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相关概念视频

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Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
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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...
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When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
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富林类型的蛋白转化酶是膜类型矩阵金属蛋白酶-pro-matrix金属蛋白酶-2蛋白质溶解级联在动脉样硬化中的中央调节者.

Philipp Stawowy1, Heike Meyborg, Dietger Stibenz

  • 1Department of Medicine/Cardiology, Deutsches Herzzentrum Berlin, Augustenburger Platz 1, D-13353 Berlin, Germany. stawowy@dhzb.de

Circulation
|May 25, 2005
PubMed
概括

巨细胞利用MT1-MMP和类似的酶 (和PC5) 来激活亲MMP-2,这是动脉样硬化的关键过程. 这些酶存在于动脉样硬化斑块内的人类单细胞和巨细胞中.

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科学领域:

  • 生物化学 生物化学
  • 细胞生物学 细胞生物学
  • 免疫学 免疫学 免疫学

背景情况:

  • 巨细胞积累和矩阵金属蛋白酶 (MMP) 表达影响斑块稳定性.
  • 膜结合的MT1-MMP的激活,对于亲MMP-2激活至关重要,需要细胞内裂变由类蛋白质转化酶 (PCs),如和PC5.

研究的目的:

  • 研究MT1-MMP和类PC在单核炎性细胞中的作用.
  • 探索MT1-MMP的激活机制及其对亲MMP-2的下游影响.

主要方法:

  • 单细胞衍生的巨细胞分化和刺激.
  • 使用decanoyl-RVKR-chloromethylketone (dec-CMK) 和小干扰RNA (siRNA) 抑制类PC.
  • 流细胞计和免疫组织化学检测酶表达和定位.

主要成果:

  • 巨细胞分化增加了furin,PC5和MT1-MMP的表达.
  • 巨MT1-MMP从血管光滑肌细胞激活了pro-MMP-2,这种效应被dec-CMK或furin siRNA抑制.
  • 富林,PC5和MT1-MMP在人体循环单细胞中被发现,并在动脉样硬化病变内的巨细胞中结合.

结论:

  • 富林类PCs (furin和PC5) 是MT1-MMP-MMP-2级联的核心,使得巨细胞MT1-MMP能够激活细胞外亲MMP-2.
  • 这些酶在人类动脉样硬化斑块中的表达和同位化表明它们是动脉样硬化的潜在治疗标.