Relevant bibliographies by topics / Pq4305

Academic literature on the topic 'Pq4305'

Author: Grafiati
Published: 25 July 2024
Last updated: 26 July 2024

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Journal articles on the topic "Pq4305"

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Engdahl, Taylor B., F. Graeme Frost, Amanda J. Schech, and Samantha L. Elliott. "Viability and migratory effects of IGF-1R inhibitor, PQ401, on triple negative breast cancer cells." BIOS 90, no. 1 (October 26, 2019): 14. http://dx.doi.org/10.1893/0005-3155-90.1.14.

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Zhou, Xiang, Xinli Zhao, Xiangsheng Li, Guanfang Ping, Sujuan Pei, Ming Chen, Zhongwei Wang, Wenke Zhou, and Baozhe Jin. "PQ401, an IGF-1R inhibitor, induces apoptosis and inhibits growth, proliferation and migration of glioma cells." Journal of Chemotherapy 28, no. 1 (January 2, 2016): 44–49. http://dx.doi.org/10.1179/1973947815y.0000000026.

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Maher, Lynn M., and Anastasia M. Raymer. "Management of Anomia." Topics in Stroke Rehabilitation 11, no. 1 (January 2004): 10–21. http://dx.doi.org/10.1310/318r-rmd5-055j-pq40.

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Ghosh, Manik C., Vijay Gorantla, Patrudu S. Makena, Charlean Luellen, Scott E. Sinclair, Andreas Schwingshackl, and Christopher M. Waters. "Insulin-like growth factor-I stimulates differentiation of ATII cells to ATI-like cells through activation of Wnt5a." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 3 (August 1, 2013): L222—L228. http://dx.doi.org/10.1152/ajplung.00014.2013.

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Alveolar type II (ATII) epithelial cells play a crucial role in the repair and remodeling of the lung following injury. ATII cells have the capability to proliferate and differentiate into alveolar type I (ATI) cells in vivo and into an ATI-like phenotype in vitro. While previous reports indicate that the differentiation of ATII cells into ATI cells is a complex biological process, the underlying mechanism responsible for differentiation is not fully understood. To investigate factors involved in this differentiation in culture, we used a PCR array and identified several genes that were either up- or downregulated in ATI-like cells ( day 6 in culture) compared with day 2 ATII cells. Insulin-like growth factor-I (IGF-I) mRNA was increased nearly eightfold. We found that IGF-I was increased in the culture media of ATI-like cells and demonstrated a significant role in the differentiation process. Treatment of ATII cells with recombinant IGF-I accelerated the differentiation process, and this effect was abrogated by the IGF-I receptor blocker PQ401. We found that Wnt5a, a member of the Wnt-Frizzled pathway, was activated during IGF-I-mediated differentiation. Both protein kinase C and β-catenin were transiently activated during transdifferentiation. Knocking down Wnt5a using small-interfering RNA abrogated the differentiation process as indicated by changes in the expression of an ATII cell marker (prosurfactant protein-C). Treatment of wounded cells with either IGF-I or Wnt5a stimulated wound closure. These results suggest that IGF-I promotes differentiation of ATII to ATI cells through the activation of a noncanonical Wnt pathway.
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Kim, Wooseong, Guijin Zou, Wen Pan, Nico Fricke, Hammad A. Faizi, Soo Min Kim, Rajamohammed Khader, et al. "The Neutrally Charged Diarylurea Compound PQ401 Kills Antibiotic-Resistant and Antibiotic-Tolerant Staphylococcus aureus." mBio 11, no. 3 (June 30, 2020). http://dx.doi.org/10.1128/mbio.01140-20.

