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Phosphoproteomic analysis reveals Smarcb1 dependent EGFR signaling in Malignant Rhabdoid tumor cells

Overview of attention for article published in Molecular Cancer, September 2015
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  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (81st percentile)

Mentioned by

blogs
1 blog
twitter
1 tweeter

Citations

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13 Dimensions

Readers on

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33 Mendeley
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Title
Phosphoproteomic analysis reveals Smarcb1 dependent EGFR signaling in Malignant Rhabdoid tumor cells
Published in
Molecular Cancer, September 2015
DOI 10.1186/s12943-015-0439-5
Pubmed ID
Authors

Jonatan Darr, Agnes Klochendler, Sara Isaac, Tami Geiger, Amir Eden

Abstract

The SWI/SNF ATP dependent chromatin remodeling complex is a multi-subunit complex, conserved in eukaryotic evolution that facilitates nucleosomal re-positioning relative to the DNA sequence. In recent years the SWI/SNF complex has emerged to play a role in cancer development as various sub-units of the complex are found to be mutated in a variety of tumors. One core-subunit of the complex, which has been well established as a tumor suppressor gene is SMARCB1 (SNF5/INI1/BAF47). Mutation and inactivation of SMARCB1 have been identified as the underlying mechanism leading to Malignant Rhabdoid Tumors (MRT) and Atypical Teratoid/Rhabdoid Tumors (AT/RT), two highly aggressive forms of pediatric neoplasms. We present a phosphoproteomic study of Smarcb1 dependent changes in signaling networks. The SILAC (Stable Isotopic Labeling of Amino Acids in Cell Culture) protocol was used to quantify in an unbiased manner any changes in the phosphoproteomic profile of Smarcb1 deficient murine rhabdoid tumor cell lines following Smarcb1 stable re-expression and under different serum conditions. This study illustrates broad changes in the regulation of multiple biological networks including cell cycle progression, chromatin remodeling, cytoskeletal regulation and focal adhesion. Specifically, we identify Smarcb1 dependent changes in phosphorylation and expression of the EGF receptor, demonstrate downstream signaling and show that inhibition of EGFR signaling specifically hinders the proliferation of Smarcb1 deficient cells. These results support recent findings regarding the effectivity of EGFR inhibitors in hindering the proliferation of human MRT cells and demonstrate that activation of EGFR signaling in Rhabdoid tumors is SMARCB1 dependent.

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 33 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 33 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 8 24%
Student > Bachelor 6 18%
Student > Ph. D. Student 4 12%
Researcher 3 9%
Student > Doctoral Student 2 6%
Other 7 21%
Unknown 3 9%
Readers by discipline Count As %
Medicine and Dentistry 10 30%
Biochemistry, Genetics and Molecular Biology 7 21%
Agricultural and Biological Sciences 7 21%
Neuroscience 2 6%
Psychology 1 3%
Other 3 9%
Unknown 3 9%

Attention Score in Context

This research output has an Altmetric Attention Score of 8. 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 01 February 2018.
All research outputs
#1,879,146
of 12,448,635 outputs
Outputs from Molecular Cancer
#75
of 1,055 outputs
Outputs of similar age
#38,613
of 210,046 outputs
Outputs of similar age from Molecular Cancer
#1
of 3 outputs
Altmetric has tracked 12,448,635 research outputs across all sources so far. Compared to these this one has done well and is in the 84th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,055 research outputs from this source. They receive a mean Attention Score of 3.4. This one has done particularly well, scoring higher than 92% 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 210,046 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 81% of its contemporaries.
We're also able to compare this research output to 3 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them