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相关概念视频

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
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

7.3K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
7.3K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

4.7K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
4.7K
Negative Regulator Molecules01:23

Negative Regulator Molecules

35.2K
Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
35.2K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.1K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.7K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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相关实验视频

Updated: Jun 11, 2025

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

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瘤抑制剂p53控制胸膜NKT17的发育.

Sofia Celli, Masashi Watanabe, Richard J Hodes

    bioRxiv : the preprint server for biology
    |October 7, 2024
    PubMed
    概括

    瘤抑制剂p53特别控制胸膜不变天然杀手T-17 (iNKT17) 细胞的发展. 失去p53会增加iNKT17细胞,这些细胞表现出增强的DNA损伤反应,这表明它在基因组稳定性中的作用.

    科学领域:

    • 免疫学 免疫学 免疫学
    • 细胞生物学 细胞生物学
    • 癌症生物学 癌症生物学

    背景情况:

    • 已知瘤抑制剂p53可以抑制瘤发生.
    • 它在T细胞生物学中的确切作用,包括胸膜T细胞的发育,仍然不完全理解.
    • 不变的自然杀手T (iNKT) 细胞是内在的类似T细胞,在胸腺中发育,包括NKT1,NKT2和NKT17子集.

    研究的目的:

    • 研究瘤抑制剂p53在不同不变的自然杀手T (iNKT) 细胞子集的发展中的作用.
    • 为了确定p53表达是否特定于某些iNKT细胞群.
    • 探索p53,DNA损伤和iNKT17细胞发育之间的关系.

    主要方法:

    • 分析不同胸膜T细胞种群中的p53表达水平.
    • 在野生型与p53缺乏的小鼠中对iNKT细胞子集发展的比较分析.
    • 在iNKT细胞子集中评估细胞因子生产和DNA损伤标记物 (γH2AX).

    主要成果:

    • 与其他T细胞群相比,p53在甲状腺NKT17细胞中表达高.
    • 在T细胞中失去p53有选择地增加了胸膜NKT17细胞的数量,而不会影响NKT1,NKT2或常规T细胞.
    • NKT17细胞表现出更高的基底γH2AX表达,表明DNA损伤,在p53缺乏的NKT17细胞中进一步升高.

    更多相关视频

    Derivation of Thymic Lymphoma T-cell Lines from Atm-/- and p53-/- Mice
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    Examination of Thymic Positive and Negative Selection by Flow Cytometry
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    Examination of Thymic Positive and Negative Selection by Flow Cytometry

    Published on: October 8, 2012

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    Yeast As a Chassis for Developing Functional Assays to Study Human P53
    14:57

    Yeast As a Chassis for Developing Functional Assays to Study Human P53

    Published on: August 4, 2019

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    Derivation of Thymic Lymphoma T-cell Lines from Atm-/- and p53-/- Mice
    17:59

    Derivation of Thymic Lymphoma T-cell Lines from Atm-/- and p53-/- Mice

    Published on: April 3, 2011

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    Examination of Thymic Positive and Negative Selection by Flow Cytometry
    14:29

    Examination of Thymic Positive and Negative Selection by Flow Cytometry

    Published on: October 8, 2012

    21.8K

    结论:

    • 瘤抑制剂p53在甲状腺NKT17细胞发育中发挥着特定的调节作用.
    • 缺少p53导致NKT17细胞的扩张,与增加的DNA损伤反应有关.
    • 这些发现表明p53在胸膜发育过程中控制NKT17细胞系内的基因组不稳定性.