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Journal articles on the topic 'PFN1'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Gau, David M., Abigail Allen, Andrew Daoud, Jessica Kunkel, Stefan Duensing, and Partha Roy. "Abstract 4584: Genetic disruption of vascular endothelial profilin-1 impacts tumor microenvironment supressing tumorigenicity of renal cancer." Cancer Research 83, no. 7_Supplement (2023): 4584. http://dx.doi.org/10.1158/1538-7445.am2023-4584.

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Abstract Renal cell carcinoma (RCC) is estimated to result in 79,000 new cases and 13,920 deaths in 2022. Clear cell renal cell carcinoma (ccRCC) is the most common subtype of RCC and is characterized by a highly vascularized tumor microenvironment (TME). While current anti-angiogenic therapies targeting VEGF signaling are initially effective, almost all patients develop resistance to these therapies. Therefore, there is a need to identify clinically relevant alternative molecular targets to suppress tumor angiogenesis and progression in ccRCC. We previously discovered transcriptional upregula

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Teyssou, Elisa, Laura Chartier, Delphine Roussel, et al. "The Amyotrophic Lateral Sclerosis M114T PFN1 Mutation Deregulates Alternative Autophagy Pathways and Mitochondrial Homeostasis." International Journal of Molecular Sciences 23, no. 10 (2022): 5694. http://dx.doi.org/10.3390/ijms23105694.

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Mutations in profilin 1 (PFN1) have been identified in rare familial cases of Amyotrophic Lateral Sclerosis (ALS). PFN1 is involved in multiple pathways that could intervene in ALS pathology. However, the specific pathogenic role of PFN1 mutations in ALS is still not fully understood. We hypothesized that PFN1 could play a role in regulating autophagy pathways and that PFN1 mutations could disrupt this function. We used patient cells (lymphoblasts) or tissue (post-mortem) carrying PFN1 mutations (M114T and E117G), and designed experimental models expressing wild-type or mutant PFN1 (cell lines

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3

Schmidt, Eric J., Salome Funes, Jeanne E. McKeon, et al. "ALS-linked PFN1 variants exhibit loss and gain of functions in the context of formin-induced actin polymerization." Proceedings of the National Academy of Sciences 118, no. 23 (2021): e2024605118. http://dx.doi.org/10.1073/pnas.2024605118.

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Profilin-1 (PFN1) plays important roles in modulating actin dynamics through binding both monomeric actin and proteins enriched with polyproline motifs. Mutations in PFN1 have been linked to the neurodegenerative disease amyotrophic lateral sclerosis (ALS). However, whether ALS-linked mutations affect PFN1 function has remained unclear. To address this question, we employed an unbiased proteomics analysis in mammalian cells to identify proteins that differentially interact with mutant and wild-type (WT) PFN1. These studies uncovered differential binding between two ALS-linked PFN1 variants, G1

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4

Nekouei, Mina, Atousa Aliahmadi, Mahmoud Kiaei, and Ali Reza Ghassempour. "Mutant Profilin1 Aggregation in Amyotrophic Lateral Sclerosis: An in Vivo Biochemical Analysis." Basic and Clinical Neuroscience Journal 12, no. 2 (2021): 213–22. http://dx.doi.org/10.32598/bcn.12.2.1631.1.

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Introduction: Profilin1 (PFN1) is a ubiquitously expressed protein known for its function as a regulator of actin polymerization and dynamics. A recent discovery linked mutant PFN1 to Amyotrophic Lateral Sclerosis (ALS), which is a fatal and progressive motor neuron disease. We have also demonstrated that Gly118Val mutation in PFN1 is a cause of ALS, and the formation of aggregates containing mutant PFN1 may be a mechanism for motor neuron death. Hence, we were interested in investigating the aggregation of PFN1 further and searching for co-aggregated proteins in our mouse model overexpressing

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Boopathy, Sivakumar, Tania V. Silvas, Maeve Tischbein, et al. "Structural basis for mutation-induced destabilization of profilin 1 in ALS." Proceedings of the National Academy of Sciences 112, no. 26 (2015): 7984–89. http://dx.doi.org/10.1073/pnas.1424108112.

