FLT3 (Phospho-Tyr599) ELISA Kit (DEIA-XYA965)

Regulatory status: For research use only, not for use in diagnostic procedures.

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2 x 96T
cultured cells
Species Reactivity
Human, Mouse
Intended Use
The FLT3 (Phospho-Tyr599) Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor FLT3 protein phosphorylation and expression profile in cells. The kit can be used for measuring the relative amounts of phosphorylated FLT3 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on FLT3 phosphorylation.
Contents of Kit
1. 96-Well Cell Culture Clear-Bottom Microplate: 2 plates
2. 10x TBS: 24 mL
3. Quenching Buffer: 24 mL
4. Blocking Buffer: 50 mL
5. 10x Wash Buffer: 50 mL
6. 100x Anti-FLT3 (Phospho-Tyr599) Antibody (Rabbit Polyclonal): 60 μL, red
7. 100x Anti-FLT3 Antibody (Rabbit Polyclonal): 60 μL, purple
8. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL, green
9. HRP-Conjugated Anti-Rabbit IgG Antibody: 12 mL, glass
10. HRP-Conjugated Anti-Mouse IgG Antibody: 12 mL, glass
11. Primary Antibody Diluent: 12 mL
12. Ready-to-Use Substrate: 12 mL
13. Stop Solution: 12 mL
14. Crystal Violet Solution: 12 mL
15. SDS Solution: 24 mL
16. Adhesive Plate Seals: 4 seals
4°C/6 Months


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Deficiency of core fucosylation activates cellular signaling dependent on FLT3 expression in a Ba/F3 cell system


Authors: Duan, Chengwei; Fukuda, Tomohiko; Isaji, Tomoya; Qi, Feng; Yang, Jie; Wang, Yuqin; Takahashi, Shinichiro; Gu, Jianguo

Fms-like tyrosine kinase 3 (FLT3) is a glycoprotein, that is a member of the class III receptor tyrosine kinase family. Approximately one-third of acute myeloid leukemia (AML) patients have mutations of this gene, and activation of the FLT3 downstream pathway plays an important role in both normal and malignant hematopoiesis. However, the role of N-glycosylation for FLT3 activation remains unclear. In this study, we showed that the N-glycan structures on wild type (WT), internal tandem duplication (ITD), and tyrosine kinase domain (TKD) mutants of FLT3 were different. Interestingly, expression of either WT or mutant FLT3 in Ba/F3 cells, an interleukin-3 (IL-3)-dependent hematopoietic progenitor cell, greatly induced core fucosylation. To elucidate the function of core fucosylation in FLT3-mediated signaling, we used a CRISPR/Cas9 system to establish alpha 1,6-fucosyltransferase (Fut8) knockout (KO) cells. Surprisingly, the Fut8KO resulted in cell proliferation in an IL-3-independent manner in FLT3-WT cells, which was not observed in the parental cells, and suggested that this proliferation is dependent on FLT3 expression. Fut8KO greatly increased cellular tyrosine phosphorylation levels, together with an activation of STAT5, AKT, and ERK signaling, which could be completely neutralized by restoration with Fut8 in the KO cells. Consistently, a tyrosine kinase inhibitor efficiently inhibited cell proliferation induced by Fut8KO or specific fucosylation inhibitor. Additionally, immunostaining with FLT3 showed that the proteins were mainly expressed on the cell surface in the KO cells, which is similar to FLT3-WT cells, but different from the ITD mutant. Finally, we found that Fut8KO could induce dimer-formation in FLT3 without ligand-stimulation. Taken together, the present study clearly defines the regulatory function of core fucosylation in FLT3, which could provide a valuable direction for development of drugs could be effective in the treatment of AML.

Modeling pediatric AML FLT3 mutations using CRISPR/Cas12a-mediated gene editing


Authors: Rivera-Torres, Natalia; Banas, Kelly; Kmiec, Eric B.

Clustered regularly interspaced palindromic repeats (CRISPR) with the associated (Cas) nuclease complexes have democratized genetic engineering through their precision and ease-of-use. We have applied a variation of this technology, known as CRISPR-directed mutagenesis (CDM), to reconstruct genetic profiles within the FLT3 gene of AML patients. We took advantage of the versatility of CDM and built expression vectors that, in combination with a specifically designed donor DNA fragment, recapitulate simple and complex mutations within the FLT3 gene. We generate insertions and point mutations including combinations of these mutations originating from individual patient samples. We then analyze how these complex genetic profiles modulate transformation of Ba/F3 cells. Our results show that FLT3 expression plasmids bearing patientspecific single or multiple mutations recapitulate cellular transformation properties induced by FLT3 ITDs and modify their sensitivity or resistance in response to established AML drugs as a function of these complex mutations.

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