Findings suggested that non-synonymous single nucleotide variants (nsSNVs) in PFN1 gene could affect PFN1 protein flexibility which could be therefore related to the development of amyotrophic lateral sclerosis.
The authors report that formins mDia1 and mDia2 dissociate faster under higher ionic strength and when actin concentration is increased. Profilin known to increase the elongation rate of formin-associated filaments surprisingly decreases the formin dissociation rate by bringing formin FH1 domains in transient contact with the barbed end.
Data suggest that profiling-1 (PFN1) preferentially binds to Huntingtin N-terminal fragment (HTT-NTF) M-phase species and destabilizes aggregation and phase separation by shifting concentration boundaries for phase separation to higher values through a process known as polyphasic linkage; this phenomena occurs irrespective of polyglutamine length in HTT-NTF.
We found that ARP3 and profilin1 were 2 binding partners of LMO2 primarily in cytoplasm. LMO2. LMO2 mediated the assembly of a complex including ARP3 profilin1 and actin monomer increased actin monomer binding to profilin1 and promoted lamellipodia/filopodia formation in basal-type breast cancer cells.
Profilin1 acts as a molecular regulator of the levels of PI(3 4)P2 and Tks5 recruitment in invadopodia to control the invasion efficiency of invadopodia.
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