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5,5'-dihydroxy-2,2'-m-phenylenedimercapto-di-benzoic acid | 111663-66-2

中文名称
——
中文别名
——
英文名称
5,5'-dihydroxy-2,2'-m-phenylenedimercapto-di-benzoic acid
英文别名
1,3-Bis-(2-carboxy-4-hydroxy-phenylmercapto)-benzol;5,5'-Dihydroxy-2,2'-m-phenylendimercapto-di-benzoesaeure
5,5'-dihydroxy-2,2'-<i>m</i>-phenylenedimercapto-di-benzoic acid化学式
CAS
111663-66-2
化学式
C20H14O6S2
mdl
——
分子量
414.46
InChiKey
WNVYUHSTSSXCRB-UHFFFAOYSA-N
BEILSTEIN
——
EINECS
——
  • 物化性质
  • 计算性质
  • ADMET
  • 安全信息
  • SDS
  • 制备方法与用途
  • 上下游信息
  • 反应信息
  • 文献信息
  • 表征谱图
  • 同类化合物
  • 相关功能分类
  • 相关结构分类

反应信息

  • 作为反应物:
    参考文献:
    名称:
    Effect of the control proliferation of astrocyte on the formation of glial scars by antisenseGFAP retrovirus
    摘要:
    Astrocytes play an important role in the formation of glial scars. In order to investigate the effect of inhibiting GFAP gene expression on normal, reactive astrocytes and on glial scar formation, the efficiency of the recombinant antisense GFAP retrovirus (PLBskG) on the growth, cell cycle, morphology and GFAP gene expression of astrocytes in vitro and on the formation of glial scars in vivo has been studied by cell growth curves, flow cytometry, immunocytochemistry, in situ hybridization, RT-PCR and Southern blot. The results confirm the recombinant retrovirus (PLBskG) produced growth suppression and G1 arrest of the normal and injured astrocytes. The infected cells become round or ellipoid. The cell processes become fine or retracted. The intensity of staining of GFAP is reduced. Expression of GFAP mRNA is down regulated. However, in the control experiment, no obvious effects on the morphology or synthesis of GFAP on cultured normal and scratched astrocytes infected by primary retrovirus vector (PLXSN) have been observed. The supernatant of PLBskG has been injected into an injured site by microinjection in vivo. The number and process lengths of GFAP positive cells are obviously reduced around the injured site. The formation of the glial scar is inhibited, showing that the recombinant antisense GFAP retrovirus can effectively inhibit the growth and GFAP expression of normal and injured astrocytes in vitro and the formation of glial scar in vivo. It is suggested that GFAP plays an important role in glial scar formation.
    DOI:
    10.1007/bf02884900
  • 作为产物:
    描述:
    alkaline earth salt of/the/ methylsulfuric acid 在 作用下, 生成 5,5'-dihydroxy-2,2'-m-phenylenedimercapto-di-benzoic acid
    参考文献:
    名称:
    Effect of the control proliferation of astrocyte on the formation of glial scars by antisenseGFAP retrovirus
    摘要:
    Astrocytes play an important role in the formation of glial scars. In order to investigate the effect of inhibiting GFAP gene expression on normal, reactive astrocytes and on glial scar formation, the efficiency of the recombinant antisense GFAP retrovirus (PLBskG) on the growth, cell cycle, morphology and GFAP gene expression of astrocytes in vitro and on the formation of glial scars in vivo has been studied by cell growth curves, flow cytometry, immunocytochemistry, in situ hybridization, RT-PCR and Southern blot. The results confirm the recombinant retrovirus (PLBskG) produced growth suppression and G1 arrest of the normal and injured astrocytes. The infected cells become round or ellipoid. The cell processes become fine or retracted. The intensity of staining of GFAP is reduced. Expression of GFAP mRNA is down regulated. However, in the control experiment, no obvious effects on the morphology or synthesis of GFAP on cultured normal and scratched astrocytes infected by primary retrovirus vector (PLXSN) have been observed. The supernatant of PLBskG has been injected into an injured site by microinjection in vivo. The number and process lengths of GFAP positive cells are obviously reduced around the injured site. The formation of the glial scar is inhibited, showing that the recombinant antisense GFAP retrovirus can effectively inhibit the growth and GFAP expression of normal and injured astrocytes in vitro and the formation of glial scar in vivo. It is suggested that GFAP plays an important role in glial scar formation.
    DOI:
    10.1007/bf02884900
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