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Mutations in profilin 1 (PFN1) are associated with amyotrophic lateral sclerosis (ALS); however, the pathological mechanism of PFN1 in this fatal disease is unknown. We demonstrate that ALS-linked mutations severely destabilize the native conformation of PFN1 in vitro and cause accelerated turnover of the PFN1 protein in cells. This mutation-induced destabilization can account for the high propensity of ALS-linked variants to aggregate and also provides rationale for their reported loss-of-function phenotypes in cell-based assays. The source of this destabilization is illuminated by the X-ray

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Zheng, Junke, and Chengcheng Zhang. "Profilin 1 Is Essential for Retention and Metabolism of Hematopoietic Stem Cells in Bone Marrow." Blood 120, no. 21 (2012): 1224. http://dx.doi.org/10.1182/blood.v120.21.1224.1224.

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Abstract Abstract 1224 How stem cells interact with the microenvironment to regulate their cell fates and metabolism is largely unknown. Here we show that, in a hematopoietic stem cell (HSC) -specific inducible knockout model, the cytoskeleton-modulating protein profilin 1 (pfn1) is essential for the maintenance of multiple cell fates and metabolism of HSCs. The deletion of pfn1 in HSCs led to bone marrow failure, loss of quiescence, increased apoptosis, and mobilization of HSCs in vivo. In reconstitution analyses, pfn1-deficient cells were selectively lost from mixed bone marrow chimeras. By

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Lee, Chang-Jin, Seon-Hwa Hong, Min-Ji Yoon, et al. "Endometrial profilin 1: a key player in embryo-endometrial crosstalk." Clinical and Experimental Reproductive Medicine 47, no. 2 (2020): 114–21. http://dx.doi.org/10.5653/cerm.2019.03454.

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Objective: Despite extensive research on implantation failure, little is known about the molecular mechanisms underlying the crosstalk between the embryo and the maternal endometrium, which is critical for successful pregnancy. Profilin 1 (PFN1), which is expressed both in the embryo and in the endometrial epithelium, acts as a potent regulator of actin polymerization and the cytoskeletal network. In this study, we identified the specific role of endometrial PFN1 during embryo implantation.Methods: Morphological alterations depending on the status of PFN1 expression were assessed in PFN1-deple

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Lee, Chang-Jin, Min-Ji Yoon, Dong Hyun Kim, Tae Uk Kim, and Youn-Jung Kang. "Profilin-1; a novel regulator of DNA damage response and repair machinery in keratinocytes." Molecular Biology Reports 48, no. 2 (2021): 1439–52. http://dx.doi.org/10.1007/s11033-021-06210-6.

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AbstractProfilin-1 (PFN1) regulates actin polymerization and cytoskeletal growth. Despite the essential roles of PFN1 in cell integration, its subcellular function in keratinocyte has not been elucidated yet. Here we characterize the specific regulation of PFN1 in DNA damage response and repair machinery. PFN1 depletion accelerated DNA damage-mediated apoptosis exhibiting PTEN loss of function instigated by increased phosphorylated inactivation followed by high levels of AKT activation. PFN1 changed its predominant cytoplasmic localization to the nucleus upon DNA damage and subsequently restor

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9

Zi, Jingjing, Jing Xu, Jintang Luo, et al. "PFN1 Inhibits Myogenesis of Bovine Myoblast Cells via Cdc42-PAK/JNK." Cells 11, no. 20 (2022): 3188. http://dx.doi.org/10.3390/cells11203188.

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Myoblast differentiation is essential for the formation of skeletal muscle myofibers. Profilin1 (Pfn1) has been identified as an actin-associated protein, and has been shown to be critically important to cellular function. Our previous study found that PFN1 may inhibit the differentiation of bovine skeletal muscle satellite cells, but the underlying mechanism is not known. Here, we confirmed that PFN1 negatively regulated the myogenic differentiation of bovine skeletal muscle satellite cells. Immunoprecipitation assay combined with mass spectrometry showed that Cdc42 was a binding protein of P

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10

Wittenmayer, Nina, Burkhard Jandrig, Martin Rothkegel, et al. "Tumor Suppressor Activity of Profilin Requires a Functional Actin Binding Site." Molecular Biology of the Cell 15, no. 4 (2004): 1600–1608. http://dx.doi.org/10.1091/mbc.e03-12-0873.

