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相关概念视频

GPCR Desensitization01:12

GPCR Desensitization

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G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
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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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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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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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相关实验视频

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加尔-3 阻断了PD-1 和 pembrolizumab 之间的结合.

Stinne Ravn Greisen1,2, Mia Bendix3, Morten Aagaard Nielsen4,2

  • 1Rheumatology, Aarhus University Hospital, Aarhus, Denmark srg@biomed.au.dk.

Journal for immunotherapy of cancer
|October 2, 2024
PubMed
概括

加勒-3 阻断了布罗利祖马布与PD-1 的结合,阻碍了转移性黑色素瘤的免疫反应. 瘤中高高的加勒-3与瘤的进展相关,而高血水平表明更长的生存期,这表明治疗反应中具有复杂的作用.

关键词:
生物标志物生物标志物免疫检查点抑制剂 免疫检查点抑制剂免疫治疗是一种免疫疗法.皮肤癌 皮肤癌 皮肤癌

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科学领域:

  • 免疫学 免疫学 免疫学
  • 在瘤学瘤学.
  • 生物化学 生化学

背景情况:

  • 免疫检查点抑制剂 (ICI) 改善了转移性恶性黑色素瘤 (MM) 的存活率.
  • 预测ICI反应的生物标记因某些患者的治疗耐药性至关重要.
  • 加勒-3 (Gal-3) 是ICI治疗的潜在生物标志物和治疗标.

研究的目的:

  • 在转移性MM中研究编程细胞死亡1 (PD-1),布罗利祖马布和Gal-3之间的相互作用.
  • 确定Gal-3是否影响pembrolizumab的疗效.
  • 探索Gal-3作为ICI治疗反应的预测生物标志物.

主要方法:

  • 表面等离子体共振 (SPR) 和低温电子显微镜 (cryo-EM) 用于可视化结合相互作用.
  • 在体外T细胞培养物中评估细胞因子的产生.
  • 用pembrolizumab治疗的转移性MM患者的可溶性PD-1和Gal-3水平的测量.

主要成果:

  • 证明Gal-3可以通过固体抑制来阻止PD-1和pembrolizumab的结合.
  • -3降低了T细胞促炎性细胞因子的产生,不受 pembrolizumab 的影响.
  • 高瘤Gal-3与疾病进展相关,而高血Gal-3与更长的无进展生存相关.
  • 可溶性PD-1水平在佩姆布里祖马布治疗后增加,与疾病进展相关.

结论:

  • PD-1和Gal-3之间的相互作用干扰着pembrolizumab的结合.
  • 瘤微环境中的Gal-3诱导的免疫抑制不能被 pembrolizumab 克服.
  • 在ICI治疗结果方面,Gal-3在血和瘤组织中表现出不同的作用.