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相关概念视频

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...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

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相关实验视频

Updated: Jun 21, 2026

Peptide-based Identification of Functional Motifs and their Binding Partners
14:28

Peptide-based Identification of Functional Motifs and their Binding Partners

Published on: July 1, 2013

人类类可以通过干扰巴克斯激活来抑制亡.

Bin Guo1, Dayong Zhai, Edelmira Cabezas

  • 1The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA.

Nature
|May 7, 2003
PubMed
概括

人类素 (HN),一种抗亡性,与Bax结合,阻止其激活和转移到线粒体. 这一发现揭示了调节编程细胞死亡的新机制,并提供了对线粒体保护的见解.

科学领域:

  • 细胞生物学 细胞生物学
  • 分子生物学分子生物学
  • 遗传学 遗传学 是一个

背景情况:

  • 巴克斯 (Bcl2关联X蛋白) 是一种促细胞亡的蛋白质,对编程细胞死亡至关重要.
  • 巴克斯激活涉及结构变化和转移到线粒体膜,导致细胞染色体c的释放.
  • 人们对巴克斯激活的调节仍然不完全理解.

研究的目的:

  • 为了研究BAX和humanin (HN) 之间的相互作用,一个抗apoptotic.
  • 阐明HN在调节巴克斯介导的亡中的作用.
  • 探索线粒体编码的人类细胞的起源和功能.

主要方法:

  • 同免疫沉测定检测巴克斯-HN相互作用.
  • 小干扰RNA (siRNA) 减少HN表达.
  • 细胞测试以评估巴克斯转位和细胞染色体c释放.
  • 在体外实验中使用孤立的线粒体进行实验.

主要成果:

  • 人类素 (HN) 与Bax直接相互作用,抑制其从细胞质转移到线粒体的转移.
  • 由siRNA减少的HN表达增强了Bax转位,并使细胞对细胞亡敏感.
  • HN可以抑制巴克斯与分离的线粒体的结合,并抑制在体内细胞染色体c的释放.

更多相关视频

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Subcellular Fractionation for ERK Activation Upon Mitochondrial-derived Peptide Treatment
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Subcellular Fractionation for ERK Activation Upon Mitochondrial-derived Peptide Treatment

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相关实验视频

Last Updated: Jun 21, 2026

Peptide-based Identification of Functional Motifs and their Binding Partners
14:28

Peptide-based Identification of Functional Motifs and their Binding Partners

Published on: July 1, 2013

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Subcellular Fractionation for ERK Activation Upon Mitochondrial-derived Peptide Treatment
07:55

Subcellular Fractionation for ERK Activation Upon Mitochondrial-derived Peptide Treatment

Published on: September 25, 2017

  • 一个线粒体开放的读取框架编码了一个人体的变体,也抑制了Bax.
  • 结论:

    • 人类素 (HN) 通过防止巴克斯激活,作为巴克斯诱导的亡的关键调节剂.
    • HN抑制Bax的能力为线粒体提供了一种保护机制.
    • 这些发现表明,HN可能起源于线粒体,并转移到核基因组.