Academic literature on the topic 'PF-562271'

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Journal articles on the topic "PF-562271"

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Fan, Guang-Pu, Wei Wang, Hui Zhao, et al. "Pharmacological Inhibition of Focal Adhesion Kinase Attenuates Cardiac Fibrosis in Mice Cardiac Fibroblast and Post-Myocardial-Infarction Models." Cellular Physiology and Biochemistry 37, no. 2 (2015): 515–26. http://dx.doi.org/10.1159/000430373.

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Background: To investigate the role of focal adhesion kinase (FAK)-mediated signaling in hypoxia-induced cardiac fibroblasts (CFs) differentiation and cardiac fibrosis post-myocardial infarction (MI) on a mice model. Methods: CFs of neonatal C57BL/6 mice were treated under normoxic, hypoxic, or hypoxic+PP2 (known as a Src kinase family inhibitor) conditions. Gene expressions of FAK, alpha-smooth muscle actin (α-SMA) and collagen type I alpha 1 (Col1α1), or α-SMA and vimentin levels were performed by RT-PCR and immunofluorescence staining, respectively. Thirty mice were surgically treated into
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Hong, Kyoung-Ok, Chi-Hyun Ahn, In-Hyoung Yang, et al. "Norcantharidin Suppresses YD-15 Cell Invasion Through Inhibition of FAK/Paxillin and F-Actin Reorganization." Molecules 24, no. 10 (2019): 1928. http://dx.doi.org/10.3390/molecules24101928.

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Norcantharidin (NCTD), a demethylated derivative of cantharidin, has been reported to exhibit activity against various types of cancers. However, the anti-invasive effects of NCTD and its molecular mechanism in human mucoepidermoid carcinoma (MEC) remain incompletely elucidated. Clonogenic, wound healing, invasion, zymography, western blotting and immunocytochemistry assays were performed in YD-15 cells to investigate the anti-invasive effect of NCTD and its molecular mechanism of action. The inhibitory effects of NCTD on invasiveness were compared with those of a novel focal adhesion kinase (
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Xu, H., D. Yin, K. J. Pierce, S. M. Shreeve, B. Duncan, and A. Bello. "Pharmacokinetics (PK) of PF-562271, a focal adhesion kinase (FAK) inhibitor, and its effect on CYP3A in patients with advanced nonhematologic malignancies." Journal of Clinical Oncology 28, no. 15_suppl (2010): 2553. http://dx.doi.org/10.1200/jco.2010.28.15_suppl.2553.

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Fenelon, Jane C., Baozeng Xu, and Jay M. Baltz. "Focal adhesion kinase PTK2 autophosphorylation is not required for the activation of sodium–hydrogen exchange by decreased cell volume in the preimplantation mouse embryo." Zygote 27, no. 3 (2019): 173–79. http://dx.doi.org/10.1017/s0967199419000212.

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SummaryRecovery from decreased cell volume is accomplished by a regulated increase of intracellular osmolarity. The acute response is activation of inorganic ion transport into the cell, the main effector of which is the Na+/H+ exchanger NHE1. NHE1 is rapidly activated by a cell volume decrease in early embryos, but how this occurs is incompletely understood. Elucidating cell volume-regulatory mechanisms in early embryos is important, as it has been shown that their dysregulation results in preimplantation developmental arrest. The kinase JAK2 has a role in volume-mediated NHE1 activation in a
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Nair, Rajesh R., Joel H. Tolentino, Milijana Ugrenovic, et al. "Mti-101 Induces Necrotic Cell Death in AML Cells Through Its Binding to Cell Surface Complexes Containing CD44 and ITGA4." Blood 120, no. 21 (2012): 869. http://dx.doi.org/10.1182/blood.v120.21.869.869.

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Abstract Abstract 869 We previously reported that the linear peptide referred to as HYD1 induces necrotic cell death in myeloma cell lines (Nair RR et al. Mol Cancer Ther. 2009 Aug;8(8):2441-51). We have now developed a more potent cyclic analog based on the active core region of the linear peptide which we now refer to as MTI-101. MTI-101, as a single agent, induces cell death in AML cell lines U937 and HL-60 with an IC50 value of 23.03 ± 0.67 and 36.06 ± 4.99 μM, respectively. Interestingly, unlike the conventional drugs therapies that succumb to cell adhesion mediated-drug resistance (CAM-D
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Du, Yuan, Shenglan Li, Tong Zhou, Jing Zhao, and Jiguang Liu. "SIPA1 boosts migration and proliferation, and blocks apoptosis of glioma by activating the phosphorylation of the FAK signaling pathway." Journal of Medical Biochemistry, September 5, 2021. http://dx.doi.org/10.5937/jomb0-32903.

