversely, overexpression of JAK2 promoted the proliferation, migration, and invasion of A549 cells. Therefore, the upregulation, mutations, and gene amplification of JAK2 detected in lung adenocarcinoma may contribute to lung cancer progression by regulating the proliferation, migration, and invasion of cancer cells.

Here, researchers investigated the effect of JAK2 overexpression on the migration and invasion capabilities of A549 cells. Transwell migration assays showed a significant increase in migration ability in JAK2-overexpressing A549 cells (Figure 1). They further conducted Matrigel invasion assays and found that the invasion ability of JAK2-overexpressing A549 cells was also enhanced (Figure 2). In summary, these results indicate that JAK2 overexpression is sufficient to induce the migration and invasion capabilities of lung adenocarcinoma cells.

Figure 1. Overexpression of JAK2 induced the migration of A549 cells.Figure 1. Overexpression of JAK2 induced the migration of A549 cells. (Xu Y, et al., 2017)

Figure 2. Overexpression of JAK2 induced the invasion of A549 cells.Figure 2. Overexpression of JAK2 induced the invasion of A549 cells. (Xu Y, et al., 2017)

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