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Profilin 1 (PFN1) is a regulator of the microfilament system and is involved in various signaling pathways. It interacts with many cytoplasmic and nuclear ligands. The importance of PFN1 for human tissue differentiation has been demonstrated by the findings that human cancer cells, expressing conspicuously low PFN1 levels, adopt a nontumorigenic phenotype upon raising their PFN1 level. In the present study, we characterize the ligand binding site crucial for profilin's tumor suppressor activity. Starting with CAL51, a human breast cancer cell line highly tumorigenic in nude mice, we establishe

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Allen, Abigail, David Gau, Paul Francoeur, et al. "Actin-binding protein profilin1 promotes aggressiveness of clear-cell renal cell carcinoma cells." Journal of Biological Chemistry 295, no. 46 (2020): 15636–49. http://dx.doi.org/10.1074/jbc.ra120.013963.

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Clear-cell renal cell carcinoma (ccRCC), the most common subtype of renal cancer, has a poor clinical outcome. A hallmark of ccRCC is genetic loss-of-function of VHL (von Hippel–Lindau) that leads to a highly vascularized tumor microenvironment. Although many ccRCC patients initially respond to antiangiogenic therapies, virtually all develop progressive, drug-refractory disease. Given the role of dysregulated expressions of cytoskeletal and cytoskeleton-regulatory proteins in tumor progression, we performed analyses of The Cancer Genome Atlas (TCGA) transcriptome data for different classes of

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Zheng, Junke, Zhigang Lu, Fatih Kocabas, et al. "Profilin 1 is essential for retention and metabolism of mouse hematopoietic stem cells in bone marrow." Blood 123, no. 7 (2014): 992–1001. http://dx.doi.org/10.1182/blood-2013-04-498469.

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Key Points The deletion of pfn1 led to bone marrow failure, loss of quiescence, increased apoptosis and mobilization, and a metabolic switch of HSCs. Pfn1 partially acts through the axis of pfn1/Gα13/EGR1 to regulate stem cell retention and metabolism in the bone marrow.

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Stritt, Simon, Markus Bender, Paquita Nurden, et al. "Aberrant Microtubule Organization and Wiskott-Aldrich Syndrome-like Defects in Platelets and Megakaryocytes of Profilin1-Deficient Mice." Blood 124, no. 21 (2014): 4200. http://dx.doi.org/10.1182/blood.v124.21.4200.4200.

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Abstract Wiskott-Aldrich syndrome (WAS) is a rare, X-chromosomal recessive disorder which is caused by mutations in the WAS gene and characterized by eczema, immunodeficiency and microthrombocytopenia (Thrasher and Burns, Nat Rev Immunol 2010). Interestingly, WAS protein (WASp)-deficient mice have normal-sized platelets and thus the molecular link between WAS mutations and its central hallmark microthrombocytopenia remains elusive. Profilin1 (Pfn1) is a key actin-regulating protein that, besides actin, interacts with phosphoinositides and multiple proline-rich proteins including the WAS protei

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Gau, David, Lucile Vignaud, Abigail Allen, et al. "Disruption of profilin1 function suppresses developmental and pathological retinal neovascularization." Journal of Biological Chemistry 295, no. 28 (2020): 9618–29. http://dx.doi.org/10.1074/jbc.ra120.012613.

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Angiogenesis-mediated neovascularization in the eye is usually associated with visual complications. Pathological angiogenesis is particularly prominent in the retina in the settings of proliferative diabetic retinopathy, in which it can lead to permanent loss of vision. In this study, by bioinformatics analyses, we provide evidence for elevated expression of actin-binding protein PFN1 (profilin1) in the retinal vascular endothelial cells (VECs) of individuals with proliferative diabetic retinopathy, findings further supported by gene expression analyses for PFN1 in experimentally induced abno

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Yang, Chunxing, Eric W. Danielson, Tao Qiao, et al. "Mutant PFN1 causes ALS phenotypes and progressive motor neuron degeneration in mice by a gain of toxicity." Proceedings of the National Academy of Sciences 113, no. 41 (2016): E6209—E6218. http://dx.doi.org/10.1073/pnas.1605964113.

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Mutations in the profilin 1 (PFN1) gene cause amyotrophic lateral sclerosis (ALS), a neurodegenerative disease caused by the loss of motor neurons leading to paralysis and eventually death. PFN1 is a small actin-binding protein that promotes formin-based actin polymerization and regulates numerous cellular functions, but how the mutations in PFN1 cause ALS is unclear. To investigate this problem, we have generated transgenic mice expressing either the ALS-associated mutant (C71G) or wild-type protein. Here, we report that mice expressing the mutant, but not the wild-type, protein had relentles

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Gau, David, Jennifer Taylor, Walter Storkus, and Partha Roy. "40 Preclinical evaluation of a novel dendritic cell vaccine for kidney cancer." Oncologist 29, Supplement_1 (2024): S24—S25. http://dx.doi.org/10.1093/oncolo/oyae181.039.