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ABSTRACT Resistance or tolerance to traditional antibiotics is a challenging issue in antimicrobial chemotherapy. Moreover, traditional bactericidal antibiotics kill only actively growing bacterial cells, whereas nongrowing metabolically inactive cells are tolerant to and therefore “persist” in the presence of legacy antibiotics. Here, we report that the diarylurea derivative PQ401, previously characterized as an inhibitor of the insulin-like growth factor I receptor, kills both antibiotic-resistant and nongrowing antibiotic-tolerant methicillin-resistant Staphylococcus aureus (MRSA) by lipid bilayer disruption. PQ401 showed several beneficial properties as an antimicrobial lead compound, including rapid killing kinetics, low probability for resistance development, high selectivity to bacterial membranes compared to mammalian membranes, and synergism with gentamicin. In contrast to well-studied membrane-disrupting cationic antimicrobial low-molecular-weight compounds and peptides, molecular dynamic simulations supported by efficacy data demonstrate that the neutral form of PQ401 penetrates and subsequently embeds into bacterial lipid bilayers more effectively than the cationic form. Lastly, PQ401 showed efficacy in both the Caenorhabditis elegans and Galleria mellonella models of MRSA infection. These data suggest that PQ401 may be a lead candidate for repurposing as a membrane-active antimicrobial and has potential for further development as a human antibacterial therapeutic for difficult-to-treat infections caused by both drug-resistant and -tolerant S. aureus. IMPORTANCE Membrane-damaging antimicrobial agents have great potential to treat multidrug-resistant or multidrug-tolerant bacteria against which conventional antibiotics are not effective. However, their therapeutic applications are often hampered due to their low selectivity to bacterial over mammalian membranes or their potential for cross-resistance to a broad spectrum of cationic membrane-active antimicrobial agents. We discovered that the diarylurea derivative compound PQ401 has antimicrobial potency against multidrug-resistant and multidrug-tolerant Staphylococcus aureus. PQ401 selectively disrupts bacterial membrane lipid bilayers in comparison to mammalian membranes. Unlike cationic membrane-active antimicrobials, the neutral form of PQ401 rather than its cationic form exhibits maximum membrane activity. Overall, our results demonstrate that PQ401 could be a promising lead compound that overcomes the current limitations of membrane selectivity and cross-resistance. Also, this work provides deeper insight into the design and development of new noncharged membrane-targeting therapeutics to combat hard-to-cure bacterial infections.
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Li, Junhong, Xin Zhou, Jialin Chen, Pernilla Eliasson, Paul J. Kingham, and Ludvig J. Backman. "Secretome from myoblasts statically loaded at low intensity promotes tenocyte proliferation via the IGF‐1 receptor pathway." FASEB Journal 37, no. 10 (September 21, 2023). http://dx.doi.org/10.1096/fj.202301097r.

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AbstractExercise is widely recognized as beneficial for tendon healing. Recently, it has been described that muscle‐derived molecules secreted in response to static exercise influence tendon healing. In this study, the optimal static loading intensity for tendon healing and the composition of secretome released by myoblasts in response to different intensities of static strain were investigated. In an in vitro coculture model, myoblasts were mechanically loaded using a Flexcell Tension System. Tenocytes were seeded on transwell inserts that allowed communication between the tenocytes and myoblasts without direct contact. Proliferation and migration assays, together with RNA sequencing, were used to determine potential cellular signaling pathways. The secretome from myoblasts exposed to 2% static loading increased the proliferation and migration of the cocultured tenocytes. RNA‐seq analysis revealed that this loading condition upregulated the expression of numerous genes encoding secretory proteins, including insulin‐like growth factor‐1 (IGF‐1). Confirmation of IGF‐1 expression and secretion was carried out using qPCR and enzyme‐linked immunosorbt assay (ELISA), revealing a statistically significant upregulation in response to 2% static loading in comparison to both control conditions and higher loading intensities of 5% and 10%. Addition of an inhibitor of the IGF‐1 receptor (PQ401) to the tenocytes significantly reduced myoblast secretome‐induced tenocyte proliferation. In conclusion, IGF‐1 may be an important molecule in the statically loaded myoblast secretome, which is responsible for influencing tenocytes during exercise‐induced healing.
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Vong, Chi Teng, Dechao Tan, Fengyun Liao, Zhejie Chen, Zhangmei Chen, Hisa Hui Ling Tseng, Wai San Cheang, Shengpeng Wang, and Yitao Wang. "Ginsenoside Rk1 Ameliorates ER Stress-Induced Apoptosis through Directly Activating IGF-1R in Mouse Pancreatic β-Cells and Diabetic Pancreas." American Journal of Chinese Medicine, May 27, 2024, 1–17. http://dx.doi.org/10.1142/s0192415x24500484.

