The chemical class labeled as PRAMEF12 Inhibitors encompasses a diverse range of compounds that can exert influence on the function and expression of the PRAMEF12 protein by targeting various cellular mechanisms and molecular pathways. The members of this class are not selective for the PRAMEF12 protein in isolation but are instead capable of modulating the intricate cellular processes that govern protein expression and activity. These inhibitors can act on DNA-related processes, such as transcription and methylation. For instance, some compounds can interfere with DNA methylation patterns, leading to alterations in gene expression profiles, which can include the modulation of PRAMEF12. Others can affect histone acetylation levels, thereby influencing chromatin structure and accessibility of transcriptional machinery to the DNA, which can alter the expression of a range of genes, including those related to PRAMEF12.
Furthermore, the chemical class includes inhibitors that can disrupt proteostasis, which encompasses the synthesis, folding, trafficking, and degradation of proteins. By inhibiting the proteasome, certain compounds can cause an accumulation of proteins within the cell, which can inadvertently affect the stability and degradation of a broad array of proteins, potentially including those that interact with or regulate PRAMEF12. Other members of this class can target signal transduction pathways. By altering kinase activity, these compounds can bring about changes in cell cycle progression and other signaling cascades that can have downstream effects on gene expression and protein activity. It is through these multifaceted mechanisms that this chemical class can exert control over the functional landscape in which PRAMEF12 operates, impacting its expression and regulatory roles within the cell. Each compound within this class can act through one or more of these pathways to influence the cellular context of PRAMEF12, thereby contributing to the modulation of its activity.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Trichostatin A | 58880-19-6 | sc-3511 sc-3511A sc-3511B sc-3511C sc-3511D | 1 mg 5 mg 10 mg 25 mg 50 mg | $149.00 $470.00 $620.00 $1199.00 $2090.00 | 33 | |
An HDAC inhibitor that could possibly inhibit PRAMEF12 by increasing histone acetylation, affecting the chromatin structure around the PRAMEF12 gene and its expression. | ||||||
Suberoylanilide Hydroxamic Acid | 149647-78-9 | sc-220139 sc-220139A | 100 mg 500 mg | $130.00 $270.00 | 37 | |
HDAC inhibitor that could possibly inhibit PRAMEF12 by inducing a similar effect on chromatin structure and gene expression as Trichostatin A. | ||||||
Bortezomib | 179324-69-7 | sc-217785 sc-217785A | 2.5 mg 25 mg | $132.00 $1064.00 | 115 | |
Proteasome inhibitor that could possibly inhibit PRAMEF12 by affecting protein turnover, including proteins that regulate PRAMEF12. | ||||||
MG-132 [Z-Leu- Leu-Leu-CHO] | 133407-82-6 | sc-201270 sc-201270A sc-201270B | 5 mg 25 mg 100 mg | $56.00 $260.00 $980.00 | 163 | |
A peptide aldehyde that inhibits proteasomes and could possibly inhibit PRAMEF12 by increasing the levels of proteins involved in its regulation. | ||||||
Palbociclib | 571190-30-2 | sc-507366 | 50 mg | $315.00 | ||
A CDK4/6 inhibitor that could possibly inhibit PRAMEF12 by inhibiting cell cycle progression, impacting expression or stability. | ||||||
Nutlin-3 | 548472-68-0 | sc-45061 sc-45061A sc-45061B | 1 mg 5 mg 25 mg | $56.00 $212.00 $764.00 | 24 | |
Disrupts the MDM2-p53 interaction and could possibly inhibit PRAMEF12 by affecting p53-dependent transcriptional responses, including regulation of PRAMEF12. | ||||||
MS-275 | 209783-80-2 | sc-279455 sc-279455A sc-279455B | 1 mg 5 mg 25 mg | $24.00 $88.00 $208.00 | 24 | |
A benzamide HDAC inhibitor that could possibly inhibit PRAMEF12 by influencing histone acetylation and gene expression. | ||||||
Vemurafenib | 918504-65-1 | sc-364643 sc-364643A | 10 mg 50 mg | $115.00 $415.00 | 11 | |
A BRAF inhibitor that could possibly inhibit PRAMEF12 by altering downstream signaling pathways, especially in the context of melanoma | ||||||