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Abstract Background Dendritic cell (DC)-based vaccines have been previously shown to promote therapeutic T cell responses in both preclinical tumor models and in cancer patients, where extended patient overall survival has been noted in many cases. The goal of the present study is to develop a novel DC-based vaccine as an effective immuno-oncology (IO) agent for the prevention/treatment of kidney cancer. We previously demonstrated that actin-binding protein profilin1 (Pfn1) is overexpressed in tumor-associated vascular endothelial cells (ECs), where it may serve as a prognostic factor in human

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17

Ling, Zhu, Hailati Aini, Shuhei Kajikawa, et al. "Osteolytic Bone Loss and Skeletal Deformities in a Mouse Model for Early-Onset Paget’s Disease of Bone with PFN1 Mutation Are Treatable by Alendronate." Pharmaceuticals 16, no. 10 (2023): 1395. http://dx.doi.org/10.3390/ph16101395.

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A novel osteolytic disorder due to PFN1 mutation was discovered recently as early-onset Paget’s disease of bone (PDB). Bone loss and pain in adult PDB patients have been treated using bisphosphonates. However, therapeutic strategies for this specific disorder have not been established. Here, we evaluated the efficiency of alendronate (ALN) on a mutant mouse line, recapitulating this disorder. Five-week-old conditional osteoclast-specific Pfn1-deficient mice (Pfn1-cKOOCL) and control littermates (33 females and 22 males) were injected with ALN (0.1 mg/kg) or vehicle twice weekly until 8 weeks o

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18

Haake, Susan Kinder, Sean C. Yoder, Gwynne Attarian, and Kara Podkaminer. "Native Plasmids of Fusobacterium nucleatum: Characterization and Use in Development of Genetic Systems." Journal of Bacteriology 182, no. 4 (2000): 1176–80. http://dx.doi.org/10.1128/jb.182.4.1176-1180.2000.

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ABSTRACT Three native plasmids of Fusobacterium nucleatum were characterized, including DNA sequence analysis of one plasmid, pFN1. A shuttle plasmid, pHS17, capable of transforming Escherichia coli and F. nucleatum ATCC 10953 was constructed with pFN1. pHS17 was stably maintained in the F. nucleatum transformants, and differences in the transformation efficiencies suggested the presence of a restriction-modification system in F. nucleatum.

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Merlotti, Daniela, Maria Materozzi, Simone Bianciardi, et al. "Mutation of PFN1 Gene in an Early Onset, Polyostotic Paget-like Disease." Journal of Clinical Endocrinology & Metabolism 105, no. 8 (2020): 2553–65. http://dx.doi.org/10.1210/clinem/dgaa252.

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Abstract Context Paget disease of bone (PDB) is a metabolic bone disease whose genetic cause remains unknown in up to 50% of familial patients. Objective Our aim was to investigate the underlying genetic defect in a large pedigree with a severe, early onset, autosomal dominant form of PDB across 3 generations. Methods Whole exome sequencing was performed in affected and unaffected family members, and then mutation screening was replicated in a sample of PDB patients with early-onset, polyostotic PDB. Results We identified a frameshift D107Rfs*3 mutation in PFN1 (encoding for profilin 1, a high

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Janke, Jürgen, Kathrin Schlüter, Burkhard Jandrig, et al. "Suppression of Tumorigenicity in Breast Cancer Cells by the Microfilament Protein Profilin 1." Journal of Experimental Medicine 191, no. 10 (2000): 1675–86. http://dx.doi.org/10.1084/jem.191.10.1675.

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Differential display screening was used to reveal differential gene expression between the tumorigenic breast cancer cell line CAL51 and nontumorigenic microcell hybrids obtained after transfer of human chromosome 17 into CAL51. The human profilin 1 (PFN1) gene was found overexpressed in the microcell hybrid clones compared with the parental line, which displayed a low profilin 1 level. A comparison between several different tumorigenic breast cancer cell lines with nontumorigenic lines showed consistently lower profilin 1 levels in the tumor cells. Transfection of PFN1 cDNA into CAL51 cells r

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Jian, Jie, and Liang Xia. "miR-1226-3p Promotes eNOS Expression of Pulmonary Arterial Endothelial Cells to Mitigate Hypertension in Rats via Targeting Profilin-1." BioMed Research International 2021 (November 3, 2021): 1–7. http://dx.doi.org/10.1155/2021/1724722.

