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Prokaryotic cells01:51

Prokaryotic cells

Prokaryotes are small unicellular organisms that include the domains—Archaea and Bacteria. Bacteria include many common organisms, such as Salmonella and E. coli, while the Archaea include extremophiles that live in harsh environments, such as volcanic springs.Like eukaryotic cells, all prokaryotic cells are surrounded by a plasma membrane, have genetic material in the form of single, circular DNA, a cytoplasm that fills the interior of the cell, and ribosomes that synthesize proteins. However,...
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Prokaryotes are small unicellular organisms that include the domains — Archaea and Bacteria. Bacteria include many common microorganisms, such as Salmonella and E. coli, while the Archaea include extremophiles that live in harsh environments, such as volcanic springs.
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High-throughput Screening for Protein-based Inheritance in S. cerevisiae
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Prions.

David W Colby1, Stanley B Prusiner

  • 1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143, USA.

Cold Spring Harbor Perspectives in Biology
|March 23, 2011
PubMed
Summary
This summary is machine-generated.

Prions are infectious proteins that cause fatal neurodegenerative diseases like Creutzfeldt-Jakob disease (CJD). They convert normal prion proteins (PrP(C)) into disease-causing forms (PrP(Sc)) through conformational changes.

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Area of Science:

  • Neurobiology
  • Infectious Diseases
  • Molecular Biology

Background:

  • The discovery of prions, infectious proteins, challenged established biological principles.
  • Prion diseases, such as Creutzfeldt-Jakob disease (CJD), are characterized by neurodegeneration and lethality.
  • Mammalian prions propagate by converting normal cellular prion proteins (PrP(C)) into abnormal, disease-associated isoforms (PrP(Sc)).

Purpose of the Study:

  • To introduce the concept of prions and the diseases they cause.
  • To explain the mechanism of prion replication and disease pathogenesis.
  • To highlight the structural differences between PrP(C) and PrP(Sc).

Main Methods:

  • Review of historical discoveries in genetics and infectious agents.
  • Analysis of structural differences between normal and abnormal prion protein isoforms.
  • Explanation of the conformational conversion process.

Main Results:

  • Prions, unlike DNA or conventional pathogens, are proteinaceous infectious agents.
  • PrP(Sc) isoforms possess distinct secondary structures (rich in beta-sheet) compared to PrP(C) (rich in alpha-helix).
  • The conformational conversion of PrP(C) to PrP(Sc) is the central event in prion disease development.

Conclusions:

  • Prion diseases represent a unique class of infectious disorders.
  • Understanding prion structure and conversion is key to addressing these neurodegenerative conditions.
  • This article provides a foundational overview of prions for researchers and clinicians.