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hPIV-2 V protein promotes F-actin formation by affecting actin-profilin2 interaction through its binding to profilin2.
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We unveil PFN2 and GAMT as molecular determinants of Charcot-Marie-Tooth type 2 neuropathy, with possible indications of the role of PFN2 in the pathogenesis and disease progression.
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Profilin 2 (PFN2) expression is significantly upregulated in Breast cancer (BC) tissues. The abnormal upregulation of PFN2 is associated with poor prognosis in patients with BC. Long noncoding RNA FOXD2 adjacent opposite strand RNA 1 and PFN2 expression is positively correlated.
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Pfn2 levels, regulated by cIAP1, affected intracellular levels of reactive oxygen species.
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Study indicated that PFN2 may function as a negative regulator of colorectal cancer (CRC) metastasis and, thus, may represent a potential target for CRC therapy.
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High PFN2 expression might serve as a valuable predictor for poor overall survival of HNSC. DNA amplification and hypomethylation might be two mechanisms of PFN2 dysregulation.
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PFN2 gene, related to regulation of actin cytoskeleton in protein complex F, might play momentous roles in the initiation and development of consecutive Trauma-Induced Sepsis.
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PFN2 has a novel role in promoting Esophageal squamous cell carcinoma progression and metastasis.
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Data suggest 2 major isoforms of profilin (Pfn1 and Pfn2) are co-regulated by a common mechanism involving the action of MKL1 [megakaryoblastic leukemia (translocation) 1 protein] that is independent of its SRF- (serum-response factor)-related activity; cellular externalization of Pfn1, rather than transcription, is affected by the perturbations of MKL1; MKL1 can influence cell migration by modulating Pfn1 expression.
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Study demonstrated that miR30a inhibits epithelial-mesenchymal transition (EMT) and invasion in highly invasive non-small cell lung cancer (NSCLC) cell lines via targeting PFN2 suggesting that miR30a with PFN2 may play an essential role in the development of NSCLC by modulating EMT and cell invasion.
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Disease causing mutations in inverted formin 2 regulate its binding to G-actin, F-actin capping protein (CapZ alpha-1) and profilin 2.
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Therefore, this study indicates that profilin 2 affects the metastatic potential and stemness of colorectal CSCs by regulating EMT- and stemness-related proteins.
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Pfn2 suppresses the recruitment of HDAC1 to Smad2 and Smad3 promoters, increasing their expression, and, in turn, enhancing TGFB1 induced epithelial-mesenchymal transformation and VEGF and CTGF production.
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effects of profilin-1 and profilin-2, the two major isoforms of profilin, on actin cytoskeletal regulation, motility, and invasion of breast cancer cells
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Oral squamous cell carcinomas with weak PFN2 expression were associated with a significantly worse prognosis than strongly expressed tumours.
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These findings raise the possibility that Rgl3 mediates interaction between Ras/Rap-family proteins and profilin II, an important activator of actin polymerization.
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A signaling pathway from ROCK1 to profilin controls polyglutamine protein aggregation.