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The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
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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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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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通过炎症介导的皮肤反应

Tugce Boran1, Özce Pala Çamlı2, Mahmoud Abudayyak3

  • 1Department of Pharmaceutical Toxicology, Faculty of Pharmacy, İstanbul University Cerrahpaşa, İstanbul, Türkiye.

Toxicology letters
|August 27, 2025
PubMed
概括
此摘要是机器生成的。

一种乳腺癌药物Abemaciclib可以引起皮肤反应. 这项研究发现,低剂量通过氧化性炎症诱导人体皮肤细胞的细胞死亡,而高剂量则无效. 需要进一步的研究.

关键词:
阿贝马西克利布细胞毒性炎症发生激酶抑制剂氧化应激

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科学领域:

  • 药理学和毒理学
  • 皮肤病学
  • 癌症学

背景情况:

  • 阿贝马西克是FDA批准的用于治疗晚期和转移性乳腺癌的循环依赖激酶 (CDK) 抑制剂.
  • 皮肤不良反应如皮肤炎与abemaciclib有关,但细胞机制尚不清楚.
  • 了解abemaciclib的细胞效应对于管理其副作用概况至关重要.

研究的目的:

  • 为了研究由abemaciclib引起的皮肤反应的细胞机制.
  • 评估abemaciclib在人类角质细胞中的细胞毒性,亡性,氧化压力和炎症诱导潜力.

主要方法:

  • 用不同度的abemaciclib (0 - 10μM) 治疗人类角质细胞 (HaCaT) 24小时.
  • 进行了检测,以评估细胞毒性 (IC50),细胞亡/死亡,氧化应激标志物和炎症媒介分泌物 (MCP-1,IL-6,IL-8,TNF-α).

主要成果:

  • 亚贝马西基布诱导的细胞毒性与IC50≥24. 18μM.
  • 低度 (0. 1μM) 显著诱导了亡,氧化损伤和炎症媒介 (MCP-1,IL-6,IL-8,TNF-α) 的分泌量增加.
  • 较高度 (1- 10μM) 对这些细胞参数的影响较小或不显著,TNF-α在5μM时增加,但在10μM时减少.

结论:

  • 通过氧化性炎症可能导致细胞死亡,特别是在低度时.
  • 观察到的效果取决于度,在0. 1μM时发现显著的细胞影响,在较高度时效果降低.
  • 这些发现强调需要对abemaciclib的风险概况进行全面研究,并鼓励对其细胞机制进行进一步研究.