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Hyperglycemia induces chronic stresses, such as oxidative stress and endoplasmic reticulum (ER) stress, which can result in [Formula: see text]-cell dysfunction and development of Type 2 Diabetes Mellitus (T2DM). Ginsenoside Rk1 is a minor ginsenoside isolated from Ginseng. It has been shown to exert anti-cancer, anti-inflammatory, anti-oxidant, and neuroprotective effects; however, its effects on pancreatic cells in T2DM have never been studied. This study aims to examine the novel effects of Ginsenoside Rk1 on ER stress-induced apoptosis in a pancreatic [Formula: see text]-cell line MIN6 and HFD-induced diabetic pancreas, and their underlying mechanisms. We demonstrated that Ginsenoside Rk1 alleviated ER stress-induced apoptosis in MIN6 cells, which was accomplished by directly targeting and activating insulin-like growth factor 1 receptor (IGF-1R), thus activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/Bcl-2-associated agonist of cell death (Bad)-B-cell lymphoma-2 (Bcl-2) pathway. This pathway was also confirmed in an HFD-induced diabetic pancreas. Meanwhile, the use of the IGF-1R inhibitor PQ401 abolished this anti-apoptotic effect, confirming the role of IGF-1R in mediating anti-apoptosis effects exerted by Ginsenoside Rk1. Besides, Ginsenoside Rk1 reduced pancreas weights and increased pancreatic insulin contents, suggesting that it could protect the pancreas from HFD-induced diabetes. Taken together, our study provided novel protective effects of Ginsenoside Rk1 on ER stress-induced [Formula: see text]-cell apoptosis and HFD-induced diabetic pancreases, as well as its direct target with IGF-1R, indicating that Ginsenoside Rk1 could be a potential drug for the treatment of T2DM.
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Small, Theodore W., and J. Geoffrey Pickering. "Abstract 270: Insulin-Like Growth Factor-1 Promotes Vascular Smooth Muscle Survival By 26S Proteasome-Mediated Degradation of Wilms’ Tumor 1-Associating Protein." Circulation 116, suppl_16 (October 16, 2007). http://dx.doi.org/10.1161/circ.116.suppl_16.ii_34-a.

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Apoptosis of vascular smooth muscle cells (SMC) is a culprit event in atherosclerotic plaque destabilization. We recently discovered that Wilms’ tumor 1-associating protein (WTAP) is a dynamically expressed transcriptional regulator that can be pro-apoptotic for human SMCs (Circ Res, 2006). To identify upstream regulators of this nuclear protein, we screened growth factors for their capacity to impact WTAP expression and found that insulin-like growth factor-1 (IGF-1), a potent survival factor for SMCs, stimulated a striking decline in WTAP protein abundance, to 10% at 12 h. We further determined that this decline in WTAP was due specifically to WTAP protein degradation, established by pulse-chase analysis of 35 S-labeled WTAP and the absence of an acute effect of IGF-1 on WTAP mRNA abundance. IGF-1-mediated WTAP degradation was blocked by two mechanistically distinct IGF-1 receptor inhibitors (picropodophyllin and PQ401) and by inhibition of phosphatidylinositol 3 (PI3)-kinase but not by MEK inhibition. In addition, IGF-1 induced the association of WTAP with ubiquitin, established by coimmunoprecipitation, and the downregulation of WTAP by IGF-1 was abrogated by inhibiting 26S proteasome activity with lactacystin or MG132. Interestingly, IGF-1 also stimulated phosphorylation of WTAP, that preceded the association of WTAP with ubiquitin, and hyperphosphorylation of WTAP through phosphatase-inhibition further accelerated WTAP degradation. Finally, to determine if WTAP downregulation was necessary for IGF-1-mediated SMC survival, surface expression of phosphatidylserine was quantified by flow cytometry of SMCs infected with retrovirus containing WTAP cDNA. Whereas IGF-1 enhanced the survival of vector-infected SMCs this was completely abrogated in WTAP-overexpressing SMCs. Conclusions: IGF-1-mediated SMC survival is dependent on the rapid depletion of WTAP from the nucleus, a degradation cascade that is heralded by WTAP phosphorylation. This WTAP phosphorylation and clearance response represents a novel consequence of PI3-kinase activation and highlights WTAP as a key negative regulator of SMC survival during vascular remodeling.
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Dissertations / Theses on the topic "Pq4305"

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Giuliana, Chiara. "Negotiating home spaces : spatial practices in Italian postcolonial literature." Thesis, University of St Andrews, 2015. http://hdl.handle.net/10023/9764.

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Books on the topic "Pq4305"

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Alighieri, Dante. L' ottimo commento della Divina commedia. [Bologna]: A. Forni, 1995.

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Alighieri, Dante. Commento alla Divina commedia. Roma: Salerno, 2008.

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Alighieri, Dante. Commedia. [Milano]: Garzanti, 1987.

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Petrocchi, Giorgio, ed. Divina comedia. Madrid, España: Cátedra, 2013.

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Alighieri, Dante. Commedia: Paradiso. Milano: Garzanti, 1986.

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Alighieri, Dante. La divina commedia: Inferno. Milano: Mondadori, 1985.

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Burton, Raffel, and Carrigan Henry L. 1954-, eds. The divine comedy. Evanston, Ill: Northwestern University Press, 2010.

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M, Chiavacci Leonardi Anna, ed. Commedia. Milano: Mondadori, 1994.

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Alighieri, Dante. The divine comedy of Dante Alighieri. New York: Oxford University Press, 1996.

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La Divina Comedia / Divine Comédie. French & European Pubns, 2000.

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