EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #73602_C
cAMP通路激活剂；激活cAMP依赖性激酶
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总览
8-Bromo-cAMP（8-溴环腺苷酸）是一种膜渗透性cAMP衍生物。它能够激活cAMP依赖性蛋白激酶，并由于其对cAMP磷酸二酯酶具有抗性而具有长效作用（Schwede et al.）。它可用于研究钙介导通路（IC₅₀= 0.84 mM；Xaus et al.）。
重编程
·与丙戊酸搭配使用可提高人新生儿包皮成纤维细胞（HFF1）的重编程效率（Wang & Adjaye）。
免疫学
·抑制M-CSF依赖性的巨噬细胞增殖（Xaus et al.）。
·保护中性粒细胞免受TNF-α诱导的细胞凋亡（Krakstad）。
癌症研究
·诱导IL-3依赖性白血病细胞系的增殖反应（Barge et al.）。
·诱导胰腺癌细胞系的膜去极化（Sorio et al.）。
别名
8‑溴环腺苷酸，8‑Bro‑cAMP；NSC 171719
细胞类型
癌细胞及细胞系，巨噬细胞，多能干细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
重编程
研究领域
癌症，免疫，干细胞生物学
CAS 编号
23583-48-4
化学式
C₁₀H₁₁BrN₅O₆P
分子量
408.1 克/摩尔
纯度
≥ 95 %
通路
cAMP
靶点
cAMP-Dependent Kinase
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Resources and Publications
Publications (6)
A cyclic AMP analog, 8-Br-cAMP, enhances the induction of pluripotency in human fibroblast cells. Stem cell reviews 2011 JUN
Abstract
Somatic cells can be reprogrammed into induced pluripotent stem (iPS) cells by ectopic expression of four transcription factors. However, the efficiency of human iPS cell generation is extremely low and therefore elucidating the mechanisms underlying cellular reprogramming is of prime importance. We demonstrate that 8-Bromoadenosine 3', 5'-cyclic monophosphate (8-Br-cAMP) improves the reprogramming efficiency of human neonatal foreskin fibroblast (HFF1) cells transduced with the four transcription factors by 2-fold. The combination of 8-Br-cAMP and VPA synergistically increases the efficiency to 6.5-fold. The effect of 8-Br-cAMP or VPA may in part be due to the up-regulation of cytokine-related and inflammatory pathways. Remarkably, the synergistic effect of 8-Br-cAMP and VPA on cellular reprogramming may be due to the transient decrease of p53 protein during the early stages of reprogramming. However, it could also be due to additional differentially regulated genes and pathways such as the up-regulation of cytokine-related, inflammatory pathways and self-renewal supporting gene, namely cyclin-encoding CCND2, and the associated genes CCNA1 and CCNE1. Conversely, we also see the down-regulation of the p53 (CCNB2, GTSE1, SERPINE1) and cell cycle (PLK1, CCNB2) pathways. Our data demonstrates that a cyclic AMP analog, 8-Br-cAMP, enhances the efficiency of cellular reprogramming. In addition, 8-Br-cAMP and VPA have a synergistic effect on cellular reprogramming, which may be in part due to the transient down-regulation of the p53 signaling pathway during the early stages of reprogramming.
Defective CFTR expression and function are detectable in blood monocytes: development of a new blood test for cystic fibrosis. PloS one 2011 JAN
Abstract
BACKGROUND Evaluation of cystic fibrosis transmembrane conductance regulator (CFTR) functional activity to assess new therapies and define diagnosis of cystic fibrosis (CF) is cumbersome. It is known that leukocytes express detectable levels of CFTR but the molecule has not been characterized in these cells. In this study we aim at setting up and validating a blood test to evaluate CFTR expression and function in leukocytes. DESCRIPTION Western blot, PCR, immunofluorescence and cell membrane depolarization analysis by single-cell fluorescence imaging, using the potential-sensitive DiSBAC(2)(3) probe were utilized. Expression of PKA phosphorylated, cell membrane-localized CFTR was detected in non-CF monocytes, being undetectable or present in truncated form in monocytes derived from CF patients presenting with nonsense mutations. CFTR agonist administration induced membrane depolarization in monocytes isolated from non-CF donors (31 subjects) and, to a lesser extent, obligate CFTR heterozygous carriers (HTZ: 15 subjects), but it failed in monocytes from CF patients (44 subjects). We propose an index, which values in CF patients are significantly (ptextless0.001) lower than in the other two groups. Nasal Potential Difference, measured in selected subjects had concordant results with monocytes assay (Kappa statistic 0.93, 95%CI: 0.80-1.00). RESULTS AND SIGNIFICANCE CFTR is detectable and is functional in human monocytes. We also showed that CFTR-associated activity can be evaluated in 5 ml of peripheral blood and devise an index potentially applicable for diagnostic purposes and both basic and translational research: from drug development to evaluation of functional outcomes in clinical trials.
cAMP protects neutrophils against TNF-alpha-induced apoptosis by activation of cAMP-dependent protein kinase, independently of exchange protein directly activated by cAMP (Epac). Journal of leukocyte biology 2004 SEP
Abstract
It is unclear by which receptor cyclic adenosine monophosphate (cAMP) acts to promote neutrophil survival. We found that 8-(4-chlorophenylthio)-2'-O-methyl-cAMP, a specific activator of the recently discovered cAMP receptor, cAMP-regulated guanosine 5'-triphosphate exchange protein directly activated by cAMP, failed to protect human neutrophils from cell death. In contrast, specific activators of cAMP-dependent protein kinase type I (cA-PKI) could protect against death receptor [tumor necrosis factor receptor 1 (TNFR-1), Fas]-mediated apoptosis as well as cycloheximide-accelerated spontaneous" apoptosis. A novel "caged" cA-PK-activating analog�
更多信息
| Molecular Weight | 408.1 g/mol |
|---|---|
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
| Alternative Names | 8-BrcAMP; 8-Bromoadenosine 3', 5'-cyclic monophosphate; NSC 171719 |
| Cas Number | 23583-48-4 |
| Chemical Formula | C₁₀H₁₁BrN₅O₆P |
| 纯度 | ≥ 95% |
| Target | cAMP-Dependent Kinase |
| Pathway | cAMP |
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