Inhibition of USP10 induces degradation of oncogenic FLT3.

doi:10.1038/nchembio.2486

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

Community

Back to search

Article

Inhibition of USP10 induces degradation of oncogenic FLT3.

Nature chemical biology - 1 Dec 2017

Weisberg Ellen L, Schauer Nathan J, Yang Jing, Lamberto Ilaria, Doherty Laura, Bhatt Shruti, Nonami Atsushi, Meng Chengcheng, Letai Anthony, Wright Renee, Tiv Hong, Gokhale Prafulla C, Ritorto Maria Stella, De Cesare Virginia, Trost Matthias, Christodoulou Alexandra, Christie Amanda, Weinstock David M, Adamia Sophia, Stone Richard, Chauhan Dharminder, Anderson Kenneth C, Seo Hyuk-Soo, Dhe-Paganon Sirano, Sattler Martin, Gray Nathanael S, Griffin James D, Buhrlage Sara J

Abstract excerpt

Oncogenic forms of the kinase FLT3 are important therapeutic targets in acute myeloid leukemia (AML); however, clinical responses to small-molecule kinase inhibitors are short-lived as a result of the rapid emergence of resistance due to point mutations or compensatory increases in FLT3 expression. We sought to develop a complementary pharmacological approach whereby proteasome-mediated FLT3 degradation could be...

Read the complete abstract on PubMed

Topics

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

Share to Drug Screening Assays, Antitumor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to fms-Like Tyrosine Kinase 3

Share to Mice, Inbred NOD

Share to Neoplasms, Experimental

Share to Small Molecule Libraries

Share to Thiophenes

Share to Ubiquitin

Share to Ubiquitin Thiolesterase

Source

Open in PubMed Open full text

Identifiers

PMID: 28967922
DOI: 10.1038/nchembio.2486
PMCID: PMC6314479

Genes

FLT3
USP10

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Inhibition of USP10 induces degradation of oncogenic FLT3.PMID 28967922Read ↗

Evolving paradigms in targeting FLT3 for acute myeloid leukemia therapy.Semantic proximity Read ↗

Targeting USP14/UCHL5: A Breakthrough Approach to Overcoming Treatment-Resistant FLT3-ITD-Positive AML.Semantic proximity Read ↗

Modulation of FLT3-ITD and CDK9 in acute myeloid leukaemia cells by novel proteolysis targeting chimera (PROTAC).Semantic proximity Read ↗

Blockade of de novo pyrimidine biosynthesis triggers autophagic degradation of oncoprotein FLT3-ITD in acute myeloid leukemia.Semantic proximity Read ↗

Rapid proteasomal degradation of mutant feline McDonough sarcoma-like tyrosine kinase-3 overcomes inhibitor resistance mechanisms of acute myeloid leukemia cellsSemantic proximity Read ↗

Targeting USP13 ‐mediated drug tolerance increases the efficacy of EGFR inhibition of mutant EGFR in non‐small cell lung cancerSemantic proximity Read ↗

Ubiquitin-specific protease 7 inhibitors reveal a differentiated mechanism of p53-driven anti-cancer activitySemantic proximity Read ↗

A combinatorial therapeutic approach to enhance FLT3-ITD AML treatment.Semantic proximity Read ↗

19S Proteasome Subunits as Oncogenes and Prognostic Biomarkers in FLT3-Mutated Acute Myeloid Leukemia (AML).Semantic proximity Read ↗

USP8 Is a Novel Target for Overcoming Gefitinib Resistance in Lung CancerSemantic proximity Read ↗

Rapid proteasomal degradation of mutant feline McDonough sarcoma-like tyrosine kinase-3 overcomes tyrosine kinase inhibitor resistance of acute myeloid leukemia cellsSemantic proximity Read ↗

Degrading FLT3-ITD protein by proteolysis targeting chimera (PROTAC).Semantic proximity Read ↗

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