FAK regulates IL-33 expression by controlling chromatin accessibility at c-Jun motifs
Abstract Focal adhesion kinase (FAK) localizes to focal adhesions and is overexpressed in many cancers. FAK can also translocate to the nucleus, where it binds to, and regulates, several transcription factors, including MBD2, p53 and IL-33, to control gene expression by unknown mechanisms. We have u...
Main Authors: | Billie G. C. Griffith, Rosanna Upstill-Goddard, Holly Brunton, Graeme R. Grimes, Andrew V. Biankin, Bryan Serrels, Adam Byron, Margaret C. Frame |
---|---|
Format: | Article |
Language: | English |
Published: |
Nature Publishing Group
2021-01-01
|
Series: | Scientific Reports |
Online Access: | https://doi.org/10.1038/s41598-020-80111-9 |
Similar Items
-
Using Chromatin Accessibility to Delineate Therapeutic Subtypes in Pancreatic Cancer Patient-Derived Cell Lines
by: Holly Brunton, et al.
Published: (2020-09-01) -
Ambra1 spatially regulates Src activity and Src/FAK-mediated cancer cell invasion via trafficking networks
by: Christina Schoenherr, et al.
Published: (2017-03-01) -
Genetic dissection of early-onset breast cancer and other genetic diseases
by: Upstill-Goddard, Rosanna
Published: (2015) -
RECL 33 - 14-Jun-78
Published: (2011) -
FAK deletion promotes p53-mediated induction of p21, DNA-damage responses and radio-resistance in advanced squamous cancer cells.
by: Kathryn Graham, et al.
Published: (2011-01-01)