Panoply™ Human ITK Over-expressing Stable Cell Line

Name: Panoply™ Human ITK Over-expressing Stable Cell Line
SKU: CSC-SC007819
Availability: InStock

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

Cat. No. : CSC-SC007819

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-SC007819
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	ITK
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	ITK IL2-inducible T-cell kinase [ Homo sapiens ]
Gene Symbol	ITK
Synonyms	EMT; LYK; PSCTK2
Gene Description	IL2-inducible T-cell kinase
GeneID	3702
Uni ProtID	Q08881
mRNA Refseq	NM_005546.3
Protein Refseq	NP_005537.3
Chromosome Location	5q31-q32
Function	ATP binding; metal ion binding; non-membrane spanning protein tyrosine kinase activity; phospholipid binding; protein binding;
Pathway	Adaptive Immune System, organism-specific biosystem; B Cell Receptor Signaling Pathway, organism-specific biosystem; Chemokine signaling pathway, organism-specific biosystem; Chemokine signaling pathway, conserved biosystem; Class I PI3K signaling events, organism-specific biosystem; Fc-epsilon receptor I signaling in mast cells, organism-specific biosystem; Generation of second messenger molecules, organism-specific biosystem;
MIM	186973

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Natural killer/T-cell lymphoma (NKTCL) is a highly aggressive non-Hodgkin lymphoma. Patients with relapsed/refractory (R/R) NKTCL have a very poor prognosis, and effective treatment options are lacking, highlighting the urgent need for new therapeutic strategies. Here, researchers found that interleukin-2-inducible T-cell kinase (ITK) expression levels were elevated in NKTCL cells and patient tumors. Higher ITK expression levels were associated with a worse clinical prognosis. In vitro experiments showed that ITK knockdown inhibited NKTCL cell growth, induced apoptosis, caused cell cycle arrest, and impaired colony formation ability; while ITK overexpression accelerated cell proliferation. In vivo experiments demonstrated that ITK knockdown significantly inhibited lymphoma growth in a mouse model, suggesting that ITK is a potential therapeutic target. Mechanistic studies revealed that ITK knockdown inhibits NKTCL cell growth by attenuating the oncogenic NF-κB signaling pathway, a mechanism revealed through transcriptome sequencing analysis and further validated by in vitro experiments and in vivo NKTCL models.

Considering the widespread expression of ITK in NKTCL and its prognostic significance, researchers explored the potential of targeting ITK in NKTCL treatment. They constructed ITK-overexpressing NK-YS and YTS cell lines, which normally exhibit low ITK expression (Figure 1A). The results showed that ITK-overexpressing cells had significantly faster growth rates (Figure 1B and C), indicating a carcinogenic role for ITK. Using KHYG-1 and YT cells with high ITK expression, researchers performed ITK gene knockdown using a Tet-on inducible system. In this system, ITK expression was effectively downregulated in shITK#1 and shITK#2 cells after treatment with 4 μg/mL Dox for 48 hours (Figure 1D). Next, the researchers cultured the stably transfected cells with 4 μg/mL Dox for 5 days and recorded the cell growth curves. The results showed that ITK gene knockdown significantly inhibited the proliferation of KHYG-1 and YT cells (Figure 1E and F), indicating that ITK plays a crucial role in NKTCL cell growth.

Figure 1. ITK downregulation inhibits NKTCL cell growth. (Cao J, et al., 2025)

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