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

It is known that the sonic hedgehog (SHH) transcriptional activator GLI1 plays key roles in a panel of cancers including medulloblastoma (MB). We previously reported that AMP-activated protein kinase (AMPK) phosphorylates GLI1 and promotes GLI1 degradation through the β-TrCP-mediated ubiquitin proteasomal pathway. Therefore, activation of AMPK is a promising venue to target cancers that arise from aberrant SHH signaling such as MB. Mice models are commonly used to elucidate SHH-regulated developmental programs as well as SHH signaling in MB pathogenesis and would continue to inform how AMPK controls SHH signaling processes. However, an important question is whether AMPK regulates Gli1 in the murine system is not fully demonstrated. Here we review and present recent findings which demostrated that AMPK downregulates Gli1 in mouse cell lines. Correspondence to: Jer-Yen Yang, Department of Basic Medical Sciences and Center for Cancer Research, Purdue University, West Lafayette, Indiana 47906, USA, Tel: 7654967363; E-mail: jyyang@purdue.edu

Activation of AMPK inhibits medulloblastoma cell growth and Gli1 activity