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In pulmonary arterial hypertension (PAH), microRNAs (miRNAs) are related with dysfunction of pulmonary arterial endothelial cells. miR-1226-3p was found to be downregulated in the serum of PAH patients, while few studies have illustrated the regulation mechanism of miR-1226-3p on PAH. In this study, we aimed to systematically investigate the role of miR-1226-3p in PAH. Sprague-Dawley (SD) rats were treated with monocrotaline (MCT) to establish the PAH models. The right ventricular systolic pressure (RVSP), ratio of the right ventricle to the left ventricle with septum (RV/(LV+S) ratio), and ni

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Michaelsen-Preusse, Kristin, Sabine Zessin, Gayane Grigoryan, et al. "Neuronal profilins in health and disease: Relevance for spine plasticity and Fragile X syndrome." Proceedings of the National Academy of Sciences 113, no. 12 (2016): 3365–70. http://dx.doi.org/10.1073/pnas.1516697113.

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Learning and memory, to a large extent, depend on functional changes at synapses. Actin dynamics orchestrate the formation of synapses, as well as their stabilization, and the ability to undergo plastic changes. Hence, profilins are of key interest as they bind to G-actin and enhance actin polymerization. However, profilins also compete with actin nucleators, thereby restricting filament formation. Here, we provide evidence that the two brain isoforms, profilin1 (PFN1) and PFN2a, regulate spine actin dynamics in an opposing fashion, and that whereas both profilins are needed during synaptogene

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Ree, Rasmus, Laura Kind, Anna Kaziales, et al. "PFN2 and NAA80 cooperate to efficiently acetylate the N-terminus of actin." Journal of Biological Chemistry 295, no. 49 (2020): 16713–31. http://dx.doi.org/10.1074/jbc.ra120.015468.

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The actin cytoskeleton is of profound importance to cell shape, division, and intracellular force generation. Profilins bind to globular (G-)actin and regulate actin filament formation. Although profilins are well-established actin regulators, the distinct roles of the dominant profilin, profilin 1 (PFN1), versus the less abundant profilin 2 (PFN2) remain enigmatic. In this study, we use interaction proteomics to discover that PFN2 is an interaction partner of the actin N-terminal acetyltransferase NAA80, and further confirm this by analytical ultracentrifugation. Enzyme assays with NAA80 and

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Klingenspor, Martin, Jackie Bodnar, Yu-Rong Xia, Carrie Welch, Aidons J. Lusis, and Karen Reue. "Localization of profilin-1 (Pfn1) and a related sequence (Pfn1-rs) to mouse Chromosomes 11 and 15 respectively." Mammalian Genome 8, no. 7 (1997): 539–40. http://dx.doi.org/10.1007/s003359900496.

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Vavlukis, Ana, Kristina Mladenovska, Katarina Davalieva, Marija Vavlukis, and Aleksandar Dimovski. "Rosuvastatin effects on the HDL proteome in hyperlipidemic patients." Acta Pharmaceutica 73, no. 3 (2023): 363–84. http://dx.doi.org/10.2478/acph-2023-0034.

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Abstract The advancements in proteomics have provided a better understanding of the functionality of apolipoproteins and lipoprotein-associated proteins, with the HDL lipoprotein fraction being the most studied. The focus of this study was to evaluate the HDL proteome in dyslipidemic subjects without an established cardiovascular disease, as well as to test whether rosuvastatin treatment alters the HDL proteome. Patients with primary hypercholesterolemia or mixed dyslipidemia were assigned to 20 mg/day rosuvastatin and blood samples were drawn at study entry and after 12 weeks of treatment. A

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Bochenek, D., G. Dercz, and D. Oleszak. "Application of Mechanical Activation in Synthesizing Multiferroic Pb(Fe1/2Nb1/2)O3 Powders." Archives of Metallurgy and Materials 56, no. 4 (2011): 1015–20. http://dx.doi.org/10.2478/v10172-011-0112-y.

