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相关概念视频

Nonsense-mediated mRNA Decay02:27

Nonsense-mediated mRNA Decay

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The Upf proteins that carry out nonsense-mediated decay (NMD) are found in all eukaryotic organisms, including humans. Each protein has an individual role, but they need to work in collaboration. Upf1 is an ATP-dependent RNA helicase that unwinds the RNA helix. Because Upf1 can unwind any RNA, Upf2 and Upf3 are required to help Upf1 discriminate between nonsense and normal mRNAs.
Usually, Upf3 binds to an Exon Junction Complex (EJC) at mRNA splice sites. If a ribosome fully translates the mRNA,...
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Translation01:31

Translation

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Lesson: Translation
Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
Translation Produces the Building Blocks of...
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Alternative RNA Splicing02:18

Alternative RNA Splicing

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Alternative RNA splicing is the regulated splicing of exons and introns to produce different mature mRNAs from a single pre-mRNA. Unlike in constitutive splicing where a single gene produces a single type of mRNA, alternative splicing allows an organism to produce multiple proteins from a single gene and plays an important role in protein diversity.
There are five types of alternative RNA splicing that vary in the ways the pre-mRNA segments are removed or retained in the mature mRNA. The first...
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Restarting Stalled Replication Forks02:37

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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
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相关实验视频

Updated: May 20, 2025

Assay to Measure Nucleocytoplasmic Transport in Real Time within Motor Neuron-like NSC-34 Cells
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Assay to Measure Nucleocytoplasmic Transport in Real Time within Motor Neuron-like NSC-34 Cells

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C9ORF72聚PR通过SRSF7破坏了ALS/FTD相关的STMN2通过SRSF7表达.

Karen S Wang1,2, Julie Smeyers1,2, Kevin Eggan3,4

  • 1Institute for Neurodegenerative Diseases, University of California, San Francisco, CA, USA.

Acta neuropathologica communications
|March 27, 2025
PubMed
概括

C9ORF72的重复扩张会导致神经退行性疾病,如ALS和FTD. 反感性聚PR破坏RNA结合蛋白,减少STMN2并损害轴突修复.

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科学领域:

  • 神经科学是一个神经科学.
  • 遗传学 遗传学 是一个
  • 分子生物学分子生物学

背景情况:

  • C9ORF72 六核酸重复扩张是肌缩侧面硬化症 (ALS) 和前性痴呆症 (FTD) 的主要遗传原因.
  • 由这种扩张产生的二重复蛋白 (DPR) 有毒的功能增益效应,但它们的神经毒性的确切机制尚不清楚.

研究的目的:

  • 研究DPRs,特别是聚烯-氨酸-氨酸 (聚PR) 导致神经退行的分子机制.
  • 确定聚PR的细胞点及其在神经元功能障碍中的作用,特别是轴突再生.

主要方法:

  • 使用人类诱导的多能干细胞 (iPSC) 衍生的神经元.
  • 采用全球基蛋白学来识别聚PR相互作用蛋白.
  • 研究了特定RNA结合蛋白 (RBPs) 和STMN2在轴突再生缺陷中的作用.

主要成果:

  • 发现Poly-PR可以抑制来自iPSC的神经元的轴突再生.
  • 聚PR可以选择性地扰乱核RNA结合蛋白 (RBPs).
  • 耗尽SRSF7,一个RBP,降低了STMN2水平和受损的轴突再生,被外源性STMN2拯救.

结论:

  • 反传感重复编码的聚PR破坏了RBPs,特别是SRSF7,导致STMN2.2的减少.
  • 这种机制将DPR功能增长与STMN2功能丧失表型联系起来,解释了C9ORF72相关的神经退行症中轴突修复缺陷.