DDAH I Activators
Dimethylarginine dimethylaminohydrolase I (DDAH I) is an essential enzyme involved in the regulation of nitric oxide (NO) signaling pathways and the maintenance of cardiovascular homeostasis. DDAH I catalyzes the hydrolysis of asymmetric dimethylarginine (ADMA), a potent inhibitor of NO synthase (NOS), into citrulline and dimethylamine, thereby promoting NO synthesis and bioavailability. NO plays a crucial role in various physiological processes, including vasodilation, neurotransmission, and immune regulation. By degrading ADMA, DDAH I effectively enhances NO production, contributing to the modulation of vascular tone, blood pressure regulation, and endothelial function. Additionally, DDAH I-mediated ADMA metabolism influences angiogenesis, platelet function, and inflammatory responses, highlighting its significance in cardiovascular health and disease.
Activation of DDAH I involves complex regulatory mechanisms that modulate its enzymatic activity and expression levels. One key regulatory aspect is post-translational modifications, such as phosphorylation and acetylation, which can alter DDAH I activity and stability. Phosphorylation, in particular, has been shown to enhance DDAH I activity, promoting ADMA hydrolysis and NO synthesis. Moreover, DDAH I expression can be regulated by various transcription factors, including NF-κB and PPARγ, in response to inflammatory stimuli or metabolic signals. Furthermore, epigenetic modifications, such as DNA methylation and histone acetylation, may also influence DDAH I expression, affecting its enzymatic function and cellular localization. Overall, the activation of DDAH I is tightly regulated at multiple levels, ensuring proper NO signaling and cardiovascular homeostasis.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Calcium | 7440-70-2 | sc-252536 | 5 g | $209.00 | ||
Intracellular calcium levels can influence DDAH-1 activity. Elevated calcium levels may stimulate DDAH-1 and promote ADMA metabolism. | ||||||
Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $80.00 $220.00 $460.00 | 64 | |
Resveratrol, through its antioxidant properties, indirectly activates DDAH I. By reducing oxidative stress, resveratrol contributes to the preservation of nitric oxide (NO) bioavailability, impacting the feedback inhibition of DDAH I and favorably modulating ADMA metabolism. | ||||||
Folic Acid | 59-30-3 | sc-204758 | 10 g | $73.00 | 2 | |
Folic Acid indirectly activates DDAH I by promoting the synthesis of Tetrahydrobiopterin (BH4), a cofactor for DDAH I. BH4 stabilizes the active conformation of DDAH I, enhancing its enzymatic function and facilitating the breakdown of asymmetric dimethylarginine (ADMA) to citrulline and methylamine. | ||||||
Ademetionine | 29908-03-0 | sc-278677 sc-278677A | 100 mg 1 g | $184.00 $668.00 | 2 | |
Ademetionine acts as a methyl donor, indirectly activating DDAH I. By providing methyl groups, SAMe supports the methylation of proteins, including DDAH I, and may influence the modulation of ADMA metabolism by promoting the enzymatic activity of DDAH I. | ||||||
L-Arginine | 74-79-3 | sc-391657B sc-391657 sc-391657A sc-391657C sc-391657D | 5 g 25 g 100 g 500 g 1 kg | $20.00 $31.00 $61.00 $219.00 $352.00 | 2 | |
L-Arginine directly activates DDAH I by serving as a substrate for the enzyme. It competes with asymmetric dimethylarginine (ADMA) for binding to the active site of DDAH I, promoting the breakdown of ADMA to citrulline and methylamine. L-Arginine thus enhances DDAH I enzymatic function and NO production. | ||||||
Melatonin | 73-31-4 | sc-207848 sc-207848A sc-207848B sc-207848C sc-207848D sc-207848E | 1 g 5 g 25 g 100 g 250 g 1 kg | $65.00 $73.00 $218.00 $697.00 $1196.00 $3574.00 | 16 | |
Melatonin indirectly activates DDAH I by reducing oxidative stress. As an antioxidant, melatonin preserves nitric oxide (NO) bioavailability by mitigating the impact of reactive oxygen species, influencing the feedback inhibition of DDAH I and favorably modulating ADMA metabolism. | ||||||
Curcumin | 458-37-7 | sc-200509 sc-200509A sc-200509B sc-200509C sc-200509D sc-200509F sc-200509E | 1 g 5 g 25 g 100 g 250 g 1 kg 2.5 kg | $37.00 $69.00 $109.00 $218.00 $239.00 $879.00 $1968.00 | 47 | |
Curcumin, with its anti-inflammatory properties, indirectly activates DDAH I. By attenuating inflammation, curcumin contributes to the preservation of nitric oxide (NO) bioavailability, impacting the feedback inhibition of DDAH I and favorably modulating ADMA metabolism. | ||||||
L-Citrulline | 372-75-8 | sc-204784 sc-204784A | 25 g 200 g | $32.00 $240.00 | ||
L-Citrulline directly activates DDAH I by serving as a substrate for the enzyme. It competes with asymmetric dimethylarginine (ADMA) for binding to the active site of DDAH I, promoting the breakdown of ADMA to citrulline and methylamine. L-Citrulline thus enhances DDAH I enzymatic function and NO production. | ||||||
L-Ascorbic acid, free acid | 50-81-7 | sc-202686 | 100 g | $46.00 | 5 | |
Vitamin C indirectly activates DDAH I by reducing oxidative stress. As an antioxidant, vitamin C preserves nitric oxide (NO) bioavailability by mitigating the impact of reactive oxygen species, influencing the feedback inhibition of DDAH I and favorably modulating ADMA metabolism. | ||||||
Pterostilbene, Pterocarpus marsupium | 537-42-8 | sc-203223 sc-203223A | 10 mg 100 mg | $211.00 $1196.00 | ||
Pterostilbene, through its antioxidant properties, indirectly activates DDAH I. By reducing oxidative stress, pterostilbene contributes to the preservation of nitric oxide (NO) bioavailability, impacting the feedback inhibition of DDAH I and favorably modulating ADMA metabolism. | ||||||