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Receptor-mediated Endocytosis01:38

Receptor-mediated Endocytosis

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Antibiotic Selection00:57

Antibiotic Selection

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Receptor-mediated Endocytosis01:20

Receptor-mediated Endocytosis

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Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
Clathrin-Mediated Endocytosis of LDL
One well-characterized example of receptor-mediated endocytosis is the...
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GPCR Desensitization01:12

GPCR Desensitization

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G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
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Selectins01:25

Selectins

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Cell adhesion is  an essential aspect of multicellularity. While stable cell interactions usually occur between cells of the same type, transient cell interactions occur between cells of different tissue types, such as between neutrophils and endothelial cells. Selectins are one class of cell adhesion molecules (CAMs) that bind carbohydrate ligands to form transient cell adhesion. They are rod-like proteins with a long extracellular part of variable length ending with the lectin domain,...
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Repressible Operon: trp Operon01:21

Repressible Operon: trp Operon

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The trp operon in Escherichia coli exemplifies a repressible operon. It regulates the synthesis of tryptophan through repressor-mediated transcriptional control and attenuation. This dual regulatory mechanism ensures tryptophan biosynthesis occurs only when needed, conserving cellular resources.Structure of the trp OperonThe trp operon consists of five structural genes (trpE, trpD, trpC, trpB, and trpA) that encode enzymes for tryptophan biosynthesis. These genes are transcribed as a single...
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相关实验视频

Updated: May 3, 2026

Real Time Measurements of Membrane Protein:Receptor Interactions Using Surface Plasmon Resonance SPR
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Real Time Measurements of Membrane Protein:Receptor Interactions Using Surface Plasmon Resonance SPR

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一个细胞表面受体的利波卡林24p3选择性介导细胞亡和铁的吸收.

Laxminarayana R Devireddy1, Claude Gazin, Xiaochun Zhu

  • 1Howard Hughes Medical Institute, Programs in Gene Function and Expression and Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.

Cell
|December 27, 2005
PubMed
概括

24p3受体 (24p3R) 调节细胞亡和铁水平. BCR-ABL coprotein 阻断了 24p3R,但是 imatinib 恢复了它,从而诱导了癌细胞的亡.

科学领域:

  • 细胞生物学 细胞生物学
  • 分子生物学分子生物学
  • 癌症研究 癌症研究

背景情况:

  • 鼠标的卡林24p3蛋白质参与了亡和铁运输.
  • 24p3 (24p3R) 的细胞表面受体以前没有表征.

研究的目的:

  • 克隆和表征24p3细胞表面受体 (24p3R).
  • 研究24p3R在铁运输和亡中的作用.
  • 探索24p3R,BCR-ABL蛋白和伊马替尼治疗之间的关系.

主要方法:

  • 对24p3R基因进行克隆.
  • 基于细胞的测试来评估铁的吸收和亡.
  • 对24p3,铁和BCR-ABL.反应中的基因表达的分析.
  • 用伊马替尼治疗BCR-ABL表达细胞.

主要成果:

  • 异位24p3R表达使细胞能够根据结合体铁含量控制铁含量和亡.
  • 含铁的24p3会增加细胞内铁;缺乏铁的24p3会诱导Bim和亡.
  • BCR-ABL激活24p3并抑制24p3R,导致对24p3.3的抵抗.
  • 伊马替尼抑制BCR-ABL,诱导BCR-ABL(+) 细胞中的24p3R表达和亡.

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Essential Metal Uptake in Gram-negative Bacteria: X-ray Fluorescence, Radioisotopes, and Cell Fractionation
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Essential Metal Uptake in Gram-negative Bacteria: X-ray Fluorescence, Radioisotopes, and Cell Fractionation
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结论:

  • 细胞内铁调节是新型亡途径的关键组成部分.
  • 这一途径与BCR-ABL诱导的骨髓增殖性疾病有关.
  • 准24p3R为BCR-ABL相关癌症提供了一个潜在的治疗策略.