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相关概念视频

Mutations01:39

Mutations

Overview
X-Inactivation01:58

X-Inactivation

The human X chromosome contains over ten times the number of genes as in the Y chromosome. Since males have only one X chromosome, and females have two, one might expect females to produce twice as many of the proteins, with undesirable results.
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Bioactivation and Tissue Toxicity01:25

Bioactivation and Tissue Toxicity

Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...

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相关实验视频

Updated: Jun 21, 2026

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
08:09

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

Published on: March 24, 2017

激活剂和抑制剂与Xeroderma pigmentosum中TFIH的缺陷相互作用

J Liu1, S Akoulitchev, A Weber

  • 1Gene Regulation Section, Laboratory of Pathology, National Cancer Institute, National Institute of Health, Bethesda, MD 20892, USA.

Cell
|March 10, 2001
PubMed
概括

在TFIIH子单元中发生的突变,Xeroderma pigmentosum (XP) B和XPD破坏了c-myc基因的转录调节. 这种微妙的转录缺陷,不仅仅是DNA修复问题,导致XP患者的癌症风险.

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Pooled shRNA Screen for Reactivation of MeCP2 on the Inactive X Chromosome
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Pooled shRNA Screen for Reactivation of MeCP2 on the Inactive X Chromosome

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A Non-random Mouse Model for Pharmacological Reactivation of Mecp2 on the Inactive X Chromosome
08:27

A Non-random Mouse Model for Pharmacological Reactivation of Mecp2 on the Inactive X Chromosome

Published on: May 22, 2019

相关实验视频

Last Updated: Jun 21, 2026

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
08:09

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

Published on: March 24, 2017

Pooled shRNA Screen for Reactivation of MeCP2 on the Inactive X Chromosome
11:15

Pooled shRNA Screen for Reactivation of MeCP2 on the Inactive X Chromosome

Published on: March 2, 2018

A Non-random Mouse Model for Pharmacological Reactivation of Mecp2 on the Inactive X Chromosome
08:27

A Non-random Mouse Model for Pharmacological Reactivation of Mecp2 on the Inactive X Chromosome

Published on: May 22, 2019

科学领域:

  • 分子生物学分子生物学
  • 遗传学 遗传学 是一个
  • 癌症研究 癌症研究

背景情况:

  • 在TFIIH螺旋酶亚单元XPB和XPD的遗传突变导致重叠的DNA修复和转录综合征.
  • 色素瘤 (XP) 患者的高癌症风险不完全由单独的DNA修复缺陷来解释.
  • 在XP中转录缺陷是微妙的,难以评估.

研究的目的:

  • 研究XPB和XPD突变对FUSE结合蛋白 (FBP) 和FBP相互作用抑制剂 (FIR) 的转录调节的影响.
  • 阐明TFIIH在FBP介导的转录激活和FIR介导的抑制中的作用.
  • 了解TFIIH功能受损对c-myc表达和恶性瘤发展的影响.

主要方法:

  • 研究了TFIIH子单位 (XPB,XPD) 与转录监管机构FBP和FIR之间的相互作用.
  • 评估了XPB和XPD突变对FBP依赖的转录激活和FIR依赖的抑制的影响.
  • 在TFIIH突变的背景下分析了c-myc基因表达的调节.

主要成果:

  • 发现XPB和XPD突变阻断了FBP的转录激活.
  • 突变还影响了FIR介导的转录抑制.
  • TFIIH促进了FBP介导的转录,直到发起者逃脱和FIR介导的延迟启动后.
  • FBP和FIR受损的TFIIH监管影响了c-myc表达.

结论:

  • 影响FBP和FIR调节的TFIIH突变破坏了适当的c-myc表达控制.
  • 这些转录失调有助于XP患者观察到的高恶性瘤风险.
  • 了解这些转录缺陷对于评估XP综合征和癌症发展至关重要.