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c-MYC Generates Repair Errors via Increased Transcription of Alternative-NHEJ Factors, LIG3 and PARP1, in Tyrosine Kinase–Activated Leukemias

Overview of attention for article published in Molecular Cancer Research, April 2015
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About this Attention Score

  • Good Attention Score compared to outputs of the same age (66th percentile)
  • Good Attention Score compared to outputs of the same age and source (72nd percentile)

Mentioned by

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1 tweeter
wikipedia
9 Wikipedia pages

Citations

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46 Dimensions

Readers on

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40 Mendeley
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Title
c-MYC Generates Repair Errors via Increased Transcription of Alternative-NHEJ Factors, LIG3 and PARP1, in Tyrosine Kinase–Activated Leukemias
Published in
Molecular Cancer Research, April 2015
DOI 10.1158/1541-7786.mcr-14-0422
Pubmed ID
Authors

Nidal Muvarak, Shannon Kelley, Carine Robert, Maria R. Baer, Danilo Perrotti, Carlo Gambacorti-Passerini, Curt Civin, Kara Scheibner, Feyruz V. Rassool

Abstract

Leukemias expressing the constitutively activated tyrosine kinases (TKs) BCR-ABL1 and FLT3/ITD activate signaling pathways that increase genomic instability through generation of reactive oxygen species (ROS), DNA double-strand breaks (DSBs) and error-prone repair. The non-homologous end-joining (NHEJ) pathway is a major pathway for DSB repair and is highly aberrant in TK-activated leukemias; an alternative form of NHEJ (ALT-NHEJ) predominates, evidenced by increased expression of DNA ligase IIIalpha (LIG3) and poly (ADP-ribose)polymerase (PARP1), increased frequency of large genomic deletions, and repair using DNA sequence microhomologies. This study, for the first time, demonstrates that the TK target c-MYC plays a role in transcriptional activation and subsequent expression of LIG3 and PARP1 and contributes to the increased error-prone repair observed in TK-activated leukemias. c-MYC negatively regulates microRNAs miR-150 and miR-22 which demonstrate an inverse correlation with LIG3 and PARP1 expression in primary and cultured leukemia cells and chronic myelogenous leukemia (CML) human patient samples. Notably, inhibition of c-MYC and overexpression of miR-150 and -22 decreases ALT-NHEJ activity. Thus, BCR-ABL1 or FLT3/ITD induces c-MYC expression leads to genomic instability via augmented expression of ALTNHEJ repair factors that generate repair errors. In the context of TK-activated leukemias c-MYC contributes to aberrant DNA repair through downstream targets LIG3 and PARP1, which represent viable and attractive therapeutic targets.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 40 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 40 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 8 20%
Student > Master 7 18%
Student > Ph. D. Student 4 10%
Student > Bachelor 4 10%
Student > Doctoral Student 2 5%
Other 7 18%
Unknown 8 20%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 19 48%
Agricultural and Biological Sciences 7 18%
Medicine and Dentistry 3 8%
Psychology 1 3%
Unknown 10 25%

Attention Score in Context

This research output has an Altmetric Attention Score of 4. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 15 May 2022.
All research outputs
#6,689,305
of 21,340,902 outputs
Outputs from Molecular Cancer Research
#557
of 1,791 outputs
Outputs of similar age
#80,313
of 248,624 outputs
Outputs of similar age from Molecular Cancer Research
#6
of 29 outputs
Altmetric has tracked 21,340,902 research outputs across all sources so far. This one has received more attention than most of these and is in the 68th percentile.
So far Altmetric has tracked 1,791 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.9. This one has gotten more attention than average, scoring higher than 67% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 248,624 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 66% of its contemporaries.
We're also able to compare this research output to 29 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 72% of its contemporaries.