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相关概念视频

The Intrinsic Apoptotic Pathway01:31

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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...
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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...
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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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Mitochondrial protein import is powered by two distinct energy sources: ATP hydrolysis and electrochemical potential across the inner membrane. Newly synthesized precursors are bound by cytosolic chaperones of the Hsp70 family, which guide them to the import receptors on the mitochondrial surface. Utilizing the energy of ATP hydrolysis, Hsp70 chaperones transfer these precursors to the TOM receptors on the mitochondrial outer membrane.
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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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相关实验视频

Updated: Jun 29, 2025

Differentiation and Imaging of Brown Adipocytes from the Stromal Vascular Fraction of Interscapular Adipose Tissue from Newborn Mice
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棕色脂肪组织通过Syntaxin 4依赖性热灭菌途径的卷入.

Xiaofan Yu1,2, Gabrielle Benitez1,2, Peter Tszki Wei3

  • 1Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, 10461, USA.

Nature communications
|April 2, 2024
PubMed
概括

老龄化导致棕色脂肪组织 (BAT) 损失. 恢复合成素4 (STX4) 或抑制热灭可以防止这种下降,揭示了热原性功能障碍的关键机制.

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Visualization and Quantification of Brown and Beige Adipose Tissues in Mice using [18F]FDG Micro-PET/MR Imaging
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相关实验视频

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科学领域:

  • 代谢过程中的代谢.
  • 细胞生物学 细胞生物学
  • 衰老研究研究 衰老研究

背景情况:

  • 棕色脂肪组织 (BAT) 卷积,以减少质量和功能为标志,随着衰老,高脂肪饮食或热中性住房发生.
  • 这种卷入涉及增加的脂质液滴大小和特定的Ucp1-低棕色脂肪细胞群体,表现出热和减少的合成素4 (STX4).

研究的目的:

  • 调查STX4和热病在衰老和发热功能障碍期间棕色脂肪组织卷积中的作用.
  • 确定将STX4缺乏与BAT功能受损和热症联系起来的机制.

主要方法:

  • 在老老鼠中单核RNA测序是BAT.
  • 基因操纵 (Ucp1-STX4KO小鼠) 来研究STX4缺乏症.
  • 评估BAT质量,热生成活性,热灭菌标记物和代谢途径 (氧化酸化,葡萄糖吸收,糖解).

主要成果:

  • 陈旧的棕色脂肪细胞和Ucp1-STX4KO小鼠表现出减少的BAT质量,热能功能障碍和增加的热亡.
  • 恢复STX4表达或抑制热致死改善了与年龄相关的BAT下降和功能障碍.
  • 缺乏STX4会损害氧化酸化,葡萄糖吸收和糖解,导致ATP水平降低并触发热.

结论:

  • 生理衰老和发热功能障碍是由棕色脂肪细胞中 pyroptotic 信号激活驱动的.
  • STX4在保持BAT质量和功能的过程中起着至关重要的作用,其缺乏会通过热致死促进进化.
  • 针对热或恢复STX4为与年龄相关的代谢衰退提供了潜在的治疗策略.