Jove
Visualize
联系我们
JoVE
x logofacebook logolinkedin logoyoutube logo
关于 JoVE
概览领导团队博客JoVE 帮助中心
作者
出版流程编辑委员会范围与政策同行评审常见问题投稿
图书馆员
用户评价订阅访问资源图书馆顾问委员会常见问题
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experiments存档
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教师资源中心教师网站
使用条款与条件
隐私政策
政策

相关概念视频

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

5.7K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.7K
The Nucleolus02:55

The Nucleolus

8.7K
The nucleolus is the most prominent substructure of the nucleus. When it was first discovered, it was considered to be an isolated organelle that forms fibrils and granules. In 1931, the relationship between the nucleolus and chromosomes was first described by Heitz. He observed that the appearance and size of nucleolus varies depending on the stage of the cell cycle. He also noticed constricted regions on different chromosomes clustered together at definite cell cycle stages. These regions,...
8.7K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

6.4K
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...
6.4K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

11.8K
Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
11.8K
Abnormal Proliferation02:23

Abnormal Proliferation

4.5K
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...
4.5K
The Tumor Microenvironment02:17

The Tumor Microenvironment

6.6K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
6.6K

您也可能阅读

相关文章

通过共同作者、期刊和引用图与本文相关的文章。

排序
Same author

Arylsulfatase L is a Golgi chondroitin sulfatase regulating skeletal development.

The Journal of biological chemistry·2026
Same author

Arylsulfatase I is a novel lysosomal chondroitin endosulfatase regulating endochondral ossification.

Matrix biology : journal of the International Society for Matrix Biology·2026
Same author

Development and characterization of a model of mucopolysaccharidosis type IVA for evaluating therapies targeting bone disease.

Disease models & mechanisms·2026
Same author

Author Correction: Defective CFTR induces aggresome formation and lung inflammation in cystic fibrosis through ROS-mediated autophagy inhibition.

Nature cell biology·2026
Same author

TFEB coordinates autophagosome biogenesis and ribophagy during starvation via SQSTM1.

Science advances·2026
Same author

A matter of selectivity: ER-phagy suppression at the onset of pancreatic cancer.

Developmental cell·2025

相关实验视频

Updated: Jun 14, 2025

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel
08:29

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Published on: May 14, 2018

9.9K

癌症中的微核崩机制

Marianna Maddaluno1,2, Carmine Settembre1,2

  • 1Telethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.

Science (New York, N.Y.)
|August 29, 2024
PubMed
概括
此摘要是机器生成的。

氧化损伤导致核膜破裂,导致DNA修复中的错误. 这种细胞损伤与各种疾病和衰老过程有关.

更多相关视频

One-step Protocol for Evaluation of the Mode of Radiation-induced Clonogenic Cell Death by Fluorescence Microscopy
06:47

One-step Protocol for Evaluation of the Mode of Radiation-induced Clonogenic Cell Death by Fluorescence Microscopy

Published on: October 23, 2017

11.2K
Combining 3D Magnetic Force Actuator and Multi-Functional Fluorescence Imaging to Study Nucleus Mechanobiology
06:54

Combining 3D Magnetic Force Actuator and Multi-Functional Fluorescence Imaging to Study Nucleus Mechanobiology

Published on: July 5, 2022

2.3K

相关实验视频

Last Updated: Jun 14, 2025

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel
08:29

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Published on: May 14, 2018

9.9K
One-step Protocol for Evaluation of the Mode of Radiation-induced Clonogenic Cell Death by Fluorescence Microscopy
06:47

One-step Protocol for Evaluation of the Mode of Radiation-induced Clonogenic Cell Death by Fluorescence Microscopy

Published on: October 23, 2017

11.2K
Combining 3D Magnetic Force Actuator and Multi-Functional Fluorescence Imaging to Study Nucleus Mechanobiology
06:54

Combining 3D Magnetic Force Actuator and Multi-Functional Fluorescence Imaging to Study Nucleus Mechanobiology

Published on: July 5, 2022

2.3K

科学领域:

  • 细胞生物学
  • 遗传学
  • 分子生物学

背景情况:

  • 氧化损伤是细胞功能障碍的一个关键因素.
  • 微核形成与基因组不稳定性有关.
  • 正确的DNA修复机制对于维持细胞健康至关重要.

研究的目的:

  • 研究氧化损伤对微核膜完整性的影响.
  • 阐明膜破裂对微核中的DNA修复过程的影响.

主要方法:

  • 使用暴露于氧化应激的细胞培养模型.
  • 使用先进的显微镜技术可视化微核膜动态.
  • 通过特定的分子标记来评估DNA修复活性.

主要成果:

  • 氧化应激导致显著的微核膜破裂.
  • 破裂的微核显示出DNA修复能力受损.
  • 微核中的缺陷修复与基因组不稳定性增加相关.

结论:

  • 微核膜的完整性对于有效的DNA修复至关重要.
  • 氧化损伤损害了这种完整性,导致故障修复.
  • 这些发现突出了导致疾病发病的新机制.