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Littérature scientifique sur le sujet « LFM-A13 »

Auteur : Grafiati

Publié le 9 mars 2023

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Articles de revues sur le sujet "LFM-A13"

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Bam, Rakesh, Angela Pennisi, Xin Li, et al. "Bruton's Tyrosine Kinase (BTK) Is Indispensable for Myeloma Cell Migration towards SDF-1 and Induction of Osteoclastogenesis and Osteolytic Bone Disease." Blood 116, no. 21 (2010): 447. http://dx.doi.org/10.1182/blood.v116.21.447.447.

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Abstract Abstract 447 Bruton's tyrosine kinase (BTK), a nonreceptor tyrosine kinase of the TEC family of protein tyrosine kinases, is preferentially expressed in the hematopoietic cells and involved in B-lymphocytes survival and differentiation, and their migration towards SDF-1 gradient. BTK is also expressed in osteoclast precursors and plays indispensable role in osteoclastogenesis (Shinohara et al., Cell 2008). LFM-A13 is small molecule inhibitor of BTK and TEC, and can be tolerated even when animals are given daily dose of 100 mg/kg. The aims of the study were to investigate the effect of

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Akker, E. van den, T. B. van Dijk, U. Schmidt, et al. "The Btk inhibitor LFM-A13 is a potent inhibitor of Jak2 kinase activity." Biological Chemistry 385, no. 5 (2004): 409–13. http://dx.doi.org/10.1515/bc.2004.045.

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AbstractLFMA13, or α-cyano-β-hydroxy-β-methyl-N-(2,5-dibromophenyl)propenamide, was shown to inhibit Brutons tyrosine kinase (Btk). Here we show that LFM-A13 efficiently inhibits erythropoietin (Epo)-induced phosphorylation of the erythropoietin receptor, Janus kinase 2 (Jak2) and downstream signalling molecules. However, the tyrosine kinase activity of immunoprecipitated or in vitro translated Btk and Jak2 was equally inhibited by LFM-A13 in in vitro kinase assays. Finally, Epo-induced signal transduction was also inhibited in cells lacking Btk. Taken together, we conclude that LFM-A13 is a p

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Zhang, Wei, Ping Zhou, Xiao Jiang, Zhe Fan, Xingxin Xu та Fei Wang. "Negative Regulation of Tec Kinase Alleviates LPS-Induced Acute Kidney Injury in Mice via theTLR4/NF-κB Signaling Pathway". BioMed Research International 2020 (20 червня 2020): 1–15. http://dx.doi.org/10.1155/2020/3152043.

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Tec kinase is an important mediator in inflammatory immune response that enhances the activity of neutrophils and macrophages. However, information on its function in lipopolysaccharide- (LPS-) induced acute kidney injury (AKI) is limited. This study is aimed at determining whether Tec kinase was a regulator in AKI. An AKI model in mice was successfully established using intraperitoneal LPS. Results showed that the serum levels of creatinine (Cr), blood urea nitrogen (BUN), and cystatin-C (Cys-C) increased after intraperitoneal LPS injection. Renal tissue sustained significantly severe injury

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Bam, Rakesh, Wen Ling, Sharmin Khan, et al. "Cell Surface CXCR4 and BTK Expression Are Associated in Myeloma Cells and Osteoclast Precursors and Mediate Myeloma Cell Homing and Clonogenicity, and Osteoclastogenesis." Blood 118, no. 21 (2011): 884. http://dx.doi.org/10.1182/blood.v118.21.884.884.

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Abstract Abstract 884 Myeloma cells typically grow in bone, recruit osteoclast precursors and induce their differentiation and activity in areas adjacent to tumor foci. Clonal B-lymphocytes and plasma cells harboring lymphocytic phenotypes have a proposed role in sustaining myeloma. Bruton's tyrosine kinase (BTK) is expressed in hematopoietic cells and is particularly involved in B-lymphocyte function and osteoclastogenesis. The SDF-1/CXCR4 signaling pathway is reportedly involved in homing to bone of myeloma cells and osteoclast precursors. The aims of the study were to investigate the possib

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Wang, Gaiqing, Zhenni Guo, Lusha Tong, et al. "TLR7 (Toll-Like Receptor 7) Facilitates Heme Scavenging Through the BTK (Bruton Tyrosine Kinase)–CRT (Calreticulin)–LRP1 (Low-Density Lipoprotein Receptor–Related Protein-1)–Hx (Hemopexin) Pathway in Murine Intracerebral Hemorrhage." Stroke 49, no. 12 (2018): 3020–29. http://dx.doi.org/10.1161/strokeaha.118.022155.

