产品号 #72382_C
维甲酸通路激活剂；可激活视黄酸受体（RAR）和类视黄醇X受体（RXR）
-顺式视黄酸可激活所有视黄酸受体 (RAR) 亚型 (Ki = 0.5-27 nM) 以及类视黄酸 X 受体 (RXR) 亚型 (Ki = 3.8-12 nM) (Umemiya et al.; Wong et al.)。RAR 能够与 RXR 形成异二聚体，而 RXR 又能与其他受体形成异二聚体，这使得 9-顺式视黄酸能够产生广泛的效应 (Dawson et al.; Kane)。
分化
·增加大鼠神经干细胞培养物中衍生的神经元数量（Laeng et al.）。
·促进培养细胞和小鼠小脑切片中少突胶质细胞前体细胞的分化和髓鞘形成（Huang et al.）。
·在胶原凝胶中培养的小鼠胚胎胰腺中诱导胰管形成，但不诱导腺泡形成 (Kadison et al.; Kobayashi et al.)。
·在体外和体内增强 BMP9 诱导的间充质祖细胞成骨分化（Zhang et al.）。
·诱导 C2C12 成肌祖细胞成肌分化（Zhu et al.）。
癌症研究
·抑制 Epstein-Barr 病毒感染的淋巴母细胞系增殖（Pomponi et al.）。
·抑制培养的人胃癌细胞的生长（Naka et al.）。
·抑制原发性套细胞淋巴瘤细胞的自发增殖和 CD40 诱导的生长（Guidoboni et al.）。
分化
·增加大鼠神经干细胞培养物中衍生的神经元数量（Laeng et al.）。
·促进培养细胞和小鼠小脑切片中少突胶质细胞前体细胞的分化和髓鞘形成（Huang et al.）。
·在胶原凝胶中培养的小鼠胚胎胰腺中诱导胰管形成，但不诱导腺泡形成 (Kadison et al.; Kobayashi et al.)。
·在体外和体内增强 BMP9 诱导的间充质祖细胞成骨分化（Zhang et al.）。
·诱导 C2C12 成肌祖细胞成肌分化（Zhu et al.）。
癌症研究
·抑制 Epstein-Barr 病毒感染的淋巴母细胞系增殖（Pomponi et al.）。
·抑制培养的人胃癌细胞的生长（Naka et al.）。
·抑制原发性套细胞淋巴瘤细胞的自发增殖和 CD40 诱导的生长（Guidoboni et al.）。
细胞类型
癌细胞及细胞系，白血病/淋巴瘤细胞，间充质干/祖细胞，肌源干/祖细胞，神经干/祖细胞，成骨细胞，胰腺细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
分化
研究领域
癌症，神经科学，干细胞生物学
CAS 编号
5300-03-8
化学式
C₂₀H₂₈O₂
纯度
≥ 90%
通路
视黄醇类
靶点
RAR，RXR
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Resources and Publications
Educational Materials (3)
Publications (12)
Analysis, occurrence, and function of 9-cis-retinoic acid. Biochimica et biophysica acta 2012 JAN
Abstract
Metabolic conversion of vitamin A (retinol) into retinoic acid (RA) controls numerous physiological processes. 9-cis-retinoic acid (9cRA), an active metabolite of vitamin A, is a high affinity ligand for retinoid X receptor (RXR) and also activates retinoic acid receptor (RAR). Despite the identification of candidate enzymes that produce 9cRA and the importance of RXRs as established by knockout experiments, in vivo detection of 9cRA in tissue was elusive until recently when 9cRA was identified as an endogenous pancreas retinoid by validated liquid chromatography-tandem mass spectrometry (LC-MS/MS) methodology. This review will discuss the current status of the analysis, occurrence, and function of 9cRA. Understanding both the nuclear receptor-mediated and non-genomic mechanisms of 9cRA will aid in the elucidation of disease physiology and possibly lead to the development of new retinoid-based therapeutics. This article is part of a Special Issue entitled Retinoid and Lipid Metabolism.
The retinoid X receptors and their ligands. Biochimica et biophysica acta 2012 JAN
Abstract
This chapter presents an overview of the current status of studies on the structural and molecular biology of the retinoid X receptor subtypes α, β, and γ (RXRs, NR2B1-3), their nuclear and cytoplasmic functions, post-transcriptional processing, and recently reported ligands. Points of interest are the different changes in the ligand-binding pocket induced by variously shaped agonists, the communication of the ligand-bound pocket with the coactivator binding surface and the heterodimerization interface, and recently identified ligands that are natural products, those that function as environmental toxins or drugs that had been originally designed to interact with other targets, as well as those that were deliberately designed as RXR-selective transcriptional agonists, synergists, or antagonists. Of these synthetic ligands, the general trend in design appears to be away from fully aromatic rigid structures to those containing partial elements of the flexible tetraene side chain of 9-cis-retinoic acid. This article is part of a Special Issue entitled Advances in High Density Lipoprotein Formation and Metabolism: A Tribute to John F. Oram (1945-2010).
Retinoid X receptor gamma signaling accelerates CNS remyelination. Nature neuroscience 2011 JAN
Abstract
The molecular basis of CNS myelin regeneration (remyelination) is poorly understood. We generated a comprehensive transcriptional profile of the separate stages of spontaneous remyelination that follow focal demyelination in the rat CNS and found that transcripts that encode the retinoid acid receptor RXR-γ were differentially expressed during remyelination. Cells of the oligodendrocyte lineage expressed RXR-γ in rat tissues that were undergoing remyelination and in active and remyelinated multiple sclerosis lesions. Knockdown of RXR-γ by RNA interference or RXR-specific antagonists severely inhibited oligodendrocyte differentiation in culture. In mice that lacked RXR-γ, adult oligodendrocyte precursor cells efficiently repopulated lesions after demyelination, but showed delayed differentiation into mature oligodendrocytes. Administration of the RXR agonist 9-cis-retinoic acid to demyelinated cerebellar slice cultures and to aged rats after demyelination caused an increase in remyelinated axons. Our results indicate that RXR-γ is a positive regulator of endogenous oligodendrocyte precursor cell differentiation and remyelination and might be a pharmacological target for regenerative therapy in the CNS.
更多信息
| Species | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 5300-03-8 |
| Chemical Formula | C₂₀H₂₈O₂ |
| Purity | ≥ 90% |
| Target | RAR, RXR |
| Pathway | Retinoid |
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