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Related Concept Videos

DNA Replication02:40

DNA Replication

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DNA replication involves the separation of the two strands of the double helix, with each strand serving as a template from which the new complementary strand is copied.  After replication, each double-stranded DNA includes one parental or “old” strand and one “new” strand. This is known as semiconservative replication. The resulting DNA molecules have the same sequence and are divided equally into the two daughter cells.
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The DNA Replication Fork01:02

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An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
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S-Cdk Initiates DNA Replication02:38

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The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
Two states at the origin of replication
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Chromosome Replication02:31

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Before a cell can divide, it must accurately replicate all of its chromosomes, including the DNA and its associated histone and non-histone proteins.  This process begins at numerous origins of replication during the S phase of the cell cycle in each of a cell’s chromosomes simultaneously. Certain nucleotides can act as origins of replication, but these sequences are not well defined - especially in complex, multi-cellular, eukaryotic species. The length of DNA that spans an origin...
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Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
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Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions

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Challenges to DNA replication in hypoxic conditions.

Natalie Ng1, Karin Purshouse1, Iosifina P Foskolou1

  • 1Department of Oncology, CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, UK.

The FEBS Journal
|December 31, 2017
PubMed
Summary
This summary is machine-generated.

Hypoxia, or insufficient oxygen, causes therapy-resistant tumors. This resistance stems from replication stress and DNA damage responses, even without detectable DNA damage, impacting cancer treatment.

Keywords:
DNA damage responsehypoxiareoxygenationreplication restartreplication stressribonucleotide reductase

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Area of Science:

  • Oncology
  • Molecular Biology
  • Radiotherapy

Background:

  • Hypoxia is defined as insufficient oxygen availability, encompassing various concentration levels.
  • Tumor regions near necrosis exhibit anoxic conditions, leading to extreme therapy resistance, termed radiobiological hypoxia.

Purpose of the Study:

  • To discuss the causes and consequences of hypoxia-induced replication stress.
  • To explore the biological response to radiobiological hypoxia in cancer therapy.

Main Methods:

  • Review of existing literature on tumor hypoxia and its biological effects.
  • Analysis of DNA damage response pathways activated under hypoxic conditions.

Main Results:

  • Radiobiological hypoxia triggers rapid replication stress and DNA damage responses.
  • ATR- and ATM-mediated signaling pathways are activated despite the absence of detectable DNA damage.

Conclusions:

  • Hypoxia-induced replication stress is a critical factor in radiobiological resistance.
  • Understanding these mechanisms is crucial for improving cancer treatment strategies.