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Background: We aimed to analyze the regulatory effects of SIPA1 (signal-induced proliferation-associated protein 1) on glioma progression and the dominant signaling pathway.
 Methods: Differential level of SIPA1 in glioma and normal tissues and cells was determined. Migratory, proliferative, apoptotic and cell cycle progression changes in A172 cells with overexpression or knockdown of SIPA1 were examined. Finally, protein levels of phosphorylated FAKs in A172 cells intervened by SIPA1 and the FAK inhibitor PF-562271 were detected.
 Results: SIPA1 was upregulated in glioma cases. Knoc
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Ali, Dalia, Sarah Abuelreich, Nora Alkeraishan, et al. "Multiple intracellular signaling pathways orchestrate adipocytic differentiation of human bone marrow stromal stem cells." Bioscience Reports 38, no. 1 (2018). http://dx.doi.org/10.1042/bsr20171252.

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Bone marrow adipocyte formation plays a role in bone homeostasis and whole body energy metabolism. However, the transcriptional landscape and signaling pathways associated with adipocyte lineage commitment and maturation are not fully delineated. Thus, we performed global gene expression profiling during adipocyte differentiation of human bone marrow stromal (mesenchymal) stem cells (hMSCs) and identified 2,589 up-regulated and 2,583 down-regulated mRNA transcripts. Pathway analysis on the up-regulated gene list untraveled enrichment in multiple signaling pathways including insulin receptor si
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Tien, Ting-Yi, Yih-Jer Wu, Cheng-Huang Su та ін. "Reduction of Connexin 43 Attenuates Angiogenic Effects of Human Smooth Muscle Progenitor Cells via Inactivation of Akt and NF-κB Pathway". Arteriosclerosis, Thrombosis, and Vascular Biology, 24 грудня 2020. http://dx.doi.org/10.1161/atvbaha.120.315650.

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Objective: Circulating progenitor cells possess vasculogenesis property and participate in repair of vascular injury. Cx (connexin) 43—a transmembrane protein constituting gap junctions—is involved in vascular pathology. However, the role of Cx43 in smooth muscle progenitor cells (SPCs) remained unclear. Approach and Results: Human SPCs cultured from CD34 + peripheral blood mononuclear cells expressed smooth muscle cell markers, such as smooth muscle MHC (myosin heavy chain), nonmuscle MHC, calponin, and CD140B, and Cx43 was the most abundant Cx isoform. To evaluate the role of Cx43 in SPCs, s
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Dissertations / Theses on the topic "PF-562271"

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Conway, Brianna. "Searching for Synergy: FAK Inhibition in Metastatic Breast Cancer Treatment." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37304.

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Breast cancer is the most common cancer among Canadian women and 14-20% will develop lethal metastases within 5 years. A potential novel therapeutic target is Focal Adhesion Kinase (FAK), a cytoplasmic tyrosine kinase. FAK’s expression is inversely correlated with survival and is known to regulate cell migration, proliferation and invasion. While tyrosine kinase inhibitors are historically ineffective as single agents, they are commonly used as part of combination therapies. Therefore, given its central role in tumor cell biology and cell signaling, we hypothesized that inhibiting FAK in comb
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Conference papers on the topic "PF-562271"

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Rolon-Reyes, Kimberleve, Luis A. Cubano, Alfredo Quiñones-Hinojosa, and Lilia Kucheryavykh. "Abstract B202: Combined therapy of temozolomide and PF-562271, a PYK2 inhibitor, reduces glioma tumor growth and dispersal compare to temozolomide monotherapy." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-b202.

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Rolon-Reyes, Kimberleve, Serguey Skatchkov, Misty Eaton, Luis Cubano, Jeffrey Harrison, and Lilia Kucheryavykh. "Abstract A26: PF-562271, a small molecule PYK2 inhibitor, reduces microglial pro-migratory effect and tumor dispersal in C57/B6 glioma bearing model." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a26.

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