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. | Product Name | Price |
|---|---|---|
| CSC-DC004161 | Panoply™ Human DDX5 Knockdown Stable Cell Line | Inquiry |
| CSC-SC004161 | Panoply™ Human DDX5 Over-expressing Stable Cell Line | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| LV10508L | human DDX5 (NM_004396) lentivirus particles | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| SHG227287 | shRNA set against Mouse Ddx5(NM_007840.3) | Inquiry |
| SHG227323 | shRNA set against Human DDX5(NM_004396.3) | Inquiry |
| SHG227413 | shRNA set against Rat Ddx5(NM_001007613.1) | Inquiry |
| SHH276089 | shRNA set against Human DDX5 (NM_004396.3) | Inquiry |
| SHH276093 | shRNA set against Mouse DDX5 (NM_007840.3) | Inquiry |
| SHH276097 | shRNA set against Rat DDX5 (NM_001007613.1) | Inquiry |
| SHW005333 | shRNA set against Chicken DDX5 (NM_204827) | Inquiry |
| SHW017777 | shRNA set against Danio rerio DDX5 (NM_212612) | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CDCB166808 | Chicken DDX5 ORF Clone (NM_204827) | Inquiry |
| CDFR001625 | Rat Ddx5 cDNA Clone(NM_001007613.1) | Inquiry |
| MiUTR1H-02738 | DDX5 miRNA 3'UTR clone | Inquiry |
| MiUTR1M-03761 | DDX5 miRNA 3'UTR clone | Inquiry |
| MiUTR1R-01418 | DDX5 miRNA 3'UTR clone | Inquiry |
| CDCB179252 | Danio rerio DDX5 ORF Clone (NM_212612) | Inquiry |
| CDCB187105 | Rabbit DDX5 ORF clone (XM_002719484.2) | Inquiry |
| CDCR054476 | Mouse Ddx5 ORF clone (NM_007840.3) | Inquiry |
| CDCR368666 | Rat Ddx5 ORF Clone(NM_001007613.1) | Inquiry |
DDX5, also known as DEAD (Asp-Glu-Ala-Asp) box helicase 5, is a captivating gene that has garnered significant attention in recent years. This gene, encoded by the DDX5 gene, belongs to the DEAD box family of proteins and plays a crucial role in various cellular processes.
DDX5 is a 522-kDa protein consisting of 11 distinct domains, each with a unique function. The N-terminal domain of DDX5 is responsible for ATP binding and hydrolysis, while the C-terminal domain is involved in RNA binding. The central region of the protein contains a series of motifs that contribute to its helicase activity. DDX5 is primarily localized in the nucleus, where it interacts with a myriad of RNA and protein partners to regulate gene expression.
DDX5 plays a pivotal role in regulating gene expression at various levels. It is involved in the transcriptional regulation of genes involved in cell proliferation, apoptosis, and stress responses. DDX5 interacts with transcription factors and coactivators to facilitate the assembly of transcriptional machinery on gene promoters. Additionally, DDX5 is involved in the processing and export of mRNA from the nucleus to the cytoplasm, thereby influencing protein synthesis.
The dysregulation of DDX5 has been implicated in the pathogenesis of various diseases. Studies have shown that DDX5 is overexpressed in certain types of cancer, including lung, breast, and colorectal cancers. The increased expression of DDX5 in these tumors correlates with tumor aggressiveness and poor patient prognosis. Moreover, DDX5 has been found to be upregulated in response to inflammation and oxidative stress, suggesting a role for this gene in the pathogenesis of inflammatory and neurodegenerative diseases. DDX5 also functions to inhibit the process of viral infection, including HBV and MYXV. In infected hepatocytes, the HBV genome is converted in the nucleus into covalently closed circular DNA (cccDNA), which is organised into a small chromosome that serves as a template for the synthesis of all viral mRNAs. Furthermore, chronic HBV infection is one of the major causes of HCC; DDX5 also plays an important role in HBV-associated HCC with a poor prognosis. However, the role of DDX5 in HBV infection is incompletely understood, and further study of the mechanism by which DDX5 inhibits HBV infection may be important for antiviral and anticancer therapy.
Given the multifaceted role of DDX5 in gene regulation and its involvement in various diseases, targeting this gene holds immense therapeutic potential. Inhibit DDX5 expression or activity has been shown to decrease tumor growth and enhance the efficacy of chemotherapeutic drugs in preclinical models. Furthermore, modulating DDX5 expression may have beneficial effects in treating inflammation and neurodegenerative diseases.
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