Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat. No. : CSC-DC007301
Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR
| Cat. No. | CSC-DC007301 |
| 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 | HSP90AA1 |
| 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 | HSP90AA1 heat shock protein 90kDa alpha (cytosolic), class A member 1 [ Homo sapiens ] |
| Gene Symbol | HSP90AA1 |
| Synonyms | HSPN; LAP2; HSP86; HSPC1; HSPCA; Hsp89; Hsp90; HSP89A; HSP90A; HSP90N; HSPCAL1; HSPCAL4 |
| Gene Description | heat shock protein 90kDa alpha (cytosolic), class A member 1 |
| GeneID | 3320 |
| Uni ProtID | P07900 |
| mRNA Refseq | NM_001017963.2 |
| Protein Refseq | NP_001017963.2 |
| Chromosome Location | 14q32.33 |
| Function | ATP binding; ATPase activity; TPR domain binding; TPR domain binding; identical protein binding; nitric-oxide synthase regulator activity; nucleotide binding; protein binding; protein homodimerization activity; unfolded protein binding; |
| Pathway | Antigen processing and presentation, organism-specific biosystem; Antigen processing and presentation, conserved biosystem; Axon guidance, organism-specific biosystem; Cell Cycle, organism-specific biosystem; Cell Cycle, Mitotic, organism-specific biosystem; Centrosome maturation, organism-specific biosystem; Class I PI3K signaling events, organism-specific biosystem; |
| MIM | 140571 |
HSP90AA1 is a chaperone protein involved in various biological processes, including inflammation and cancer. HSP90AA1 is highly expressed in lung adenocarcinoma (LUAD), but its exact function remains unclear. Here, prognostic analysis of survival data from the TCGA database showed that HSP90AA1 expression is associated with clinicopathological staging. The overall survival (OS) and disease-specific survival (DSS) were significantly higher in the low-expression group of HSP90AA1 compared to the high-expression group. Furthermore, CancerSEA functional similarity analysis revealed that HSP90AA1 is involved in multiple cellular functions, including cell cycle stimulation, DNA damage response, invasion, and proliferation. Analysis of immune scores and immune cell infiltration using the ESTIMATE and TIMER databases showed that high levels of HSP90AA1 were associated with decreased infiltration of CD8+ T cells and plasmacytoid dendritic cells (pDCs), while infiltration of Th2 cells and helper T cells was increased. In vitro experiments further confirmed that knockdown of HSP90AA1 expression significantly inhibited the proliferation of H1299 cells. These findings suggest that silencing HSP90AA1 expression or using HSP90AA1 inhibitors could effectively improve the treatment of LUAD. Targeting HSP90AA1 may be an effective strategy for treating LUAD.
Compared to the control group, the proliferation of HSP90AA1-knockdown H1299 cells was inhibited (Figure 1C). To confirm the reason for the inhibited cell proliferation, researchers used PI staining to detect the cell cycle of H1299 cells. The results showed that, compared to the control group, the number of cells in the G1 phase increased, while the number of cells in the S and G2/M phases decreased in HSP90AA1-knockdown cells (Figure 1D-G). This indicates that the absence of HSP90AA1 leads to H1299 cell cycle arrest in the G1 phase. Furthermore, Western blot experiments confirmed that knocking down HSP90AA1 effectively downregulated the expression of cell cycle-related proteins CCNB1 and CCND1 (Figure 1H, I). These findings suggest that HSP90AA1 may regulate the cell cycle by modulating these specific proteins.
Figure 1. HSP90AA1 is crucial for the proliferation of LUAD cells. (Xiang S, et al., 2025)
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