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Study revealed an essential role for FMNL3 in regulating the RhoC/FAK pathway and actin assembly dynamics, and the subsequent promotion of colorectal carcinoma invasion.
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FMNL3, the target gene of miR-127, is upregulated and acting as an oncogene in ESCC
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we use a simple cellular system to examine fundamental features of formin-mediated filopodial assembly, using constitutively active constructs of the formins mDia2 and FMNL3
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FMNL3 interacts with Cdc42 and RhoJ, two Rho family GTPases known to be required for lumen formation. FMNL3 and RhoJ are concentrated at the early apical surface, or AMIS, and regulate the formation of radiating actin cables from this site.
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FMNL3 functions in assembly of actin-based protrusions that are specialized for cell-cell adhesion.
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FMNL3 plays an important role in the progression and metastasis of colorectal carcinoma and may be a novel potential prognostic predictor in colorectal carcinoma.
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miR-335 regulates the expression of at least five formin family members, three of which are validated, FMNL3, FMN2 and DAAM2.
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Formin-like 3 (FMNL3) is a crucial regulator of endothelial cell elongation during angiogenesis.
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Protein N-myristoylation plays critical roles in the cellular morphological changes induced by FMNL2 and FMNL3.
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Data suggest that the FH2 domain of FRL2 possesses properties not shared by FRL1 that allow it to generate filopodia.