Date published: 2026-1-9

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MAN2C1 Inhibitors

MAN2C1 inhibitors represent a specific class of chemical compounds designed to target and modulate the activity of the enzyme alpha-mannosidase 2C1 (MAN2C1), a critical enzyme in the glycosylation pathway. MAN2C1 is involved in the processing of N-linked glycans, which are essential carbohydrate structures attached to proteins during their synthesis and folding. The enzyme plays a pivotal role in the trimming and remodeling of mannose residues in glycoproteins, which is crucial for their proper folding, stability, and function. Inhibitors of MAN2C1 are thus important tools for studying the biochemical pathways involved in protein glycosylation, offering insights into the regulation of glycoprotein biosynthesis, cellular glycome composition, and the overall dynamics of cellular carbohydrate processing.The inhibition of MAN2C1 can lead to alterations in glycoprotein structure, resulting in changes in the functional properties of these proteins, including their trafficking, degradation, and interactions with other cellular components. Researchers often use MAN2C1 inhibitors to dissect the roles of specific glycan structures in various biological processes, such as cell signaling, immune response, and protein quality control mechanisms within the endoplasmic reticulum and Golgi apparatus. By understanding how MAN2C1 inhibitors affect glycan processing, scientists can gain a deeper understanding of the glycosylation machinery's complexity and its broader implications in cellular biology. This exploration can also shed light on the evolutionary significance of glycan diversity in different organisms and the role of specific glycan structures in cellular adaptation and survival.

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Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

5-Aza-2′-Deoxycytidine

2353-33-5sc-202424
sc-202424A
sc-202424B
25 mg
100 mg
250 mg
$218.00
$322.00
$426.00
7
(1)

5-Aza-2′-Deoxycytidine (Decitabine) may decrease MAN2C1 expression by reducing methylation levels at the MAN2C1 gene promoter, which can lead to the recruitment of repressive transcriptional machinery to the locus.