7-methylsulfanyl-heptan-1-ol | 101397-91-5

• 分子结构分类: 有机化合物 - 有机硫化合物 - 硫醚类
• 英文名称: 7-methylsulfanyl-heptan-1-ol
• 英文别名: Methyl-(7-hydroxy-heptyl)-sulfid；7-Methylmercapto-heptan-1-ol；7-Methylsulfanylheptan-1-ol
• CAS: 101397-91-5
• 化学式: C₈H₁₈OS
• 分子量: 162.296
• InChiKey: JLASRTSTQMCFMA-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.2
• 重原子数：
  10
• 可旋转键数：
  7
• 环数：
  0.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  45.5
• 氢给体数：
  1
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  7-methylsulfanyl-heptan-1-ol 在 氯化亚砜 作用下， 生成 1-chloro-7-methylsulfanyl-heptane
  参考文献：
  名称：

  Familial Head and Neck Cancer: Molecular Analysis of a New Clinical Entity

  摘要：

  AbstractObjective The tumor suppressor gene p16 encodes a cyclin‐dependent kinase inhibitor that normally inhibits cell proliferation by causing a G1 cell cycle arrest. The p16 gene is frequently mutated in a variety of somatic tumors, as well as in familial melanoma and familial pancreatic carcinoma. We identified a family with a high incidence of head and neck squamous cell carcinoma (HNSCC) and melanoma. Molecular analyses of the p16 gene locus in blood and tumor DNA from this family was performed to determine whether an association between germline p16 gene mutation and HNSCC exists.Study Design Molecular pedigree analyses.Methods Exon 2 of p16 was polymerase chain reaction amplified from blood, tumor, or nontumor DNA isolated from affected and unaffected members, then directly sequenced and compared with consensus p16 sequence. Cell cycle position of cells expressing wild‐type or mutant p16 was determined by flow cytometry.Results Molecular analyses revealed a nonfunctional germline point mutation within exon 2 of the p16 gene that encodes a mutant p16 protein substituting proline at amino acid position 87 for the wild‐type arginine (p16R87P). Relative to wild‐type p16, p16R87P lost ability to cause a growth arrest following ectopic expression. The mutant (p16R87P) allele segregated with cancer predisposition in tested family members, and analyses of HNSCC tumor tissues demonstrated universal loss of wild‐type allele.Conclusions Significance of the mutant p16 (p16R87P) in HNSCC tumorigenesis is strongly suggested by its loss of cell cycle arrest activity and its retention in tumor tissue with simultaneous loss of the wild‐type allele. Further, the germline p16 mutation segregated with cancer predisposition within the family. In aggregate, these data suggest that there is a direct causal relationship between the germline p16 mutation in this family and HNSCC tumorigenesis. Based on our observations, the spectrum of familial cancers associated with p16 mutations should include a new clinical entity, familial HNSCC.

  DOI：

  10.1097/00005537-200209000-00010
• 作为产物：
  描述：

  7-氯-1-庚醇 、 potassium methanethiolate 在 乙醇 作用下， 生成 7-methylsulfanyl-heptan-1-ol
  参考文献：
  名称：

  Familial Head and Neck Cancer: Molecular Analysis of a New Clinical Entity

  摘要：

  AbstractObjective The tumor suppressor gene p16 encodes a cyclin‐dependent kinase inhibitor that normally inhibits cell proliferation by causing a G1 cell cycle arrest. The p16 gene is frequently mutated in a variety of somatic tumors, as well as in familial melanoma and familial pancreatic carcinoma. We identified a family with a high incidence of head and neck squamous cell carcinoma (HNSCC) and melanoma. Molecular analyses of the p16 gene locus in blood and tumor DNA from this family was performed to determine whether an association between germline p16 gene mutation and HNSCC exists.Study Design Molecular pedigree analyses.Methods Exon 2 of p16 was polymerase chain reaction amplified from blood, tumor, or nontumor DNA isolated from affected and unaffected members, then directly sequenced and compared with consensus p16 sequence. Cell cycle position of cells expressing wild‐type or mutant p16 was determined by flow cytometry.Results Molecular analyses revealed a nonfunctional germline point mutation within exon 2 of the p16 gene that encodes a mutant p16 protein substituting proline at amino acid position 87 for the wild‐type arginine (p16R87P). Relative to wild‐type p16, p16R87P lost ability to cause a growth arrest following ectopic expression. The mutant (p16R87P) allele segregated with cancer predisposition in tested family members, and analyses of HNSCC tumor tissues demonstrated universal loss of wild‐type allele.Conclusions Significance of the mutant p16 (p16R87P) in HNSCC tumorigenesis is strongly suggested by its loss of cell cycle arrest activity and its retention in tumor tissue with simultaneous loss of the wild‐type allele. Further, the germline p16 mutation segregated with cancer predisposition within the family. In aggregate, these data suggest that there is a direct causal relationship between the germline p16 mutation in this family and HNSCC tumorigenesis. Based on our observations, the spectrum of familial cancers associated with p16 mutations should include a new clinical entity, familial HNSCC.

