Panoply™ Human MAPK14 Over-expressing Stable Cell Line

Name: Panoply™ Human MAPK14 Over-expressing Stable Cell Line
SKU: CSC-SC009198
Availability: InStock

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

Cat. No. : CSC-SC009198

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

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Cell Line Information

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Gene Information

Cat. No.	CSC-SC009198
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	MAPK14
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	MAPK14 mitogen-activated protein kinase 14 [ Homo sapiens ]
Gene Symbol	MAPK14
Synonyms	MAPK14; mitogen-activated protein kinase 14; CSBP1, CSBP2, CSPB1; Mxi2; p38; p38 MAP kinase; PRKM14; PRKM15; MAP kinase 14; p38alpha Exip; MAP kinase Mxi2; MAP kinase p38 alpha; CSAID-binding protein; Csaids binding protein; MAX-interacting protein 2; stress-activated protein kinase 2A; p38 mitogen activated protein kinase; mitogen-activated protein kinase p38 alpha; cytokine suppressive anti-inflammatory drug binding protein; cytokine suppressive anti-inflammatory drug-binding protein; RK; CSBP; EXIP; CSBP1; CSBP2; CSPB1; SAPK2A; p38ALPHA;
GeneID	1432
Uni ProtID	Q16539
mRNA Refseq	BC000092
Chromosome Location	6p21.3-p21.2
Pathway	ADP signalling through P2Y purinoceptor 1, organism-specific biosystem; ATF-2 transcription factor network, organism-specific biosystem; Activated TLR4 signalling, organism-specific biosystem; Activation of the AP-1 family of transcription factors, organism-specific biosystem; Amyotrophic lateral sclerosis (ALS), organism-specific biosystem; Amyotrophic lateral sclerosis (ALS), conserved biosystem; Angiopoietin receptor Tie2-mediated signaling, organism-specific biosystem;
MIM	600289

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Sepsis-induced acute lung injury (ALI) is driven by inflammation, oxidative stress, and immunosuppression. MAPK14 (p38α) plays a role in ferroptosis and immune regulation, but its specific function in pediatric sepsis remains unclear. Here, researchers performed bioinformatics analysis of GSE26440 and FerrDb to identify MAPK14 as a ferroptosis-related gene in pediatric sepsis. MAPK14 expression was upregulated in sepsis patient samples, LPS-treated MLE-12 cells, and CLP mouse lung tissue. MAPK14 overexpression led to increased MDA and Fe2+ levels, decreased GSH levels, and increased ROS fluorescence intensity, confirming its role in promoting ferroptosis. Mechanistically, MAPK14 upregulated TTP53, which in turn inhibited SLC7A11 and GPX4, further driving ferroptosis. MAPK14 overexpression stabilized TTP53 and enhanced its activity. Furthermore, MAPK14 enhanced the expression of MPO and PD-L1, promoting neutrophil infiltration and immunosuppression. In addition, MAPK14 overexpression inhibited neutrophil apoptosis, promoting neutrophil infiltration and enhancing immunosuppression. These studies indicate that MAPK14 drives ferroptosis through the TTP53/SLC7A11/GPX4 pathway and exacerbates immunosuppression by promoting neutrophil infiltration.

To investigate the role of MAPK14 in ferroptosis, researchers constructed MLE-12 cells with MAPK14 knockdown and MAPK14 overexpression (Figure 1A-B). Ferroptosis is characterized by increased reactive oxygen species (ROS) production and iron accumulation. Using DCFH-DA staining, researchers observed that ROS levels were significantly increased in MAPK14-overexpressing MLE-12 cells after LPS treatment, while ROS accumulation was reduced in MAPK14-knockdown MLE-12 cells (Figure 1C-E). Furthermore, MAPK14 knockdown reversed the LPS-induced decrease in MLE-12 cell viability, while MAPK14 overexpression further exacerbated the LPS-induced decrease in MLE-12 cell viability (Figure 1F). Biochemical analysis showed that MAPK14 silencing led to decreased MDA and Fe2+ levels and increased GSH content. Conversely, in MAPK14-overexpressing cells, MDA and Fe2+ levels were increased, while GSH content was decreased (Figure 1G-I). Therefore, MAPK14 primarily regulates ferroptosis in MLE-12 cells by enhancing oxidative stress and iron accumulation.

Figure 1. MAPK14 enhanced ferroptosis in MLE-12 cells. (Zhang N, et al., 2025)

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