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Application of Mechanical Activation in Synthesizing Multiferroic Pb(Fe1/2Nb1/2)O3 Powders In the study, the method of high-energy powder milling - mechanical activation (MA) was used for synthesizing Pb(Fe1/2Nb1/2)O3 (PFN) powders. For the purpose of comparing the influence of high-energy milling on PFN synthesis, two groups of powder samples were used. The first mixture consisting of simple oxide powders; the second one consisting of compound oxide powders. The obtained powders were subjected to structural analysis with the use of XRD and Mőssbauer spectroscopy. Tests revealed that during th

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Zou, Zhang-Yu, Shi-Dong Chen, Shu-Yan Feng, et al. "Familial flail leg ALS caused by PFN1 mutation." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 2 (2019): 223–24. http://dx.doi.org/10.1136/jnnp-2019-321366.

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Kakurina, G. V., E. E. Sereda, O. V. Cheremisina, et al. "The relationship between gene expression of cytoskeletal protein genes and the epithelial-mesenchymal vimentin marker in squamous cell carcinoma of the larynx." Yakut Medical Journal, no. 2 (June 22, 2025): 19–23. https://doi.org/10.25789/ymj.2025.90.04.

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Aggressive laryngeal squamous cell carcinoma (LSCC) is characterized by a high metastatic potential, which is closely associated with epithelial-mesenchymal transition (EMT). Initiation of EMT is manifested by changes in the expression of some genes, including those associated with cytoskeleton reorganization. Currently, there are no effective methods for predicting metastasis in LSCC patients. In this regard, the study of SCC molecular characteristics remains relevant. In our study we assessed the relationship between the mRNA level of vimentin (VIM) and mRNA of cytoskeleton proteins: fascin-

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Pereira, Gabriel Rodrigues Coutinho, Giovanni Henrique Almeida Silva Tellini, and Joelma Freire De Mesquita. "In silico analysis of PFN1 related to amyotrophic lateral sclerosis." PLOS ONE 14, no. 6 (2019): e0215723. http://dx.doi.org/10.1371/journal.pone.0215723.

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Daoud, Hussein, Sylvia Dobrzeniecka, William Camu, et al. "Mutation analysis of PFN1 in familial amyotrophic lateral sclerosis patients." Neurobiology of Aging 34, no. 4 (2013): 1311.e1–1311.e2. http://dx.doi.org/10.1016/j.neurobiolaging.2012.09.001.

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Cànaves-Gómez, Laura, Aarne Fleischer, Josep Muncunill-Farreny, et al. "Effect of Obstructive Sleep Apnea during Pregnancy on Fetal Development: Gene Expression Profile of Cord Blood." International Journal of Molecular Sciences 25, no. 10 (2024): 5537. http://dx.doi.org/10.3390/ijms25105537.

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Obstructive sleep apnea (OSA) is quite prevalent during pregnancy and is associated with adverse perinatal outcomes, but its potential influence on fetal development remains unclear. This study investigated maternal OSA impact on the fetus by analyzing gene expression profiles in whole cord blood (WCB). Ten women in the third trimester of pregnancy were included, five OSA and five non-OSA cases. WCB RNA expression was analyzed by microarray technology to identify differentially expressed genes (DEGs) under OSA conditions. After data normalization, 3238 genes showed significant differential exp

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Kakurina, Gelena V., Marina N. Stakheeva, Islombek A. Bakhronov, et al. "Circulating Actin-Binding Proteins in Laryngeal Cancer: Its Relationship with Circulating Tumor Cells and Cells of the Immune System." Acta Naturae 13, no. 4 (2021): 64–68. http://dx.doi.org/10.32607/actanaturae.11413.

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We previously exposed the role of actin-binding proteins (ABPs) in cancer development and progression. In this paper, we studied the relationship between circulating ABPs and the number of ABP-expressing leukocytes and circulating tumor cells (CTCs) in patients with highly aggressive laryngeal squamous cell carcinoma (LSCC). The levels of cofilin (CFL1), profilin (PFN1), ezrin (EZR), fascin (FSCN1), and adenylate cyclase-associated protein 1 (CAP1) were determined using enzyme immunoassay. The ABP expression by the cellular pools was analyzed by flow cytometry. The highest levels of FSCN1 and

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Ulyanova, Vera, Raihan Shah Mahmud, Alexander Laikov, et al. "Anti-Influenza Activity of the Ribonuclease Binase: Cellular Targets Detected by Quantitative Proteomics." International Journal of Molecular Sciences 21, no. 21 (2020): 8294. http://dx.doi.org/10.3390/ijms21218294.

