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Drug: Nilotinib

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Total 12 results found since Jan 2013.

ABL1 and Cofilin1 promote T-cell acute lymphoblastic leukemia cell migration
Acta Biochim Biophys Sin (Shanghai). 2021 Sep 11:gmab117. doi: 10.1093/abbs/gmab117. Online ahead of print.ABSTRACTThe fusion gene of ABL1 is closely related to tumor proliferation, invasion, and migration. It has been reported recently that ABL1 itself is required for T-cell acute lymphoblastic leukemia (T-ALL) cell migration induced by CXCL12. Further experiments revealed that ABL1 inhibitor Nilotinib inhibited leukemia cell migration induced by CXCL12, indicating the possible application of Nilotinib in T-ALL leukemia treatment. However, the interacting proteins of ABL1 and the specific mechanisms of their involvement i...
Source: Acta Biochimica et Biophysica Sinica - September 11, 2021 Category: Biochemistry Authors: Jixian Luo Huiguang Zheng Sen Wang Dingyun Li Wenli Ma Lan Wang M James C Crabbe Source Type: research

Inhibition of ABL1 tyrosine kinase reduces HTLV-1 proviral loads in peripheral blood mononuclear cells from patients with HTLV-1-associated myelopathy/tropical spastic paraparesis
by Daisuke Kodama, Masakazu Tanaka, Toshio Matsuzaki, Kimiko Izumo, Nobuaki Nakano, Eiji Matsuura, Mineki Saito, Masahiro Nagai, Masahisa Horiuchi, Atae Utsunomiya, Hiroshi Takashima, Ryuji Kubota, Shuji Izumo Human T-cell leukemia virus type 1 (HTLV-1) causes incurable adult T-cell leukemia and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Patients with HAM/TSP have increased levels of HTLV-1-infected cells compared with asymptomatic HTLV-1 carriers. However, the roles of cellula r genes in HTLV-1-infected CD4+ T cells await discovery. We performed microarray analysis of CD4+ T cells from HAM/TSP p...
Source: PLoS Neglected Tropical Diseases - July 14, 2020 Category: Tropical Medicine Authors: Daisuke Kodama Source Type: research

DDR1 and MT1-MMP Expression Levels Are Determinant for Triggering BIK-Mediated Apoptosis by 3D Type I Collagen Matrix in Invasive Basal-Like Breast Carcinoma Cells
In conclusion, and in agreement with the other studies (Ford et al., 2007; Koh et al., 2015; Toy et al., 2015; Takai et al., 2018), our data suggest that during the acquisition of mesenchymal features, the level of full-length DDR1 expression should be considered, in addition to the other markers, as an important biomarker in the prognosis of aggressive breast carcinomas. As summarized in Figure 9, the regulation of cell proliferation and apoptosis by the collagen/DDR1 axis involves a differential activation of DDR1 signaling pathway and thus BIK expression. In the case of the basal-like bre...
Source: Frontiers in Pharmacology - May 2, 2019 Category: Drugs & Pharmacology Source Type: research

Novel Application of Radotinib for the Treatment of Solid Tumors via Natural Killer Cell Activation.
This study provides the first evidence that radotinib could be used as an effective and strong therapeutic to treat solid tumors via upregulation of NK cell cytotoxicity, suggesting that radotinib has indirect killing mechanisms via upregulation of antitumor innate immune responses as well as direct killing activities for CML cells. PMID: 30687767 [PubMed - in process]
Source: Journal of Immunology Research - January 29, 2019 Category: Allergy & Immunology Tags: J Immunol Res Source Type: research

c-Abl phosphorylation of Yin Yang 1's conserved tyrosine 254 in the spacer region modulates its transcriptional activity
In conclusion, we demonstrate the novel role of c-Abl kinase in regulation of YY1's transcriptional activity, linking YY1 regulation with c-Abl tyrosine kinase signaling pathways.Graphical abstract
Source: Biochimica et Biophysica Acta (BBA) Molecular Cell Research - July 11, 2018 Category: Molecular Biology Source Type: research

c-Abl phosphorylation of Yin Yang 1's conserved tyrosine 254 in the spacer region modulates its transcriptional activity.
In conclusion, we demonstrate the novel role of c-Abl kinase in regulation of YY1's transcriptional activity, linking YY1 regulation with c-Abl tyrosine kinase signaling pathways. PMID: 29807053 [PubMed - as supplied by publisher]
Source: Biochimica et Biophysica Acta - May 25, 2018 Category: Biochemistry Authors: Daraiseh SI, Kassardjian A, Alexander KE, Rizkallah R, Hurt MM Tags: Biochim Biophys Acta Source Type: research

Caspase-Independent Pathway is Related to Nilotinib Cytotoxicity in Cultured Cardiomyocytes
Conclusion: Our findings demonstrate that nilotinib increases autophagy and cathepsin B activity, leading to mitochondrial AIF release and nuclear translocation, which is responsible for p53 and apoptosis induction in H9C2 cells.Cell Physiol Biochem 2017;42:2182 –2193
Source: Cellular Physiology and Biochemistry - August 16, 2017 Category: Cytology Source Type: research

Abstract 3378: Discoidin domain receptor 2 differentially controls HT-1080 cell proliferation in young-adult and old type I collagen 3D matrices
In this study, we analyzed the effect of collagen aging on human HT-1080 fibrosarcoma cell proliferation in 3D matrix model. For this, type I collagen was extracted from tail tendons of young-adult (2 months) and old (2 years) rats. In 3D matrix, the rate of HT-1080 cell growth was significantly lower in young-adult collagen. This was accompanied by a down-regulation of ERK1/2 phosphorylation and an increase in the cyclin-dependent kinase inhibitor p21 expression. Blocking antibodies and siRNA strategy against β1 integrin and AGEs receptor (RAGE) did not increase cell growth in young-adult collagen.Accumulating evidence s...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Saby, C., Garnotel, R., El Btaouri, H., Van Gulick, L., Jeannesson, P., Morjani, H. Tags: Tumor Biology Source Type: research

Imatinib and Nilotinib inhibit Bcr–Abl-induced ROS through targeted degradation of the NADPH oxidase subunit p22phox
In this study, using the K562 CML cell line we showed that inhibition of Bcr–Abl signalling, by either Imatinib or Nilotinib, led to a significant reduction in ROS levels which was concurrent with the GSK-3β dependent, post-translational down-regulation of the small membrane-bound protein p22phox, an essential component of the Nox complex. Furthermore, siRNA knockdown of p22phox in these cells established its importance in ROS production and proliferation. Taken together we believe our results provide a possible link between Bcr–Abl signalling and ROS production through Nox activity and demonstrate a novel mechanism o...
Source: Leukemia Research - December 5, 2012 Category: Hematology Authors: William D. Landry, John F. Woolley, Thomas G. Cotter Tags: Laboratory Studies Source Type: research