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Receptor-mediated Endocytosis

Receptor-mediated Endocytosis

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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Updated: Jun 14, 2025

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance

Published on: January 3, 2012

艰难的Clostridioides的毒性需要高效的霍林中介毒素分泌.

Nicholas V DiBenedetto^1,2, Marine Oberkampf³, Aline Crouzols³

¹Massachusetts Host-Microbiome Center, Department Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

|June 11, 2025

概括

类似霍林的蛋白TcdE对于释放来自Clostridioides difficile的毒素至关重要. 移除TcdE通过防止毒素分泌来保护小鼠免受致命的感染.

关键词:

细菌学细菌学是一门学科.生物科学生物科学微生物学微生物学自然科学自然科学

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Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291

Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291

Published on: December 10, 2016

相关实验视频

Last Updated: Jun 14, 2025

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance

Published on: January 3, 2012

Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells

Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells

Published on: August 19, 2016

Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291

Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291

Published on: December 10, 2016

科学领域:

微生物学微生物学
病原体生物学病原体生物学
分子机制的分子机制

背景情况:

困难类 Clostridioides 通过 TcdA 和 TcdB 毒素引起伪膜性结肠炎.
这些毒素缺乏标准的分泌信号,这意味着有替代的释放途径.
潜在的机制包括TcdE介导的分泌或细胞溶解的被动释放.

研究的目的:

研究霍林类蛋白TcdE在Clostridioides difficile毒素分泌中的作用.
在体内确定TcdE对毒性和宿主疾病的贡献.
阐明高毒素产生的菌株中毒素释放的机制.

主要方法:

在高毒素产生的C. difficile菌株 (UK1和VPI10463) 中,tcdE基因的遗传删除.
评估毒素分泌水平,独立于细胞溶解.
使用易受感染的 gnotobiotic 小鼠的感染模型来评估毒性和存活率.

主要成果:

删除tcdE显著减少了两种测试菌株的毒素分泌.
在感染DtcdE突变的小鼠中,毒素水平无法检测.
被 ΔtcdE 突变病毒感染的小鼠,尽管有活性的毒素基因表达,但仍能长期存活.

结论:

在生物体内,TcdE霍林在Clostridioides difficile毒素分泌中起着主导作用.
TcdE介导的分泌是毒性Clostridia中保存的,非的机制.
向TcdE代表了对抗C. difficile感染的潜在治疗策略.