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Unpredictable influenza pandemics, annual epidemics, and sporadic poultry-to-human avian influenza virus infections with high morbidity and mortality rates dictate a need to develop new antiviral approaches. Targeting cellular pathways and processes is a promising antiviral strategy shown to be effective regardless of viral subtypes or viral evolution of drug-resistant variants. Proteomics-based searches provide a tool to reveal the druggable stages of the virus life cycle and to understand the putative antiviral mode of action of the drug(s). Ribonucleases (RNases) of different origins not on

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Huang, Yongguo, Hong Sun, Xiang Ma, et al. "HLA-F-AS1/miR-330-3p/PFN1 axis promotes colorectal cancer progression." Life Sciences 254 (August 2020): 117180. http://dx.doi.org/10.1016/j.lfs.2019.117180.

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Chen, YongPing, Zhen-Zhen zheng, Rui Huang, et al. "PFN1 mutations are rare in Han Chinese populations with amyotrophic lateral sclerosis." Neurobiology of Aging 34, no. 7 (2013): 1922.e1–1922.e5. http://dx.doi.org/10.1016/j.neurobiolaging.2013.01.013.

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Nekouei, Mina, Parviz Ghezellou, Atousa Aliahmadi, Sareh Arjmand, Mahmoud Kiaei, and Alireza Ghassempour. "Changes in biophysical characteristics of PFN1 due to mutation causing amyotrophic lateral sclerosis." Metabolic Brain Disease 33, no. 6 (2018): 1975–84. http://dx.doi.org/10.1007/s11011-018-0305-4.

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Syriani, Enrique, Candi Salvans, Maria Salvadó, et al. "PFN1 mutations are also rare in the Catalan population with amyotrophic lateral sclerosis." Journal of Neurology 261, no. 12 (2014): 2387–92. http://dx.doi.org/10.1007/s00415-014-7501-x.

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Garitano-Trojaola, Andoni, Ana Sancho, Ralph Goetz, et al. "RAC1 Inhibitor EHT1864 and Venetoclax Overcome Midostaurin Resistance in Acute Myeloid Leukemia." Blood 134, Supplement_1 (2019): 1277. http://dx.doi.org/10.1182/blood-2019-129762.

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Introduction Acute Myeloid Leukemia (AML) is a genetically heterogeneous disease characterized by clonal expansion of immature myeloid progenitor cells in the bone marrow (BM). Mutations of the FMS-like tyrosine kinase 3 (FLT3) gene occur in approximately 30% of AML cases, with Internal Tandem Duplications (ITD) being the most common type of mutation. Several FLT3 specific inhibitors (TKI) have been developed such as quizartinib, crenolanib and midostaurin (recently approved for clinical use). Nevertheless FLT3-ITD is associated with unfavorable prognosis and patients develop drug resistance w

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Wu, Suwen, Yutong Cui, Huanqiang Zhao, et al. "Trophoblast Exosomal UCA1 Induces Endothelial Injury through the PFN1-RhoA/ROCK Pathway in Preeclampsia: A Human-Specific Adaptive Pathogenic Mechanism." Oxidative Medicine and Cellular Longevity 2022 (September 15, 2022): 1–19. http://dx.doi.org/10.1155/2022/2198923.

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Preeclampsia is regarded as an evolution-related disease that has only been observed in humans and our closest relatives, and the important factor contributing to its pathogenesis is endothelial dysregulation secondary to a stressed placenta. Hypoxia-inducible factor 1 subunit alpha (HIF1α), a highly conserved molecule in virtually all mammals, is regarded as a crucial regulator of the hypoxia adaptation and evolution. Persistent high expression of HIF1α in the placenta is one of the pathogenic mechanisms of preeclampsia. Therefore, human-specific molecules should link increased HIF1α to preec

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Shih, Ping-Cheng, I.-Shiang Tzeng, Yi-Chyan Chen, and Mao-Liang Chen. "Gastrodin Mitigates Ketamine-Induced Inhibition of F-Actin Remodeling and Cell Migration by Regulating the Rho Signaling Pathway." Biomedicines 13, no. 3 (2025): 649. https://doi.org/10.3390/biomedicines13030649.

