EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #73382_C
cAMP通路激活剂；抑制4型环核苷酸磷酸二酯酶（PDE4）
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总览
Rolipram是一种具有细胞渗透性的选择性4型环核苷酸磷酸二酯酶（PDE4）抑制剂，该酶介导环磷酸腺苷（cAMP）的降解。Rolipram对PDE4同工酶A（IC₅₀=3 nM）的抑制作用优于对PDE4同工酶B和D（IC₅₀=130 nM和240 nM；MacKenzie和Houslay）等其他同工酶的抑制作用。它通过抑制PDE4B和/或PDE4D同工酶来抑制干扰素IFN-γ刺激的p38丝裂原活化蛋白（MAP）激酶的磷酸化（MacKenzie和Houslay）。
分化
·增强BMP-2诱导的小鼠间充质干细胞（MSC）的成骨分化（Munisso等）
·诱导人骨髓来源间充质干细胞的神经分化（Alexanian等）
重编程
·结合A83-01、CHIR99021、丁酸钠、LPA、SP600125和外源性OCT4表达，诱导成人人类真皮成纤维细胞（AHDF）重编程为诱导神经干细胞（Zhu等）
疾病建模
·促进小鼠缺血模型中新形成的小鼠海马神经元的存活（Sasaki等）
·逆转C57BL/6J小鼠精神分裂症模型中苯丙胺引起的听觉诱发电位降低（Maxwell等）
免疫学
·通过抑制白细胞功能，抑制人嗜酸性粒细胞中C5a刺激的白三烯C4（LTC4）合成（Tenor等）
·抑制人单核细胞中脂多糖（LPS）诱导的肿瘤坏死因子（TNF）的合成（Souness等）
细胞类型
间充质干/祖细胞，单核细胞，神经干/祖细胞，神经元，成骨细胞
种属
人，小鼠，非人灵长类，其他物种，大鼠
应用
分化，重编程
研究领域
疾病建模，免疫，干细胞生物学
CAS 编号
61413-54-5
化学式
C₁₆H₂₁NO₃
纯度
≥98%
通路
cAMP
靶点
PDE
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
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相关材料与文献
技术资料 (3)
文献 (8)
Action of rolipram on specific PDE4 cAMP phosphodiesterase isoforms and on the phosphorylation of cAMP-response-element-binding protein (CREB) and p38 mitogen-activated protein (MAP) kinase in U937 monocytic cells.
The Biochemical journal 2000
Abstract
U937 monocytic cells are shown here to express a range of PDE4,cAMP-specific phosphodiesterase (PDE) isoenzymes: the long isoenzymes,PDE4A4,PDE4D5 and PDE4D3,plus the short isoenzyme,PDE4B2. These isoenzymes provide around 76% of the total cAMP PDE activity of U937 cells. The specific activities of the total PDE4A,PDE4B and PDE4D activities were 0.63+/-0.09,8.8+/-0.2 and 34.4+/-2.9 pmol/min per mg of protein respectively. The PDE4 selective inhibitor,rolipram,inhibited immunopurified PDE4B and PDE4D activities similarly,with IC(50) values of approx. 130 nM and 240 nM respectively. In contrast,rolipram inhibited immunopurified PDE4A activity with a dramatically lower IC(50) value of around 3 nM. Rolipram increased phosphorylation of cAMP-response-element-binding protein (CREB) in U937 cells in a dose-dependent fashion,which implied the presence of both high affinity (IC(50) value approx. 1 nM) and low affinity (IC(50) value approx. 120 nM) components. Rolipram dose-dependently inhibited the interferon-gamma (IFN-gamma)-stimulated phosphorylation of p38 mitogen-activated protein (MAP) kinase in a simple monotonic fashion with an IC(50) value of approx. 290 nM. On this basis,it is suggested that rolipram inhibition of PDE4A4 is involved in regulating CREB phosphorylation but not IFN-gamma-stimulated p38 MAP kinase phosphorylation. PDE4A4 was also selectively activated by challenge of U937 cells with either bacterial lipopolysaccharide (LPS) or IFN-gamma through a process which was attenuated by both wortmannin and rapamycin. It is proposed that the PDE4A4 isoform is involved in compartmentalized cAMP signalling responses in U937 monocytes.
