Publications
43 results found
Hu M, Khorashad JS, Chaidos A, et al., 2012, Contrasting Effects of Enhanced Sirt1 Activity in Normal and BCR-ABL1-Depedent Haematopoiesis, 54th Annual Meeting and Exposition of the American-Society-of-Hematology (ASH), Publisher: AMER SOC HEMATOLOGY, ISSN: 0006-4971
Nteliopoulos G, Gordon MY, 2012, Protein Segregation Between Dividing Hematopoietic Progenitor Cells in the Determination of the Symmetry/Asymmetry of Cell Division, STEM CELLS AND DEVELOPMENT, Vol: 21, Pages: 2565-2580, ISSN: 1547-3287
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- Citations: 7
Bazeos A, Lowe R, Apperley J, et al., 2012, A DNA METHYLATION CLASSIFIER PREDICTS RESPONSE TO IMATINIB IN PRE-TREATMENT CML SAMPLES, Publisher: FERRATA STORTI FOUNDATION, Pages: 65-65, ISSN: 0390-6078
Koumallos N, Nteliopoulos G, Paschalis A, et al., 2011, Therapeutic interventions to renin-angiotensin-aldosterone system, and vascular redox state., Recent Pat Cardiovasc Drug Discov, Vol: 6, Pages: 115-122
It is well established that RAS plays a key role in the development of hypertension, cardiovascular and renal disease. On the other hand oxidative stress is a key feature in vascular homeostasis. Many of the cellular effects of Ang II appear to be mediated by ROS generated by NAD(P)H oxidase. In this review, we provide an overview of ROS physiology in human vessels especially in relation with RAS. We also discuss how therapeutic interventions on RAS affect redox signaling in the vascular wall at a clinical level with the discussion of recent patents.
Patel H, Nteliopoulos G, Nikolakopoulou Z, et al., 2011, Antibody arrays identify protein-protein interactions in chronic myeloid leukaemia, BRITISH JOURNAL OF HAEMATOLOGY, Vol: 152, Pages: 611-614, ISSN: 0007-1048
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- Citations: 4
Sears D, Luong P, Yuan M, et al., 2010, Functional phosphoproteomic analysis reveals cold-shock domain protein A to be a Bcr-Abl effector-regulating proliferation and transformation in chronic myeloid leukemia, CELL DEATH & DISEASE, Vol: 1, ISSN: 2041-4889
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- Citations: 15
Nteliopoulos G, Marley SB, Gordon MY, 2009, Influence of PI-3K/Akt pathway on Wnt signalling in regulating myeloid progenitor cell proliferation. Evidence for a role of autocrine/paracrine Wnt regulation, BRITISH JOURNAL OF HAEMATOLOGY, Vol: 146, Pages: 637-651, ISSN: 0007-1048
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- Citations: 13
Nteliopoulos G, Levicar N, Dimarakis I, 2009, Overview of Adult Stem Cell Therapy in Cardiac Disease, Handbook of Cardiac Stem Cell Therapy, Editors: Dimarakis, Menashe, Habib, Gordon, Publisher: Imperial College Press, Pages: 7-28
Nteliopoulos G, Marley SB, Gordon MY, 2008, Influence of PI-3K/Akt Pathway on Wnt Signalling in Myeloid Progenitor Cells. Evidence for a Role of Autocrine/Paracrine Wnt Regulation in CFU-GM Proliferation, 50th Annual Meeting of the American-Society-of-Hematology, Publisher: AMER SOC HEMATOLOGY, Pages: 995-995, ISSN: 0006-4971
Nteliopoulos G, Marley SB, Gordon MY, 2007, Involvement of WNT signalling in myeloid progenitor cell self-renewal, 36th Annual Meeting of the International-Society-for-Experimental-Hematology, Publisher: ELSEVIER SCIENCE INC, Pages: 30-30, ISSN: 0301-472X
Nteliopoulos G, Marley SB, Gordon MY, 2007, Involvement of Wnt signalling in myeloid progenitor cell self-renewal, 36th Annual Meeting of the International-Society-for-Experimental-Hematology, Publisher: ELSEVIER SCIENCE INC, Pages: 94-95, ISSN: 0301-472X
Sears D, Luong P, Yuan M, et al., Functional phosphoproteomic analysis reveals cold-shock domain protein A to be a Bcr-Abl effector-regulating proliferation and transformation in chronic myeloid leukemia, Cell Death Dis, Vol: 1, ISSN: 2041-4889
One proposed strategy to suppress the proliferation of imatinib-resistant cells in chronic myeloid leukemia (CML) is to inhibit key proteins downstream of Bcr-Abl. The PI3K/Akt pathway is activated by Bcr-Abl and is specifically required for the growth of CML cells. To identify targets of this pathway, we undertook a proteomic screen and identified several proteins that differentially bind 14-3-3, dependent on Bcr-Abl kinase activity. An siRNA screen of candidates selected by bioinformatics analysis reveals cold-shock domain protein A (CSDA), shown previously to regulate cell cycle progression in epithelial cells, to be a positive regulator of proliferation in a CML cell line. We show that Akt can phosphorylate the serine 134 residue of CSDA but, downstream of Bcr-Abl activity, this modification is mediated through the activation of MEK/p90 ribosomal S6 kinase (RSK) signaling. Inhibition of RSK, similarly to treatment with imatinib, blocked proliferation specifically in Bcr-Abl-positive leukemia cell lines, as well as cells from CML patients. Furthermore, these primary CML cells showed an increase in CSDA phosphorylation. Expression of a CSDA phospho-deficient mutant resulted in the decrease of Bcr-Abl-dependent transformation in Rat1 cells. Our results support a model whereby phosphorylation of CSDA downstream of Bcr-Abl enhances proliferation in CML cells to drive leukemogenesis.
Patel H, Nteliopoulos G, Nikolakopoulou Z, et al., Antibody arrays identify protein-protein interactions in chronic myeloid leukaemia, Br J Haematol, Vol: 152, Pages: 611-614, ISSN: 1365-2141
Multiprotein complex formation with p210(BCR-ABL1) is likely to play a major role in determining cellular abnormalities in chronic myeloid leukaemia (CML). Although many p210(BCR-ABL1) binding partners have been identified, it is likely that many have not. We evaluated the use of co-immunoprecipitation and antibody arrays and found that this approach is capable of identifying new p210(BCR-ABL1) binding partners, and may contribute to the search for new therapeutic targets in CML.
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