Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Aberrant GSK3β nuclear localization promotes AML growth and drug resistance

1 Nov 2018

Abstract excerpt

Abstract Acute myeloid leukemia (AML) is a devastating disease with poor patient survival. As targetable mutations in AML are rare, novel oncogenic mechanisms are needed to define new therapeutic targets. We identified AML cells that exhibit an aberrant pool of nuclear glycogen synthase kinase 3β (GSK3β). This nuclear fraction drives AML growth and drug resistance. Nuclear, but not cytoplasmic, GSK3β enhances AML...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acute Myeloid Leukemia Research
Share to Cancer-related gene regulation
Share to Genomics and Chromatin Dynamics

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 30385433
DOI: 10.1182/bloodadvances.2018016006

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Aberrant GSK3β nuclear localization promotes AML growth and drug resistancePMID 30385433Read ↗

Glycogen synthase kinase-3β is a pivotal mediator of cancer invasion and resistance to therapy.Semantic proximity Read ↗

Inhibition of glycogen synthase kinase-3 activity leads to epigenetic silencing of nuclear factor κB target genes and induction of apoptosis in chronic lymphocytic leukemia B cellsSemantic proximity Read ↗

Proteasome 26S subunit, non-ATPases 1 (PSMD1) and 3 (PSMD3), play an oncogenic role in chronic myeloid leukemia by stabilizing nuclear factor-kappa BSemantic proximity Read ↗

The Landscape of Glycogen Synthase Kinase-3 Beta Genomic Alterations in Cancer.Semantic proximity Read ↗

Glycogen synthase kinase-3 and alternative splicing.Semantic proximity Read ↗

Targeting NLRP3 inhibits AML progression by inducing PERK/eIF2-mediated apoptosisSemantic proximity Read ↗

Nuclear translocation of p85β promotes tumorigenesis of PIK3CA helical domain mutant cancer.Semantic proximity Read ↗

Kinase-Inactive Glycogen Synthase Kinase 3β Promotes Wnt Signaling and Mammary TumorigenesisSemantic proximity Read ↗

The enzyme glycogen synthase kinase-3 is associated with specific forms of oncogenesis; what more do we need to know to achieve clinical benefit?Semantic proximity Read ↗

Nuclear translocation of p85β promotes tumorigenesis of PIK3CA helical domain mutant cancerSemantic proximity Read ↗

Glucosylceramide synthase inhibitor PDMP sensitizes chronic myeloid leukemia T315I mutant to Bcr-Abl inhibitor and cooperatively induces glycogen synthase kinase-3-regulated apoptosis.Semantic proximity Read ↗

LncRNA-mediated organization of oncogenic chromatin state is a targetable vulnerability in leukemiaSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.