Phosphodiesterase inhibitors: a novel mechanism for receptor-independent antipsychotic medications.
Neuroscience 2004
Abstract
OVERVIEW: All current antipsychotic medications work by binding to Gi-coupled dopamine (DA) D2 receptors. Such medications are thought to affect cellular function primarily by decreasing DA-mediated regulation of intracellular cyclic adenosine monophosphate (cAMP).However,several studies indicate that cAMP signal transduction abnormalities in schizophrenia may not be limited to D2-containing cells. The current study examines the potential of using non-receptor-based agents that modify intracellular signal transduction as potential antipsychotic medications. METHODS: The indirect DA agonist amphetamine has been used to model the auditory sensory processing deficits in schizophrenia. Such pharmacologically induced abnormalities are reversed by current antipsychotic treatments. This study examines the ability of the phosphodiesterase-4 inhibitor,rolipram,to reverse amphetamine-induced abnormalities in auditory-evoked potentials that are characteristic of schizophrenia. RESULTS: Rolipram reverses amphetamine-induced reductions in auditory-evoked potentials. CONCLUSION: This finding could lead to novel approaches to receptor-independent treatments for schizophrenia.
The phosphodiesterase inhibitor rolipram promotes survival of newborn hippocampal neurons after ischemia.
Stroke; a journal of cerebral circulation 2007
Abstract
BACKGROUND AND PURPOSE: Brain ischemia stimulates neurogenesis. However,newborn neurons show a progressive decrease in number over time. Under normal conditions,the cAMP-cAMP responsive element binding protein (CREB) pathway regulates the survival of newborn neurons. Constitutive activation of CREB after brain ischemia also stimulates hippocampal neurogenesis. Thus,activation of cAMP-CREB signaling may provide a promising strategy for enhancing the survival of newborn neurons. We examined whether treatment of mice with the phosphodiesterase-4 inhibitor rolipram enhances hippocampal neurogenesis after ischemia. METHODS: Both common carotid arteries in mice were occluded for 12 minutes. Bromodeoxyuridine (BrdU) was used to label proliferating cells. Mice were perfused transcardially with 4% paraformaldehyde,and immunohistochemistry was performed. To evaluate the role of CREB in the survival of newborn neurons after ischemia,intrahippocampal injection of a CRE-decoy oligonucleotide was delivered for 1 week. We examined whether the activation of cAMP-CREB signaling by rolipram enhanced the proliferation and survival of newborn neurons. RESULTS: Phospho-CREB immunostaining was markedly upregulated in immature neurons,decreasing to low levels in mature neurons. The number of BrdU-positive cells 30 days after ischemia was significantly less in the CRE-decoy treatment group than in the vehicle group. Rolipram enhanced the proliferation of newborn cells under physiologic conditions but not under ischemic conditions. Rolipram significantly increased the survival of nascent BrdU-positive neurons,accompanied by an enhancement of phospho-CREB staining and decreased newborn cell death after ischemia. CONCLUSIONS: CREB phosphorylation regulates the survival of newborn neurons after ischemia. Chronic pharmacological activation of cAMP-CREB signaling may be therapeutically useful for the enhancement of neurogenesis after ischemia.
更多信息
| 物种 | 人, 其它物种, 大鼠, 小鼠, 非人灵长类 |
|---|---|
| Cas Number | 61413-54-5 |
| Chemical Formula | C₁₆H₂₁NO₃ |
| 纯度 | ≥ 98% |
| Target | PDE |
| Pathway | cAMP |
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