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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...
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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

6.3K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.3K
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
Caspases01:24

Caspases

12.4K
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...
12.4K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.8K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.8K
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

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相关实验视频

Updated: Jun 14, 2025

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
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Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

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TRIM2:一种双刃剑,可以防止细胞亡.

Thomas Hollemann1

  • 1Institute for Physiological Chemistry, Martin-Luther-University Halle-Wittenberg, Germany.

The FEBS journal
|December 2, 2024
PubMed
概括

这项研究揭示了TRIM2蛋白通过两个不同的机制抑制细胞亡:激活脂肪酸吸收能量和降解亲细胞亡蛋白. 这种双重功能对于饥饿期间的细胞生存至关重要.

科学领域:

  • 细胞生物学 细胞生物学
  • 细胞死亡的分子机制
  • 代谢调节 代谢调节 代谢调节

背景情况:

  • 三方基因含有蛋白2 (TRIM2) 是一种属于TRIM-NHL类的泛素E3酶.
  • TRIM2已涉及抑制亡,但其精确的机制仍在研究中.
  • 细胞压力,如谷氨酸缺乏,可以触发细胞亡.

研究的目的:

  • 阐明TRIM2在抑制亡中的双重功能.
  • 研究TRIM2在饥饿条件下调节细胞代谢中的作用.
  • 了解氨酸缺乏期间TRIM2转录如何调节.

主要方法:

  • 在缺乏谷氨胺的情况下,对ATF4的TRIM2转录激活的分析.
  • 研究TRIM2与CPT1 (卡尼丁棕转移酶1) 的相互作用.
  • 对TRIM2的E3无素结合酶活性对亲细胞亡的BIM蛋白的评估.

主要成果:

  • 在谷氨酸缺乏期间,ATF4会激活TRIM2转录.
  • TRIM2通过直接激活CPT1,独立于其结合酶活性来增强长脂肪酸进入线粒体的吸收.
  • 此外,TRIM2还通过其E3无素结合酶活性通过向蛋白质体降解的亲位BIM来抑制亡.
关键词:
在ATF4中使用ATF4.在TRIM2中,TRIM2是TRIM2.灭症 (apoptosis) 是一种死亡的过程.谷氨胺是一种胺.蛋白质酶体蛋白质组是什么饥饿 饥饿 饥饿 饥饿 饥饿

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Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries
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Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

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相关实验视频

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Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

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Establishing Cell Lines Overexpressing DR3 to Assess the Apoptotic Response to Anti-mitotic Therapeutics
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Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries
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Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

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结论:

  • TRIM2采用双重策略来预防亡:增强能量代谢和促进亲亡因素的降解.
  • TRIM2刺激能量代谢的能力独立于其E3无素结合酶功能.
  • 这些发现凸显了TRIM2作为在代谢压力下细胞存活的关键调节者.