The chemical class known as DSEL Inhibitors encompasses a range of compounds designed to modulate the activity of Dermatan Sulfate Epimerase-Like (DSEL), an enzyme integral to the biosynthesis and modification of dermatan sulfate in the extracellular matrix. These inhibitors operate through various mechanisms to influence the functional dynamics of DSEL. One primary approach within this class is the modulation of the biosynthetic pathway of dermatan sulfate. By targeting key steps in this pathway, such as the sulfation process or the chain elongation stages, these inhibitors can effectively disrupt the normal functioning of DSEL. This disruption can lead to alterations in the structure and function of dermatan sulfate, which is crucial for maintaining the integrity of the extracellular matrix and facilitating various cellular interactions. The ability to modulate the biosynthesis pathway provides a strategic avenue to influence the overall activity of DSEL in the extracellular matrix, offering insights into the complex interplay of enzymatic actions and matrix formation.
Another significant method employed by DSEL inhibitors involves interfering with the cellular signaling pathways that intersect with DSEL's activity. This can include targeting cell signaling mechanisms that are upstream or downstream of DSEL's action, such as growth factor interactions or tyrosine kinase pathways. By influencing these signaling cascades, DSEL inhibitors can indirectly affect the enzyme's role in the extracellular matrix organization and cellular processes like adhesion, proliferation, and migration. Additionally, these inhibitors may affect the enzyme's interaction with other molecules within the cell, further modulating its functional capacity. This approach underscores the multifaceted nature of DSEL's role in cellular biology, highlighting the enzyme not only as a participant in the biosynthesis of dermatan sulfate but also as a key player in a broader network of cellular signals and interactions. In summary, DSEL Inhibitors represent a diverse group of compounds that employ various strategies to regulate the activity of DSEL. From direct interference in the glycosaminoglycan biosynthesis process to the modulation of related cell signaling pathways and molecular interactions, each method offers a unique perspective on controlling the function of this crucial enzyme. The development of these inhibitors is grounded in a deep understanding of DSEL's role in the extracellular matrix and its involvement in a wide array of cellular functions. This chemical class is a testament to the intricate relationship between enzymatic activity, matrix biology, and cellular signaling in the complex environment of the cell.
Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
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LY 294002 | 154447-36-6 | sc-201426 sc-201426A | 5 mg 25 mg | $121.00 $392.00 | 148 | |
As a PI3K inhibitor, LY294002 can affect cell signaling pathways involved in extracellular matrix formation, which could possibly inhibit DSEL activity. | ||||||
Tunicamycin | 11089-65-9 | sc-3506A sc-3506 | 5 mg 10 mg | $169.00 $299.00 | 66 | |
Inhibits glycosylation, crucial for glycosaminoglycan synthesis, which could potentially inhibit DSEL activity. | ||||||
Swainsonine | 72741-87-8 | sc-201362 sc-201362C sc-201362A sc-201362D sc-201362B | 1 mg 2 mg 5 mg 10 mg 25 mg | $135.00 $246.00 $619.00 $799.00 $1796.00 | 6 | |
This inhibitor of glycoprotein processing might indirectly affect glycosaminoglycan biosynthesis and potentially inhibit DSEL's role in it. | ||||||
D-Mannose | 3458-28-4 | sc-211180 sc-211180A | 100 g 250 g | $101.00 $158.00 | 1 | |
Inhibits glycosaminoglycan chain elongation, which could potentially inhibit DSEL's substrate processing. | ||||||
Genistein | 446-72-0 | sc-3515 sc-3515A sc-3515B sc-3515C sc-3515D sc-3515E sc-3515F | 100 mg 500 mg 1 g 5 g 10 g 25 g 100 g | $26.00 $92.00 $120.00 $310.00 $500.00 $908.00 $1821.00 | 46 | |
As a tyrosine kinase inhibitor, Genistein can influence cell signaling pathways, which could possibly affect those regulated by DSEL and inhibit its activity. |