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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 transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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库尔库利戈酸上调调节BMAL1以通过抑制JAK/STAT3通路来降低细胞核亡的细胞亡.

Linchuan Lei1, Hua Wang2, Zhuoyang Zhao1

  • 1Department of Spine Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, PR China; Guangdong Province Key Laboratory of Orthopedics and Traumatology, Guangzhou 510080, PR China; Laboratory of General Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, PR China.

Osteoarthritis and cartilage
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PubMed
概括

库尔库利戈 (CUR) 通过上调BMAL1,减少细胞亡和改善细胞外基质来缓解椎间盘退化 (IVDD). 这为IVDD提供了一个新的治疗策略.

关键词:
细胞灭亡 (apoptosis) 是一种死亡的过程.在BMAL1中,库尔库利戈化物 (curculigoside) 是一种椎间盘退化 椎间盘退化

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科学领域:

  • 生物化学 生物化学
  • 分子生物学分子生物学
  • 再生医学是一种再生医学.

背景情况:

  • 椎间盘退化 (IVDD) 是一个常见的衰老过程,也是腰部疼痛的主要原因.
  • 基本螺旋环螺旋ARNT样1 (BMAL1) 涉及到各种疾病病理.
  • 库尔库利戈 (CUR) 在疾病背景下被研究其潜在的抗丧性质.

研究的目的:

  • 研究BMAL1在IVDD中的作用.
  • 探索CUR在缓解IVDD方面的治疗潜力.
  • 阐明CUR对IVDD的影响背后的分子机制.

主要方法:

  • RNA测序 (RNA-seq) 用于识别失调的基因.
  • 西部涂抹 (WB),免疫组织化学和免疫光 (IF) 来评估BMAL1的表达.
  • 流细胞计和基于细胞的测试,以评估细胞核细胞核 (NP) 细胞中的亡和细胞外矩阵 (ECM) 组成部分.
  • 使用BMAL1-Knockout和IVDD小鼠模型的体内研究,以及CUR注射的治疗评估.

主要成果:

  • 在退行性NP细胞中,BMAL1表达与IVDD严重程度相反相关,在退行性NP细胞中较低.
  • 通过BMAL1的淘汰,增加了NP细胞的亡,而过度表达则减少了它.
  • 通过通过JAK-STAT3通路抑制STAT3酸化,CUR治疗上调了BMAL1.
  • CUR治疗缓解了NP细胞亡和增强了ECM的产生,从而减轻了IVDD.

结论:

  • 通过对BMAL1.1进行上调调节,CUR有效地抑制了亡并增强了IVDD中的ECM产生.
  • 这种机制为炎症诱导的IVDD提供了一个新的治疗途径.
  • 这些发现强调了CUR作为管理IVDD的潜在治疗剂.