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Background and Purpose— Heme and iron are considered to be key factors responsible for secondary insults after intracerebral hemorrhage (ICH). Our previous study showed that LRP1 (low-density lipoprotein receptor–related protein-1)–Hx (hemopexin) facilitates removal of heme. The TLR7 (Toll-like receptor 7)–BTK (Bruton tyrosine kinase)–CRT (calreticulin) pathway regulates the expression of LRP1-Hx. This study is designed to clarify whether TLR7 activation facilitates heme scavenging and to establish the potential role of the BTK-CRT-LRP1-Hx signaling pathway in the pathophysiology of ICH. Metho

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Vijayan, Vijith, Eveline Baumgart-Vogt, Srivatsava Naidu, Guofeng Qian, and Stephan Immenschuh. "Bruton's Tyrosine Kinase and Nrf2 mediate TLR-induced activation of Heme oxygenase-1 gene expression in macrophages (116.16)." Journal of Immunology 186, no. 1_Supplement (2011): 116.16. http://dx.doi.org/10.4049/jimmunol.186.supp.116.16.

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Abstract The inducible isoform of heme oxygenase (HO)-1, is involved in heme degradation producing CO and biliverdin, mediating cytoprotection against oxidative stress. Recently, HO-1 has been shown to evoke potent anti-inflammatory and immunomodulatory effects in macrophages. Here we demonstrate that Bruton's tyrosine kinase (Btk), the gene of which is mutated in human immunodeficiency X-linked agammaglobulinemia, is involved in toll-like receptor (TLR)-induced gene expression of HO-1 in macrophages. The Btk inhibitor LFM-A13 blocked the induction of HO-1 by LPS (TLR4 ligand) in RAW264.7 macr

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Tankiewicz-Kwedlo, Anna, Justyna Magdalena Hermanowicz, Tomasz Domaniewski, et al. "Simultaneous use of erythropoietin and LFM-A13 as a new therapeutic approach for colorectal cancer." British Journal of Pharmacology 175, no. 5 (2018): 743–62. http://dx.doi.org/10.1111/bph.14099.

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Uckun, Fatih M. "Chemosensitizing Anti-Cancer Activity of LFM-A13, a Leflunomide Metabolite Analog Targeting Polo-like Kinases." Cell Cycle 6, no. 24 (2007): 3021–26. http://dx.doi.org/10.4161/cc.6.24.5096.

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Hermanowicz, J. M., A. Tankiewicz-Kwedlo, A. Surażyński, K. Pawlak, and D. A. Pawlak. "Simultaneous use of erythropoietin and LFM-A13 as a new therapeutic approach for colorectal cancer." Annals of Oncology 29 (March 2018): iii17. http://dx.doi.org/10.1093/annonc/mdy047.030.

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Uckun, Fatih M., Ilker Dibirdik, Sanjive Qazi, et al. "Anti-breast cancer activity of LFM-A13, a potent inhibitor of Polo-like kinase (PLK)." Bioorganic & Medicinal Chemistry 15, no. 2 (2007): 800–814. http://dx.doi.org/10.1016/j.bmc.2006.10.050.

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Thèses sur le sujet "LFM-A13"

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NARLOCH, ROBERT. "Characterization of a novel isoform of Bruton's Tyrosine Kinase (BTK) involved in resistance to drug-induced apoptosis of carcinoma cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2010. http://hdl.handle.net/10281/10304.

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Cancer is a multistep process in which mutation of 4 to 6 genes has to occur for the cell to become fully oncogenic. Very often, genes affected by such mutations encode for molecules belonging to the pathways allowing DNA repair or controlling the apoptotic process. Many anticancer drugs act by inducing DNA damage, which in turn triggers apoptosis. Inability of tumour cells to undergo chemotherapy-induced apoptosis is a main mechanism of drug resistance. Therefore, in order to find rational targets to tailor therapy is necessary to identify novel genes involved in modulating apoptosis induced

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