The Placental RNase inhibitor is a crucial protein that plays a significant role in cellular homeostasis by providing robust inhibition of ribonucleases, enzymes that degrade RNA. This inhibition is essential for the stability and integrity of RNA molecules within the cell, which are fundamental for various biological processes such as protein synthesis, gene regulation, and cellular communication. The Placental RNase inhibitor, with its high affinity for ribonucleases, ensures the protection of RNA from unwarranted degradation, thereby maintaining the intricate balance of cellular function. The protein is ubiquitously expressed in human tissues, with particularly high levels noted in the placenta, an indication of its vital role during embryonic development where RNA integrity is paramount.
In the quest to understand and manipulate the expression of vital proteins such as the Placental RNase inhibitor, research has delved into various chemical activators that could potentially induce its expression. Compounds such as 17β-Estradiol have been hypothesized to upregulate gene expression by engaging with specific receptor pathways that trigger transcriptional activation. Similarly, DNA methylation inhibitors like 5-Azacytidine could lead to the demethylation of gene promoter regions, thereby allowing for the transcription of genes that may have been previously silenced, including that of the Placental RNase inhibitor. Histone deacetylase inhibitors, such as Trichostatin A and Sodium Butyrate, might facilitate a more relaxed chromatin state, enhancing the transcriptional activity of certain genes. Furthermore, small molecule activators like Forskolin, which increases cellular cAMP levels, might stimulate a cascade that culminates in the transcriptional upregulation of various genes. While these insights into the molecular mechanisms that govern gene expression offer pathways to potentially increase the expression of proteins like the Placental RNase inhibitor, the specific interactions and effects are subject to rigorous scientific verification.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
β-Estradiol | 50-28-2 | sc-204431 sc-204431A | 500 mg 5 g | $63.00 $182.00 | 8 | |
β-Estradiol may bind to estrogen receptors and initiate a cascade that leads to the upregulation of gene transcription, possibly including Placental RNase inhibitor. | ||||||
5-Azacytidine | 320-67-2 | sc-221003 | 500 mg | $280.00 | 4 | |
This compound could hypothetically demethylate the promoter region of the Placental RNase inhibitor gene, leading to its increased expression. | ||||||
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 | $152.00 $479.00 $632.00 $1223.00 $2132.00 | 33 | |
Trichostatin A may promote hyperacetylation of histones associated with the Placental RNase inhibitor gene, theoretically resulting in enhanced transcription. | ||||||
Forskolin | 66575-29-9 | sc-3562 sc-3562A sc-3562B sc-3562C sc-3562D | 5 mg 50 mg 1 g 2 g 5 g | $78.00 $153.00 $740.00 $1413.00 $2091.00 | 73 | |
Forskolin might stimulate the production of cAMP, which could activate protein kinase A and possibly lead to the upregulation of Placental RNase inhibitor expression. | ||||||
Imatinib | 152459-95-5 | sc-267106 sc-267106A sc-267106B | 10 mg 100 mg 1 g | $26.00 $119.00 $213.00 | 27 | |
Imatinib may theoretically inhibit tyrosine kinases that repress Placental RNase inhibitor expression, thereby leading to its increased expression. | ||||||
Dexamethasone | 50-02-2 | sc-29059 sc-29059B sc-29059A | 100 mg 1 g 5 g | $91.00 $139.00 $374.00 | 36 | |
Dexamethasone might bind to glucocorticoid receptors that interact with the promoter of the Placental RNase inhibitor gene, potentially stimulating its expression. | ||||||
Hydrogen Peroxide | 7722-84-1 | sc-203336 sc-203336A sc-203336B | 100 ml 500 ml 3.8 L | $31.00 $61.00 $95.00 | 28 | |
Hydrogen Peroxide could induce oxidative stress response elements within the Placental RNase inhibitor gene promoter, conceivably leading to higher expression levels. | ||||||
Doxorubicin | 23214-92-8 | sc-280681 sc-280681A | 1 mg 5 mg | $176.00 $426.00 | 43 | |
Doxorubicin might intercalate into DNA and inadvertently upregulate transcription of certain stress response genes, which could include Placental RNase inhibitor. | ||||||
PMA | 16561-29-8 | sc-3576 sc-3576A sc-3576B sc-3576C sc-3576D | 1 mg 5 mg 10 mg 25 mg 100 mg | $41.00 $132.00 $214.00 $500.00 $948.00 | 119 | |
PMA could theoretically activate protein kinase C, which may then stimulate transcription factors that increase Placental RNase inhibitor gene expression. | ||||||
Retinoic Acid, all trans | 302-79-4 | sc-200898 sc-200898A sc-200898B sc-200898C | 500 mg 5 g 10 g 100 g | $66.00 $325.00 $587.00 $1018.00 | 28 | |
Retinoic Acid may act on its nuclear receptors to initiate transcription of target genes, potentially including the Placental RNase inhibitor gene. | ||||||