NFYB, or Nuclear Transcription Factor Y Subunit Beta, is a pivotal component of the trimeric NF-Y complex, which plays an essential role in the transcriptional regulation of numerous genes. The NF-Y complex, composed of three subunits (NFYA, NFYB, and NFYC), is distinguished by its ability to specifically bind to the CCAAT box, a crucial promoter element that is ubiquitous in eukaryotic genes. The presence of this complex is critical for the initiation of transcription in various genes implicated in a wide array of biological processes, including cell cycle progression, differentiation, and response to stress. The role of NFYB within this complex is particularly important as it contributes to the DNA-binding and transcriptional activity of the entire NF-Y complex. This transcriptional regulation is a highly orchestrated process, involving the precise interaction of NFYB with other subunits and the recruitment of additional coactivators or corepressors that modulate gene expression.
The expression of NFYB itself is subject to regulation by various chemical compounds, which can serve as activators, leading to its upregulation. These activators engage with cellular mechanisms at multiple levels, from transcription factor activation to epigenetic modifications. For instance, compounds like retinoic acid and vitamin D3 can stimulate the transcription of NFYB by interacting with their respective receptors, which then bind to specific sites on DNA to promote gene expression. Histone deacetylase inhibitors, such as Trichostatin A and sodium butyrate, induce a relaxed chromatin structure, thereby enhancing the accessibility of transcription factors to the NFYB gene promoter. Moreover, agents like Forskolin and lithium chloride can initiate signaling cascades that culminate in the phosphorylation and activation of proteins involved in the transcriptional machinery, thereby amplifying the expression of NFYB. Through such diverse mechanisms, these chemical activators can orchestrate the upregulation of NFYB expression, reflecting the intricate network of cellular signaling pathways that govern gene regulation.
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产品名称 | CAS # | 产品编号 | 数量 | 价格 | 应用 | 排名 |
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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 | |
维甲酸可通过与维甲酸受体结合上调基因表达,而维甲酸受体可能直接与 NF-Y 结合位点相互作用,从而可能刺激 NFYB 转录物。 | ||||||
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 | |
佛司可林能提高细胞内的 cAMP 水平,从而激活蛋白激酶 A (PKA),使参与 NFYB 表达的转录因子和共激活因子磷酸化。 | ||||||
Cholecalciferol | 67-97-0 | sc-205630 sc-205630A sc-205630B | 1 g 5 g 10 g | $70.00 $160.00 $290.00 | 2 | |
胆钙化醇的活性代谢物可与维生素 D 受体(VDR)结合,后者可与 NF-Y 等转录因子形成复合物,刺激 NFYB 的转录。 | ||||||
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 | |
作为组蛋白去乙酰化酶抑制剂,曲古抑菌素A可以导致组蛋白过度乙酰化,从而形成更开放的染色质结构,这可能有助于NF-Y招募到其目标启动子,包括NFYB的启动子。 | ||||||
5-Azacytidine | 320-67-2 | sc-221003 | 500 mg | $280.00 | 4 | |
5-Azacytidine 可以抑制 DNA 甲基化,有可能导致 NFYB 启动子去甲基化,从而消除沉默标记,导致 NFYB 基因转录物增加。 | ||||||
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 | 18 | |
丁酸钠通过抑制组蛋白去乙酰化酶,导致组蛋白乙酰化增加,从而增强转录机制对NFYB基因的访问,导致其表达增加。 | ||||||
Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $60.00 $185.00 $365.00 | 64 | |
白藜芦醇可能会激活 SIRT1,导致与 NF-Y 有关的转录因子或辅助激活因子去乙酰化,从而导致 NFYB 基因转录激增。 | ||||||
(−)-Epigallocatechin Gallate | 989-51-5 | sc-200802 sc-200802A sc-200802B sc-200802C sc-200802D sc-200802E | 10 mg 50 mg 100 mg 500 mg 1 g 10 g | $42.00 $72.00 $124.00 $238.00 $520.00 $1234.00 | 11 | |
表没食子儿茶素没食子酸酯可能会引发一系列事件,导致染色质动态变化,从而刺激基因的转录活性,包括编码NFYB的基因。 | ||||||
Lithium | 7439-93-2 | sc-252954 | 50 g | $214.00 | ||
氯化锂会抑制 GSK-3,从而导致转录因子的稳定和激活,增强 NFYB 的表达。 | ||||||
Dexamethasone | 50-02-2 | sc-29059 sc-29059B sc-29059A | 100 mg 1 g 5 g | $76.00 $82.00 $367.00 | 36 | |
地塞米松通过糖皮质激素受体可导致辅助激活剂的招募,并在 NFYB 启动子处组装转录物,从而导致表达量增加。 |