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Androgen Receptor Exon 1 Mutation Causes Androgen Insensitivity by Creating Phosphorylation Site and Inhibiting Melanoma Antigen-A11 Activation of NH2- and Carboxyl-terminal Interaction-dependent…

Overview of attention for article published in Journal of Biological Chemistry, February 2012
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Mentioned by

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1 Wikipedia page

Citations

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25 Dimensions

Readers on

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27 Mendeley
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Title
Androgen Receptor Exon 1 Mutation Causes Androgen Insensitivity by Creating Phosphorylation Site and Inhibiting Melanoma Antigen-A11 Activation of NH2- and Carboxyl-terminal Interaction-dependent Transactivation*
Published in
Journal of Biological Chemistry, February 2012
DOI 10.1074/jbc.m111.336081
Pubmed ID
Authors

William H. Lagarde, Amanda J. Blackwelder, John T. Minges, Andrew T. Hnat, Frank S. French, Elizabeth M. Wilson

Abstract

Naturally occurring germ line mutations in the X-linked human androgen receptor (AR) gene cause incomplete masculinization of the external genitalia by disrupting AR function in males with androgen insensitivity syndrome. Almost all AR missense mutations that cause androgen insensitivity syndrome are located in the highly structured DNA and ligand binding domains. In this report we investigate the functional defect associated with an AR exon 1 missense mutation, R405S, that caused partial androgen insensitivity. The 46,XX heterozygous maternal carrier had a wild-type Arg-405 CGC allele but transmitted an AGC mutant allele coding for Ser-405. At birth, the 46,XY proband had a bifid scrotum, hypospadias, and micropenis consistent with clinical stage 3 partial androgen insensitivity. Androgen-dependent transcriptional activity of AR-R405S expressed in CV1 cells was less than wild-type AR and refractory in androgen-dependent AR NH(2)- and carboxyl interaction transcription assays that depend on the coregulator effects of melanoma antigen-A11. This mutation created a Ser-405 phosphorylation site evident by the gel migration of an AR-R405S NH(2)-terminal fragment as a double band that converted to the wild-type single band after treatment with λ-phosphatase. Detrimental effects of the R405S mutation were related to the proximity of the AR WXXLF motif (433)WHTLF(437) required for melanoma antigen-A11 and p300 to stimulate transcriptional activity associated with the AR NH(2)- and carboxyl-terminal interaction. We conclude that the coregulator effects of melanoma antigen-A11 on the AR NH(2)- and carboxyl-terminal interaction amplify the androgen-dependent transcriptional response to p300 required for normal human male sex development in utero.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Spain 1 4%
Unknown 26 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 26%
Student > Master 4 15%
Researcher 4 15%
Lecturer 3 11%
Professor 1 4%
Other 3 11%
Unknown 5 19%
Readers by discipline Count As %
Agricultural and Biological Sciences 8 30%
Biochemistry, Genetics and Molecular Biology 6 22%
Medicine and Dentistry 3 11%
Neuroscience 1 4%
Chemistry 1 4%
Other 0 0%
Unknown 8 30%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. 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 May 2014.
All research outputs
#8,534,976
of 25,373,627 outputs
Outputs from Journal of Biological Chemistry
#32,956
of 85,238 outputs
Outputs of similar age
#76,013
of 257,479 outputs
Outputs of similar age from Journal of Biological Chemistry
#204
of 544 outputs
Altmetric has tracked 25,373,627 research outputs across all sources so far. This one is in the 43rd percentile – i.e., 43% of other outputs scored the same or lower than it.
So far Altmetric has tracked 85,238 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.1. This one is in the 15th percentile – i.e., 15% of its peers scored the same or lower than it.
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 257,479 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 40th percentile – i.e., 40% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 544 others from the same source and published within six weeks on either side of this one. This one is in the 36th percentile – i.e., 36% of its contemporaries scored the same or lower than it.