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Related Concept Videos

Translation01:31

Translation

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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 Life
Proteins are...
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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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Amyloid Fibrils03:03

Amyloid Fibrils

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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
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Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

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Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show...
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[MicroRNAs and polyglutamine diseases].

Li Zhang1, Hong Jiang

  • 1Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China. jianghong73868@yahoo.com.cn.

Zhonghua Yi Xue Yi Chuan Xue Za Zhi = Zhonghua Yixue Yichuanxue Zazhi = Chinese Journal of Medical Genetics
|December 12, 2013
PubMed
Summary
This summary is machine-generated.

Polyglutamine (PolyQ) diseases are inherited neurodegenerative disorders. MicroRNAs show promise in understanding PolyQ disease progression and developing new therapies.

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Area of Science:

  • Neurodegenerative diseases
  • Genetics
  • Molecular biology

Context:

  • Polyglutamine (PolyQ) diseases are a group of inherited neurodegenerative disorders.
  • These diseases share a common mechanism involving expanded CAG trinucleotide repeats.
  • Clinical features and genetic heterogeneity vary among PolyQ diseases, with no specific treatments currently available.

Purpose:

  • To review the roles of microRNAs in the pathogenesis of PolyQ diseases.
  • To explore the potential therapeutic applications of microRNAs for PolyQ diseases.

Summary:

  • MicroRNAs are emerging as significant post-transcriptional regulators affecting PolyQ disease progression.
  • This review focuses on how microRNAs influence the development and advancement of Polyglutamine diseases.
  • The discussion highlights the potential of microRNAs as therapeutic targets.

Impact:

  • Provides a comprehensive overview of microRNA involvement in PolyQ disease pathogenesis.
  • Highlights novel therapeutic strategies targeting microRNAs for neurodegenerative disorders.
  • Contributes to the understanding of genetic heterogeneity and treatment development for PolyQ diseases.