• Glycosylation of FLT3 determines its subcellular localization and downstream signaling activation, with implications for AML pathogenesis.
• Ubiquitination regulates FLT3 stability and function, and its dysregulation may contribute to disease progression.
• Combining FLT3 tyrosine kinase inhibitors with drugs targeting glycosylation or ubiquitination represents a promising therapeutic strategy.
• Understanding PTMs of FLT3 is crucial for developing targeted therapies in AML, especially for mutant forms.
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