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Related Concept Videos

Base Excision Repair01:54

Base Excision Repair

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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...
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Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

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Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
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Nucleotide Excision Repair01:08

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Overview
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Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
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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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Related Experiment Videos

Arginase-mediated "field" defects in AML.

Guido Marcucci1

  • 1Ohio State University Comprehensive Cancer Center.

Blood
|August 3, 2013
PubMed
Summary
This summary is machine-generated.

Acute myeloid leukemia (AML) blasts can suppress the immune system and blood cell development via high arginase II activity. This finding offers new insights into AML resistance mechanisms and potential therapeutic targets.

Related Experiment Videos

Area of Science:

  • Hematology
  • Immunology
  • Oncology

Background:

  • Acute myeloid leukemia (AML) is a complex and heterogeneous disease with significant treatment challenges.
  • Current therapies, including chemotherapy and targeted agents, have limited long-term efficacy for many patients.
  • Relapse remains a significant issue even after potentially curative treatments like stem cell transplantation (SCT).

Purpose of the Study:

  • To investigate the role of arginase II activity in acute myeloid leukemia (AML) blasts.
  • To understand how AML blasts inhibit immune function and hematopoiesis.
  • To explore novel mechanisms contributing to AML treatment resistance.

Main Methods:

  • The study by Mussai et al. focuses on the enzymatic activity of arginase II in AML blasts.
  • Analysis of the impact of aberrant arginase II levels on immune cells and hematopoietic processes.
  • Investigation into the contribution of arginase II to leukemia stem cell populations and treatment resistance.

Main Results:

  • AML blasts exhibit aberrantly high levels of arginase II activity.
  • This elevated arginase II activity impairs immune system function.
  • Arginase II also inhibits normal hematopoiesis, contributing to disease progression and resistance.

Conclusions:

  • Aberrant arginase II activity in AML blasts is a key mechanism for immune suppression and impaired hematopoiesis.
  • Targeting arginase II may represent a novel therapeutic strategy to overcome AML resistance.
  • Further research into arginase II's role is crucial for improving AML treatment outcomes.