ADAM5, a member of the A Disintegrin And Metalloproteinase family, plays a crucial role in cell adhesion and proteolytic processing of various proteins. While the precise biological functions of ADAM5 remain to be fully elucidated, it is known to be predominantly expressed in reproductive tissues and has been implicated in processes such as sperm-egg fusion. Understanding the regulatory mechanisms that control the expression of ADAM5 is essential to decipher its role in cellular physiology. The expression of ADAM5, like many other genes, can be induced or upregulated by a variety of biochemical compounds through diverse cellular signaling pathways and mechanisms that alter the transcriptional landscape of cells.
Compounds such as retinoic acid and tretinoin are known to interact with nuclear hormone receptors, which then bind to DNA at specific response elements to initiate the transcription of target genes, including potentially ADAM5. Similarly, steroid hormones like testosterone can trigger a cascade of transcriptional events by engaging with their specific receptors that may lead to the stimulation of ADAM5 expression. Other compounds, such as forskolin, can elevate intracellular cyclic AMP (cAMP), thus activating protein kinase A and other factors that can promote the transcription of a range of genes. DNA methylation inhibitors, such as 5-Aza-2'-deoxycytidine, could stimulate gene expression by reducing methylation levels at gene promoters, thereby enhancing their transcriptional activity. Meanwhile, histone deacetylase inhibitors, such as Trichostatin A and sodium butyrate, may increase the acetylation of histones, resulting in a more open chromatin state favorable for transcription. Lithium chloride's inhibition of GSK-3 may lead to transcriptional changes conducive to ADAM5 expression. Collectively, these chemicals represent a spectrum of bioactive molecules that could be employed in research to elucidate the complex regulatory network governing ADAM5 expression. This understanding could subsequently contribute to a deeper insight into the physiological roles of ADAM5 in the context of cellular and molecular biology.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Retinoic Acid, all trans | 302-79-4 | sc-200898 sc-200898A sc-200898B sc-200898C | 500 mg 5 g 10 g 100 g | $65.00 $319.00 $575.00 $998.00 | 28 | |
Retinoic acid may upregulate ADAM5 by binding to nuclear retinoic acid receptors, which then interact with retinoic acid response elements in the promoter region of ADAM5 to stimulate 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 | $76.00 $150.00 $725.00 $1385.00 $2050.00 | 73 | |
Forskolin might elevate ADAM5 levels by activating adenylate cyclase, thereby increasing intracellular cAMP, which subsequently activates protein kinase A (PKA) and leads to the initiation of ADAM5 gene transcription. | ||||||
5-Aza-2′-Deoxycytidine | 2353-33-5 | sc-202424 sc-202424A sc-202424B | 25 mg 100 mg 250 mg | $214.00 $316.00 $418.00 | 7 | |
This compound could upregulate ADAM5 by inhibiting DNA methyltransferase, decreasing methylation levels at the ADAM5 gene locus, and thereby enhancing gene transcription. | ||||||
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 | |
Trichostatin A may promote ADAM5 transcription by inhibiting histone deacetylases, which increases acetylation of histones around the ADAM5 gene, leading to a more transcriptionally active chromatin state. | ||||||
Dibutyryl-cAMP | 16980-89-5 | sc-201567 sc-201567A sc-201567B sc-201567C | 20 mg 100 mg 500 mg 10 g | $45.00 $130.00 $480.00 $4450.00 | 74 | |
Dibutyryl-cAMP, a cAMP analog, could boost ADAM5 expression through the cAMP-dependent signaling pathway, leading to activation of transcription factors that target the ADAM5 gene promoter. | ||||||
PMA | 16561-29-8 | sc-3576 sc-3576A sc-3576B sc-3576C sc-3576D | 1 mg 5 mg 10 mg 25 mg 100 mg | $40.00 $129.00 $210.00 $490.00 $929.00 | 119 | |
PMA may stimulate ADAM5 gene expression by activating protein kinase C (PKC), which then phosphorylates transcription factors that bind to the ADAM5 promoter, enhancing its transcription. | ||||||
Dexamethasone | 50-02-2 | sc-29059 sc-29059B sc-29059A | 100 mg 1 g 5 g | $76.00 $82.00 $367.00 | 36 | |
Dexamethasone could induce ADAM5 expression by interacting with glucocorticoid receptors that bind to glucocorticoid response elements within the ADAM5 promoter region, promoting gene transcription. | ||||||
Sodium Butyrate | 156-54-7 | sc-202341 sc-202341B sc-202341A sc-202341C | 250 mg 5 g 25 g 500 g | $30.00 $46.00 $82.00 $218.00 | 19 | |
Sodium butyrate may enhance ADAM5 expression by serving as a histone deacetylase inhibitor, causing an increase in histone acetylation and a consequent upsurge in transcriptional activity at the ADAM5 gene locus. | ||||||
Lithium | 7439-93-2 | sc-252954 | 50 g | $214.00 | ||
Lithium chloride may stimulate the expression of ADAM5 through inhibition of glycogen synthase kinase 3 (GSK-3), altering intracellular signaling pathways and leading to transcriptional activation of the ADAM5 gene. | ||||||
Valproic Acid | 99-66-1 | sc-213144 | 10 g | $85.00 | 9 | |
Valproic acid might promote the expression of ADAM5 by exerting histone deacetylase inhibitory effects, which would result in hyperacetylation of histones and an open chromatin conformation conducive to ADAM5 gene transcription. | ||||||