Panoply™ Human GRIN2B Knockdown Stable Cell Line

Name: Panoply™ Human GRIN2B Knockdown Stable Cell Line
SKU: CSC-DC006660
Availability: InStock

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

Cat. No. : CSC-DC006660

Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR

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Cell Line Information

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Gene Information

Cat. No.	CSC-DC006660
Description	Creative Biogene's Knockdown Cell Lines are target specific shRNA lentivirus transduced cells. The percent knockdown levels range from 75-99% depending on the gene, as evaluated by Real-Time RCR. Cells are rigorously qualified and mycoplasma free.
Target Gene	GRIN2B
Host Cell	HEK293 (Hela and other cell types are also available)
Host Cell Species	Homo sapiens (Human)
Applications	(1) Studying gene functions (2) Studying gene interactions and signaling pathways (3) Target validation and drug discovery (4) Designing diseases models
Size	>1 × 10⁶ cells / vial
Stability	Validated for at least 10 passages
Validation	Real-Time RCR
Quality Control	Negative for bacteria, yeast, fungi and mycoplasma.
Storage	Liquid Nitrogen
Shipping	Dry Ice

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	GRIN2B glutamate receptor, ionotropic, N-methyl D-aspartate 2B [ Homo sapiens ]
Gene Symbol	GRIN2B
Synonyms	MRD6; NR2B; hNR3; GluN2B; NMDAR2B
Gene Description	glutamate receptor, ionotropic, N-methyl D-aspartate 2B
GeneID	2904
Uni ProtID	Q13224
mRNA Refseq	NM_000834.3
Protein Refseq	NP_000825.2
Chromosome Location	12p12
Function	D2 dopamine receptor binding; N-methyl-D-aspartate selective glutamate receptor activity; beta-catenin binding; calcium channel activity; cell adhesion molecule binding; drug binding; extracellular-glutamate-gated ion channel activity; glycine binding; ionotropic glutamate receptor binding; neurotransmitter binding; protein binding; protein heterodimerization activity; zinc ion binding;
Pathway	Activation of NMDA receptor upon glutamate binding and postsynaptic events, organism-specific biosystem; Alcoholism, organism-specific biosystem; Alcoholism, conserved biosystem; Alzheimers disease, organism-specific biosystem; Alzheimers disease, conserved biosystem; Alzheimers Disease, organism-specific biosystem; Amphetamine addiction, organism-specific biosystem;
MIM	138252

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Endometrial cancer (EC) remains a lethal gynecological malignancy, with limited therapeutic options due to its poorly understood pathogenesis. Cellular senescence is a key barrier to cancer cell tumorigenesis, making investigation of its role in EC progression a critical research avenue to address these challenges. Here, researchers revealed a critical role for cellular senescence in EC progression through multi-omics analysis and functional validation. Integrative analysis of RNA sequencing and clinical datasets revealed that Na+/H+ exchanger 7 (NHE7), a prognostic biomarker, is significantly overexpressed in EC tissue. Functional studies revealed that NHE7 overexpression promotes cell proliferation, motility, and cell cycle progression, while inhibiting senescence-associated markers and cytokine secretion. Conversely, knockdown of NHE7 reversed these oncogenic phenotypes. Mechanistically, NHE7 binds to the cAMP-related transcription factor, thereby increasing GRIN2B expression, which in turn enhances intracellular Ca²⁺ influx, delaying cellular senescence and promoting cancer progression in vitro and in vivo. These findings suggest that NHE7 plays a crucial role in delaying cellular senescence and promoting endometrial cancer (EC) progression through the cAMP pathway, revealing a key driver of EC pathogenesis and indicating a viable therapeutic target.

Here, the researchers constructed GRIN2B knockdown Ishikawa cells and confirmed its knockdown efficiency by Western blotting (WB) experiments (Figure 1A). Similarly, the data showed that GRIN2B knockdown partially reversed NHE7-induced EC cell senescence resistance, as reflected in calcium levels, β-galactosidase activity, and cell cycle distribution (Figure 1B-D). This also inhibited proliferation, altered the expression of senescence-related molecules, and reduced the expression of SASP-related molecules, which was caused by NHE7-induced senescence resistance (Figure 1E-F). In summary, GRIN2B knockdown effectively reversed NHE7-induced EC cell senescence resistance, highlighting the key role of GRIN2B in NHE7-regulated EC senescence.

Figure 1. Knocking down GRIN2B reverses NHE7-mediated senescence resistance of EC cells. (Yang S, et al., 2025)

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