  DOI：

  10.1097/00005537-200209000-00010

文献信息

• [EN] FUNGICIDES TO PREVENT AND CONTROL FUNGAL PATHOGENS<br/>[FR] FONGICIDES POUR LA PRÉVENTION ET LA LUTTE CONTRE DES PATHOGÈNES FONGIQUES
  申请人：UNIV LAUSANNE

  公开号：WO2020011750A1

  公开（公告）日：2020-01-16

  The invention relates to the field of biological fungicides with a broad range of antifungal activity coming from plant extracts from the order of Brassicales or molecules revealing similar chemical structure. In particular, Applicants surprisingly provided a new usage of a combination of sulfonyl and sulfinyl containing aliphatic glucosinolates, their by-products and synthetic analogues as efficient antifungal compounds with broad spectrum of activity.

  本发明涉及一种生物杀菌剂领域，其具有来自十字花目植物提取物或具有类似化学结构的分子的广谱抗真菌活性。特别地，申请人惊奇地提供了一种新的用途，即使用含有磺酰基和亚磺酰基的脂肪族葡萄糖苷、其副产物和合成类似物的组合作为具有广谱活性的高效抗真菌化合物。
• NOVEL BIOMIMETIC HYDROGEL MATERIALS
  申请人：The Regents of the University of California

  公开号：EP1017737A1

  公开（公告）日：2000-07-12
• EP1017737A4
  申请人：——

  公开号：EP1017737A4

  公开（公告）日：2002-06-26
• [EN] NOVEL BIOMIMETIC HYDROGEL MATERIALS<br/>[FR] NOUVELLES MATIERES BIOMIMETIQUES DU TYPE HYDROGEL
  申请人：THE REGENTS OF THE UNIVERSITY OF CALIFORNIA

  公开号：WO1999011692A1

  公开（公告）日：1999-03-11

  (EN) Novel biomimetic hydrogel materials and methods for their preparation. Hydrogels containing acrylamide-functionalized carbohydrate, sulfoxide, sulfide or sulfone copolymerized with a hydrophilic or hydrophobic copolymerizing material selected from the group consisting of an acrylamide, methacrylamide, acrylate, methacrylate, vinyl and a derivative thereof present in concentration from about 1 to about 99 wt.% and methods for their preparation. The method of use of the new hydrogels for fabrication of soft contact lenses and biomedical implants.(FR) L'invention concerne des nouvelles matières biomimétiques du type hydrogel, ainsi que des procédés de préparation associés. Elle concerne notamment des hydrogels contenant un glucide fonctionnalisé par acrylamide, un sulfoxyde, un sulfure ou une sulfone, copolymérisés à l'aide d'un agent de copolymérisation hydrophile ou hydrophobe choisi dans le groupe constitué par un acrylamide, méthacrylamide, acrylate, méthacrylate, vinyle et un dérivé de ceux-ci, et présent selon une concentration comprise entre environ 1 et environ 99 % en poids. L'invention concerne encore des procédés de préparation de ces nouveaux hydrogels, un procédé d'utilisation de ceux-ci dans la fabrication de lentilles de contact souples et d'implants biomédicaux.
• Familial Head and Neck Cancer: Molecular Analysis of a New Clinical Entity
  作者：Kathy K. Yu、Adam M. Zanation、Jonathan R. Moss、Wendell G. Yarbrough

  DOI：10.1097/00005537-200209000-00010

  日期：2002.9

  AbstractObjective The tumor suppressor gene p16 encodes a cyclin‐dependent kinase inhibitor that normally inhibits cell proliferation by causing a G1 cell cycle arrest. The p16 gene is frequently mutated in a variety of somatic tumors, as well as in familial melanoma and familial pancreatic carcinoma. We identified a family with a high incidence of head and neck squamous cell carcinoma (HNSCC) and melanoma. Molecular analyses of the p16 gene locus in blood and tumor DNA from this family was performed to determine whether an association between germline p16 gene mutation and HNSCC exists.Study Design Molecular pedigree analyses.Methods Exon 2 of p16 was polymerase chain reaction amplified from blood, tumor, or nontumor DNA isolated from affected and unaffected members, then directly sequenced and compared with consensus p16 sequence. Cell cycle position of cells expressing wild‐type or mutant p16 was determined by flow cytometry.Results Molecular analyses revealed a nonfunctional germline point mutation within exon 2 of the p16 gene that encodes a mutant p16 protein substituting proline at amino acid position 87 for the wild‐type arginine (p16R87P). Relative to wild‐type p16, p16R87P lost ability to cause a growth arrest following ectopic expression. The mutant (p16R87P) allele segregated with cancer predisposition in tested family members, and analyses of HNSCC tumor tissues demonstrated universal loss of wild‐type allele.Conclusions Significance of the mutant p16 (p16R87P) in HNSCC tumorigenesis is strongly suggested by its loss of cell cycle arrest activity and its retention in tumor tissue with simultaneous loss of the wild‐type allele. Further, the germline p16 mutation segregated with cancer predisposition within the family. In aggregate, these data suggest that there is a direct causal relationship between the germline p16 mutation in this family and HNSCC tumorigenesis. Based on our observations, the spectrum of familial cancers associated with p16 mutations should include a new clinical entity, familial HNSCC.