English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Significance Mutational inactivation of theVHL tumor suppressor gene is the signature lesion in the most common form of kidney cancer and causes inappropriate accumulation of the HIF transcription factor, which activates genes that normally facilitate adaptation to hypoxia but, in the context of kidney cancer, also promote tumorigenesis. Additional mutational events are needed, in conjunction with VHL loss, to cause kidney cancer. The most common of these are inactivating mutations of the PBRM1 tumor suppressor gene, which encodes a component [BRG1-associated factor 180 (BAF180)] of a multiprotein complex [Polybromo- and BRG1-associated factors-containing complex (PBAF)] that regulates the positions of nucleosomes throughout the genome. We describe here kidney cancer cell-based models for monitoring BAF180 function and show that loss of BAF180 accentuates the transcriptional response to HIF.

Inactivation of the PBRM1 tumor suppressor gene amplifies the HIF-response in VHL −/− clear cell renal carcinoma

Inactivation of the PBRM1 tumor suppressor gene amplifies the HIF-response in VHL ^−/− clear cell renal carcinoma