Asset Details
Do you wish to reserve the book?
Assembly of methylated KDM1A and CHD1 drives androgen receptor–dependent transcription and translocation
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Assembly of methylated KDM1A and CHD1 drives androgen receptor–dependent transcription and translocation
Do you wish to request the book?
Assembly of methylated KDM1A and CHD1 drives androgen receptor–dependent transcription and translocation
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Assembly of methylated KDM1A and CHD1 drives androgen receptor–dependent transcription and translocation
2016
Overview
Methylation of the lysine demethylase KDM1A and the recognition of this modification by the chromodomain helicase CHD1 control androgen-dependent gene transcription and
TMPRSS2-ERG
gene fusion, a common translocation event in prostate cancer.
Prostate cancer evolution is driven by a combination of epigenetic and genetic alterations such as coordinated chromosomal rearrangements, termed chromoplexy.
TMPRSS2-ERG
gene fusions found in human prostate tumors are a hallmark of chromoplexy.
TMPRSS2-ERG
fusions have been linked to androgen signaling and depend on androgen receptor (AR)-coupled gene transcription. Here, we show that dimethylation of KDM1A at K114 (to form K114me2) by the histone methyltransferase EHMT2 is a key event controlling androgen-dependent gene transcription and
TMPRSS2-ERG
fusion. We identified CHD1 as a KDM1A K114me2 reader and characterized the KDM1A K114me2–CHD1 recognition mode by solving the cocrystal structure. Genome-wide analyses revealed chromatin colocalization of KDM1A K114me2, CHD1 and AR in prostate tumor cells. Together, our data link the assembly of methylated KDM1A and CHD1 with AR-dependent transcription and genomic translocations, thereby providing mechanistic insight into the formation of
TMPRSS2-ERG
gene fusions during prostate-tumor evolution.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ 13/1
/ 13/109
/ 14
/ 14/32
/ 38/1
/ 38/22
/ Analysis
/ DNA-Binding Proteins - analysis
/ DNA-Binding Proteins - metabolism
/ Gene Expression Regulation, Neoplastic
/ Histocompatibility Antigens - metabolism
/ Histone Demethylases - analysis
/ Histone Demethylases - metabolism
/ Histone-Lysine N-Methyltransferase - metabolism
/ Histones
/ Humans
/ Male
/ Oncogene Proteins, Fusion - genetics
/ Prostatic Neoplasms - genetics
/ Prostatic Neoplasms - metabolism
/ Receptors, Androgen - analysis
/ Receptors, Androgen - metabolism
/ Tumors
