ReviewActa biochimica et biophysica Sinica2024
Importance of PTM of FLT3 in acute myeloid leukemia.
Review in Acta biochimica et biophysica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- RNF126 writes a non-canonical ubiquitin code on midnolin to tune protein stability.Acta biochimica et biophysica Sinica · 2026Article
- The prognostic marker NRIP1 is associated with tumor progression and immune infiltration in acute myeloid leukemia.Acta biochimica et biophysica Sinica · 2025Article
- Review
- Exploring the association between circadian rhythms and osteoporosis: new diagnostic and therapeutic targets identified via machine learning.Frontiers in molecular biosciences · 2025Article
- Exploring glyco-signatures and their clinical implications: a special issue focused on glycosylation studies.Acta biochimica et biophysica Sinica · 2024Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FMS-like tyrosine kinase 3 (FLT3) is a receptor tyrosine kinase expressed in hematopoietic cells. Internal-tandem duplication domain (ITD) mutation and tyrosine kinase domain (TKD) mutation are the two most common mutations in acute myeloid leukemia (AML). Post-translational modifications (PTMs) of FLT3, such as glycosylation and ubiquitination, have been shown to impact various aspects of the protein in both wild-type (WT) and mutant forms of FLT3. In this review, we describe how the glycosylation status of FLT3 affects its subcellular localization, which significantly impacts the activation of downstream signaling, and the impact of specific ubiquitination on FLT3 function and stability, which may be associated with disease progression. Moreover, potential novel therapeutic strategies involving a combination of FLT3 tyrosine kinase inhibitors and drugs targeting glycosylation or ubiquitination are discussed.
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