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

Template-activating factor Iβ (TAF-Iβ) has been associated with numerous pathophysiological processes and has been reported as an oncogene responsible for the regulation of important signaling pathways in various types of solid tumor; however, few studies have investigated the role of TAF-Iβ in leukemia. The present study reported the upregulated expression of TAF-Iβ in 36 patients with acute leukemia and six leukemic cell lines. In addition, TAF-Iβ-knockdown (KD) cells were generated via RNA interference. TAF-Iβ KD not only inhibited the proliferation of leukemia cells but also induced apoptosis. Furthermore, it was revealed that the mechanism underlying these effects may be associated with the upregulation of protein phosphatase type 2A and inhibition of the protein kinase B/glycogen synthase kinase-3β signaling pathway. Collectively, the findings demonstrated that TAF-Iβ serves an important role in various types of leukemia and may be considered as a potential therapeutic target for the treatment of leukemia.

TAF‑Iβ deficiency inhibits proliferation and promotes apoptosis by rescuing PP2A and inhibiting the AKT/GSK‑3β pathway in leukemic cells