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December 8, 2025BloodOpen Access

TTLL4 glutamyltransferase is a therapeutic target for NPM1-mutated Acute Myeloid Leukemia

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Authors

HIHumaira IlyasMMMaxim I. MaronJSJeffrey Shabanowitz

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Overview

Findings demonstrate glutamyltransferase TTLL4 regulates gene expression and differentiation in NPM1-mutated AML, suggesting a therapeutic target.

Key Points

  • This research aims to investigate TTLL4's role in NPM1-mutated acute myeloid leukemia.
  • Utilized CRISPR-Cas9 and shRNA to inactivate TTLL4 in NPM1-mutated OCI-AML3 cells.
  • Performed RNA sequencing post TTLL4 knockdown to assess gene expression changes.
  • Conducted mass spectrometry analysis to study NPM1 and NPM1c substrate interaction with TTLL4.
  • TTLL4 knockdown reduced NPM1c glutamylation and impaired cell proliferation and colony formation.
  • Activated myeloid differentiation markers CD11b and CD14 in TTLL4-deficient cells.
  • Identified EN7 as a small molecule inhibitor of TTLL4, promoting differentiation in NPM1c AML cell lines.

Cite This Study

Ilyas et al. (2025) studied this question.

synapsesocial.com/papers/693624d44fa91c937236d06ehttps://doi.org/10.1182/blood-2025-869
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Disrupting the PA2G4-NPM1 axis induces nucleolar stress in NPM1c AML2025
  2. 2Targeting the METTL1/m7G axis as a therapeutic strategy in myeloid leukemia2025 · 1 citations
  3. 3The KMT2A-PTD oncoprotein depends on ENL but not menin to drive AML gene expression2025 · 1 citations
  4. 4Pharmacological targeting of CTPS1 elicits macrophage-mediated anti-leukemia immunity2025
  5. 5Targeting CCL3+mono like LSC overcomes chemotherapy resistance in NPM1 mutant AML2025