Transfected Stable Cell Lines
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Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
| Cat.No. | Product Name | Price |
|---|---|---|
| CSC-DC004114 | Panoply™ Human DDAH1 Knockdown Stable Cell Line | Inquiry |
| CSC-SC004114 | Panoply™ Human DDAH1 Over-expressing Stable Cell Line | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| AD04668Z | Human DDAH1 adenoviral particles | Inquiry |
| LV10442L | human DDAH1 (NM_001134445) lentivirus particles | Inquiry |
| LV10443L | human DDAH1 (NM_012137) lentivirus particles | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| SHG225413 | shRNA set against Rat Ddah1(NM_022297.2) | Inquiry |
| SHH275541 | shRNA set against Human DDAH1 (NM_012137.3) | Inquiry |
| SHH275545 | shRNA set against Mouse DDAH1 (NM_026993.3) | Inquiry |
| SHW004895 | shRNA set against Chicken DDAH1 (NM_204382) | Inquiry |
| SHW018355 | shRNA set against Danio rerio DDAH1 (NM_213276) | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CDFH004865 | Human DDAH1 cDNA Clone(NM_001134445.1) | Inquiry |
| CDFR011978 | Rat Ddah1 cDNA Clone(NM_022297.2) | Inquiry |
| MiUTR1R-01401 | DDAH1 miRNA 3'UTR clone | Inquiry |
| CDCB166370 | Chicken DDAH1 ORF Clone (NM_204382) | Inquiry |
| CDCB179830 | Danio rerio DDAH1 ORF Clone (NM_213276) | Inquiry |
| CDCB193689 | Rabbit DDAH1 ORF clone (XM_002715885.2) | Inquiry |
| CDCH385085 | Mouse DDAH1 ORF clone(NM_026993.3) | Inquiry |
| CDCR054166 | Human DDAH1 ORF clone (NM_001134445.1) | Inquiry |
| CDCR378981 | Rat Ddah1 ORF Clone(NM_022297.2) | Inquiry |
Dimethylarginine dimethylaminohydrolase 1 (DDAH1) is an enzyme that plays a crucial role in the metabolism of arginine, a versatile amino acid with diverse functions in various cellular processes. The DDAH1 gene encodes for the enzyme dimethylarginine dimethylaminohydrolase 1, which is primarily involved in the degradation of dimethylarginine (DMA) and other polyamine substrates. In recent years, research on the DDAH1 gene has gained significant attention due to its potential involvement in various pathological conditions, including cancer, cardiovascular diseases, and neurodegenerative disorders.
The DDAH1 enzyme is a member of the amidohydrolase superfamily, which consists of enzymes that catalyze the hydrolysis of various substrates, including amides, esters, and other nitrogen-containing compounds. The DDAH1 enzyme has a characteristic alpha/beta-hydrolase fold, which is a common structural feature of amidohydrolases. The active site of DDAH1 contains a His-His-Asp catalytic triad, which is responsible for the hydrolysis of substrates.
The function of DDAH1 is to hydrolyze dimethylarginine (DMA) to generate L-arginine and dimethylamine. DMA is a natural product of protein metabolism and is also synthesized in the body through the methylation of L-arginine. The generated L-arginine serves as a precursor for various biological processes, including the synthesis of proteins, polyamines, and nitric oxide (NO). NO is a crucial signaling molecule involved in vascular relaxation, neurotransmission, and immune response. Therefore, DDAH1 plays a vital role in maintaining the appropriate levels of arginine and its metabolites, which are essential for normal cellular function.
Altered DDAH1 expression has been observed in various pathological conditions, including cancer, cardiovascular diseases, and neurodegenerative disorders. In cancer, DDAH1 has been reported to be overexpressed, which leads to increased production of polyamines, promoting tumor growth and survival. In cardiovascular diseases, DDAH1 is involved in the pathophysiology of atherosclerosis, where it modulates endothelial function and vascular tone. Moreover, decreased DDAH1 expression has been associated with neurodegenerative disorders such as Alzheimer's and Parkinson's diseases, likely due to its role in the metabolism of polyamines and maintenance of neuronal function.
The role of DDAH1 in human health also extends to its involvement in the regulation of immune response and inflammation. The enzyme has been shown to modulate the production of cytokines and other pro-inflammatory mediators, which can impact the immune response and the development of various autoimmune diseases.
The involvement of DDAH1 in various pathological conditions has led to its consideration as a potential therapeutic target. In cancer, targeting DDAH1 can lead to decreased polyamine production, thereby inhibiting tumor growth and survival. Similarly, in cardiovascular diseases and neurodegenerative disorders, modulating DDAH1 activity can have a significant impact on the disease progression.
Several approaches have been proposed to target DDAH1 for therapeutic purposes. These include the development of small molecules that inhibit the enzyme's activity, as well as the use of antisense oligonucleotides to decrease DDAH1 expression. Additionally, gene therapy approaches have been explored to increase DDAH1 expression in cases where its reduced expression is associated with disease pathophysiology.
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