mProX™ Human FLT4 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 KDR and FLT4 in HDMECs, HUVECs and leukemia cell lines.
Quantitative real-time PCR was used to quantify the KDR and FLT4 mRNA expression levels, which are listed beneath the cell line name. The endogenous control utilized in this study was TBP expression, whereas the normalization cell lines employed were CMK (KDR) and HEL (FLT4).
Ref: Quentmeier, Hilmar, et al. "DNA methylation regulates expression of VEGF-R2 (KDR) and VEGF-R3 (FLT4)." BMC cancer 12.1 (2012): 1-10.
Pubmed: 22251800
DOI: 10.1186/1471-2407-12-19
Research Highlights
Coordinated expression of multiple essential regulators is necessary for the formation of the lymphatic system, including vascular endothelial growth factor C (VEGFC), its receptor FLT4, and a crucial transcriptional effector called PROX1.
Gauvrit, Sébastien, et al. "HHEX is a transcriptional regulator of the VEGFC/FLT4/PROX1 signaling axis during vascular development." Nature communications 9.1 (2018): 2704.
Pubmed:
30006544
DOI:
10.1038/s41467-018-05039-1
In macrophages harboring the mutant FLT4, the AMPK agonist AICAR may be able to reverse glycolytic reprogramming and inflammasome activation. This could have translational implications for patients with Flt4 mutations, as it may help prevent repeated infections.
Ma, Li, et al. "FLT4/VEGFR3 activates AMPK to coordinate glycometabolic reprogramming with autophagy and inflammasome activation for bacterial elimination." Autophagy 18.6 (2022): 1385-1400.
Pubmed:
34632918
DOI:
10.1080/15548627.2021.1985338