Ethylphosphonsaeure-isopropylester-chlorid | 28829-95-0

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 有机膦酸及其衍生物
• 英文名称: Ethylphosphonsaeure-isopropylester-chlorid
• 英文别名: ethyl-phosphonic acid-chloride isopropyl ester；Aethyl-phosphonsaeure-chlorid-isopropylester；Phosphonochloridic acid, ethyl-, 1-methylethyl ester；2-[chloro(ethyl)phosphoryl]oxypropane
• CAS: 28829-95-0
• 化学式: C₅H₁₂ClO₂P
• 分子量: 170.576
• InChiKey: DEMOFDHAHKVQGA-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.4
• 重原子数：
  9
• 可旋转键数：
  3
• 环数：
  0.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  26.3
• 氢给体数：
  0
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  Ethylphosphonsaeure-isopropylester-chlorid 在 吡啶 、 水 作用下， 生成 Diethyl-diphosphonsaeure-diisopropylester
  参考文献：
  名称：

  Coe et al., Journal of the Chemical Society, 1957, p. 3604,3606

  摘要：

  DOI：
• 作为产物：
  描述：

  isopropyl hydrogen ethylphosphonate 在 五氯化磷 作用下， 生成 Ethylphosphonsaeure-isopropylester-chlorid
  参考文献：
  名称：

  Coe et al., Journal of the Chemical Society, 1957, p. 3604,3606

  摘要：

  DOI：

文献信息

• Sosnovsky,S.; Konieczny,M., Phosphorus and the Related Group V Elements, 1974, vol. 4, p. 255 - 264
  作者：Sosnovsky,S.、Konieczny,M.

  DOI：——

  日期：——
• Chymase Participates in Chronic Dermatitis by Inducing Eosinophil Infiltration
  作者：Yoshiaki Tomimori、Tsuyoshi Muto、Harukazu Fukami、Kayo Saito、Chika Horikawa、Nobuo Tsuruoka、Masayuki Saito、Namino Sugiura、Kyoko Yamashiro、Motoo Sumida、Saki Kakutani、Yoshiaki Fukuda

  DOI：10.1097/01.lab.0000018827.78602.f4

  日期：2002.6

  An epicutaneous application of 2,4-dinitrofluorobenzene (DNFB) to a mouse ear caused a transient skin swelling, and the repetition of the challenge enlarged the contact dermattis. The repeated challenge with DNFB also induced eosinophil infiltration on the application site. Administration of a chymase inhibitor significantly inhibited the ear swelling as well as eosinophil accumulation. An intradermal injection of human chymase to the mouse ear also elicited transient skin swelling and eosinophil infiltration, both of which were augmented in proportion to the number of injections. Human serum albumin and heat-inactivated chymase failed to induce such skin reactions, suggesting the participation of proteolytic activity of the enzyme. In addition, chymase stimulated eosinophil migration in vitro in a concentration-dependent manner. Taken together, these observations suggest that mast cell chymase may contribute to development of the DNFB-induced dermatitis, probably by promoting eosinophil infiltration. It is therefore possible that chymase plays a role in pathogenesis of chronic dermatitis such as atopic dermatitis.
• Michalski; Skowronska, Roczniki Chemii, 1956, vol. 30, p. 799,808,810
  作者：Michalski、Skowronska

  DOI：——

  日期：——
• Rasumow et al., Zhurnal Obshchei Khimii, 1957, vol. 27, p. 2394; engl. Ausg. S. 2455
  作者：Rasumow et al.

  DOI：——

  日期：——
• Induction of p53 Accumulation by Moloney Murine Leukemia Virus-ts1 Infection in Astrocytes Via Activation of Extracellular Signal-Regulated Kinases 1/2
  作者：Hun-Taek Kim、Serban Tasca、Wenan Qiang、Paul K Y Wong、George Stoica

  DOI：10.1097/01.lab.0000017373.82871.45

  日期：2002.6

  We previously reported that Moloney murine leukemia virus-ts1-mediated neuronal degeneration in mice is likely a result of both loss of glial support and release of cytokines and neurotoxins from ts1-infected glial cells. Viral infection in some cell types regulates expression of p53 protein, a key regulator of cell proliferation and death. Therefore, we hypothesized that p53 and its dependent genes may be linked with ts1-mediated neuropathology. We examined the presence of p53 and its dependent gene product, a proapoptotic protein bax-alpha, in ts1-induced spongiform encephalomyelopathy. Compared with controls, the lesions of infected animals contained increased levels of p53 and bax-a in astrocytes, as shown by strong nuclear p53 and cytoplasmic bax-alpha immunoreactivity in astrocytes. To determine how ts1 affects p53 expression in astrocytes, we then assessed the expression of p53 and its dependent genes, such as bax-alpha and p21, in infected and uninfected immortalized C1 astrocytes and studied possible pathways responsible for p53 accumulation in infected astrocytes. In these studies using mitogen-activated protein kinase inhibitors, infection-induced increases in the p53 level were partially blocked by PD98059, a synthetic inhibitor of MEK1 that is the immediate upstream kinase of extracellular signal-regulated kinases 1/2 (ERK1/2), but not by SB202190, a potent p38 kinase inhibitor. Furthermore, treatment with PD98059 significantly decreased the level of p21 protein, a p53-dependent gene product. These results suggest that ts1 infection may stabilize p53 protein through activation of ERKs in C1 astrocytes, leading to increased expression of the p21 and bax-alpha proteins, both of which induce cell cycle arrest and apoptosis. Our studies suggest that ts1 neuropathology in mice may result from changes in expression and activity of p53, brought about in part by ts1 activation of ERK.