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Background/Objects: Rho signaling plays a role in calcium-regulated cytoskeletal reorganization and cell movement, processes linked to neuronal function and cancer metastasis. Gastrodia elata, a traditional herbal medicine, can regulate glutamate-induced calcium influx in PC12 cells and influence cell function by modulating neuronal cytoskeleton remodeling via the monoaminergic system and Rho signaling. This study investigates the effects of gastrodin, a key component of Gastrodia elata, on Rho signaling, cytoskeleton remodeling, and cell migration in B35 and C6 cells. It also explores gastrod

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Tiloca, Cinzia, Nicola Ticozzi, Viviana Pensato, et al. "Screening of the PFN1 gene in sporadic amyotrophic lateral sclerosis and in frontotemporal dementia." Neurobiology of Aging 34, no. 5 (2013): 1517.e9–1517.e10. http://dx.doi.org/10.1016/j.neurobiolaging.2012.09.016.

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Yang, Shu, Jennifer A. Fifita, Kelly L. Williams, et al. "Mutation analysis and immunopathological studies of PFN1 in familial and sporadic amyotrophic lateral sclerosis." Neurobiology of Aging 34, no. 9 (2013): 2235.e7–2235.e10. http://dx.doi.org/10.1016/j.neurobiolaging.2013.04.003.

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Zhang, Shaoyang, Xuemin Guo, Xiufeng Liu, Zhixiong Zhong, Shulan Yang, and Haihe Wang. "Correction to: Adaptor SH3BGRL promotes breast cancer metastasis through PFN1 degradation by translational STUB1 upregulation." Oncogene 41, no. 8 (2021): 1227. http://dx.doi.org/10.1038/s41388-021-02129-1.

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Tomasello, Laura, Antonina Coppola, Maria Pitrone та ін. "PFN1 and integrin‐β1/mTOR axis involvement in cornea differentiation of fibroblast limbal stem cells". Journal of Cellular and Molecular Medicine 23, № 11 (2019): 7210–21. http://dx.doi.org/10.1111/jcmm.14438.

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Zhang, Leili, David R. Bell, Binquan Luan, and Ruhong Zhou. "Exploring the binding mechanism between human profilin (PFN1) and polyproline-10 through binding mode screening." Journal of Chemical Physics 150, no. 1 (2019): 015102. http://dx.doi.org/10.1063/1.5053922.

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Chi, Jieshan, Junling Chen, Yan Li, Zhiheng Huang, Lijuan Wang, and Yuhu Zhang. "A Familial Phenotypic and Genetic Study of Mutations in PFN1 Associated with Amyotrophic Lateral Sclerosis." Neuroscience Bulletin 36, no. 2 (2019): 174–78. http://dx.doi.org/10.1007/s12264-019-00448-8.

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Wu, Chi-Hong, Anthony Giampetruzzi, Helene Tran, Claudia Fallini, Fen-Biao Gao, and John E. Landers. "A Drosophila model of ALS reveals a partial loss of function of causative human PFN1 mutants." Human Molecular Genetics 26, no. 11 (2017): 2146–55. http://dx.doi.org/10.1093/hmg/ddx112.

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Chen, Yi-Chyan, Chang-Ti Lee, Fu-Ming Tsai, and Mao-Liang Chen. "The Effects of Poria cocos on Rho Signaling-Induced Regulation of Mobility and F-Actin Aggregation in MK-801-Treated B35 and C6 Cells." Behavioural Neurology 2022 (July 12, 2022): 1–10. http://dx.doi.org/10.1155/2022/8225499.

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Background and Aim. We recently investigated whether Poria cocos water extract modulates ketamine-induced Rho signaling regulation and reverses ketamine-inhibited cell mobility and F-actin reconstruction in B35 and C6 cells. Various studies have mentioned that drugs of abuse induce changes in neuronal plasticity in the brain’s reward circuitry. Modulations in neuronal plasticity are closely related to Rho signaling regulation in cells. Rho signaling has also been implicated in the addictive behavior induced by chronic opiate or morphine administration. MK-801 could induce Rho signaling regulat

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Bai, Ni, Ying Ma, Jia Zhao, and Bo Li. "Knockdown of lncRNA HCP5 Suppresses the Progression of Colorectal Cancer by miR-299-3p/PFN1/AKT Axis." Cancer Management and Research Volume 12 (June 2020): 4747–58. http://dx.doi.org/10.2147/cmar.s255866.

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Li, Juexing, Lei Zhou, Yuanliang Jiang, Hailan Gao, Tuersuntuoheti Maierhaba, and Hui Gong. "Long noncoding RNA RMRP ameliorates doxorubicin-induced apoptosis by interacting with PFN1 in a P53-Dependent manner." Molecular and Cellular Probes 72 (December 2023): 101937. http://dx.doi.org/10.1016/j.mcp.2023.101937.

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