The Genomic Atlas of Breast Cancer — the non-coding theme

Update News

  • GABC update 2020.06.15
  • GABC update 2019.03.20
  • GABC online 2018.08.09
  • Data collection 2018.04.09

About Us

  • Steven Xi Chen:
    steven.chen@miami.edu
  • Yunpeng Zhang:
    YXZ1418@med.miami.edu
  • Peng Wang:
    wpgqy@163.com
  • Shangwei Ning:
    ningsw@ems.hrbmu.edu.cn
  • Xia Li:
    lixia@hrbmu.edu.cn

Detail


Chr chr1
start 238480384
end 238486023
lncRNA name LINK-A
entrez id 339535
hgnc id HGNC:27924
ensg id ENSG00000215808
refseq id NR_015407
methods Cell transfection, Fluorescence quenching assay, Lipid-RNA pulldown assay etc.
regulated differential expression
function description LINK-A directly interacts with the AKT pleckstrin homology domain and PIP3 at the single-nucleotide level, facilitating AKT-PIP3 interaction and consequent enzymatic activation. LINK-A-dependent AKT hyperactivation leads to tumorigenesis and resistance to AKT inhibitors. Genomic deletions of the LINK-A PIP3-binding motif dramatically sensitized breast cancer cells to AKT inhibitors.
pubmed id 28218907
year 2017
title The LINK-A lncRNA interacts with PtdIns(3,4,5)P3 to hyperactivate AKT and confer resistance to AKT inhibitors.
drug X
circulating X
survival V

CopyRight © University of Miami, USA; Harbin Medical University, China