MTI-101 treatment inducing activation of Stim1 and TRPC1 expression is a determinant of response in multiple myeloma
暂无分享,去创建一个
A. Silva | L. Hazlehurst | J. Cuevas | M. McLaughlin | Shengyu Yang | M. Emmons | Nagaraju Anreddy | Kayla J. Steinberger
[1] F. Chan,et al. Regulation of RIPK3- and RHIM-dependent Necroptosis by the Proteasome* , 2016, The Journal of Biological Chemistry.
[2] A. Silva,et al. An Organotypic High Throughput System for Characterization of Drug Sensitivity of Primary Multiple Myeloma Cells. , 2015, Journal of visualized experiments : JoVE.
[3] Yun Dai,et al. A Bim-targeting strategy overcomes adaptive bortezomib resistance in myeloma through a novel link between autophagy and apoptosis. , 2014, Blood.
[4] L. Núñez,et al. A Reciprocal Shift in Transient Receptor Potential Channel 1 (TRPC1) and Stromal Interaction Molecule 2 (STIM2) Contributes to Ca2+ Remodeling and Cancer Hallmarks in Colorectal Carcinoma Cells* , 2014, The Journal of Biological Chemistry.
[5] S. Cha,et al. Orai1 and STIM1 are critical for cell migration and proliferation of clear cell renal cell carcinoma. , 2014, Biochemical and biophysical research communications.
[6] K. Ahn,et al. Establishment and characterization of bortezomib-resistant U266 cell line: Constitutive activation of NF-κB-mediated cell signals and/or alterations of ubiquitylation-related genes reduce bortezomib-induced apoptosis , 2014, BMB reports.
[7] Ling-gang Wu,et al. Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis , 2013, Nature Cell Biology.
[8] W. Catterall,et al. Structural basis for Ca2+ selectivity of a voltage-gated calcium channel , 2013, Nature.
[9] Lori Hazlehurst,et al. A preclinical assay for chemosensitivity in multiple myeloma. , 2014, Cancer research.
[10] L. Hazlehurst,et al. MTI-101 (Cyclized HYD1) Binds a CD44 Containing Complex and Induces Necrotic Cell Death in Multiple Myeloma , 2013, Molecular Cancer Therapeutics.
[11] Hsien-Chang Chang,et al. The ER Ca2+ sensor STIM1 regulates actomyosin contractility of migratory cells , 2013, Journal of Cell Science.
[12] Forest M White,et al. Systems-pharmacology dissection of a drug synergy in imatinib-resistant CML. , 2012, Nature chemical biology.
[13] Michael L. Wang,et al. Calcium blockers decrease the bortezomib resistance in mantle cell lymphoma via manipulation of tissue transglutaminase activities. , 2012, Blood.
[14] Xiaodong Wang,et al. Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 Kinase , 2012, Cell.
[15] Richard S Lewis,et al. Store-operated calcium channels: new perspectives on mechanism and function. , 2011, Cold Spring Harbor perspectives in biology.
[16] A. Cress,et al. Acquisition of Resistance toward HYD1 Correlates with a Reduction in Cleaved α4 Integrin Expression and a Compromised CAM-DR Phenotype , 2011, Molecular Cancer Therapeutics.
[17] Joseph P. Yuan,et al. STIM1-dependent and STIM1-independent Function of Transient Receptor Potential Canonical (TRPC) Channels Tunes Their Store-operated Mode* , 2010, The Journal of Biological Chemistry.
[18] P. Vandenabeele,et al. Molecular mechanisms of necroptosis: an ordered cellular explosion , 2010, Nature Reviews Molecular Cell Biology.
[19] T. Chou. Drug combination studies and their synergy quantification using the Chou-Talalay method. , 2010, Cancer research.
[20] Brij B. Singh,et al. Activation of TRPC1 by STIM1 in ER-PM microdomains involves release of the channel from its scaffold caveolin-1 , 2009, Proceedings of the National Academy of Sciences.
[21] W. Dalton,et al. HYD1-induced increase in reactive oxygen species leads to autophagy and necrotic cell death in multiple myeloma cells , 2009, Molecular Cancer Therapeutics.
[22] M. Zhu,et al. A role for Orai in TRPC-mediated Ca2+ entry suggests that a TRPC:Orai complex may mediate store and receptor operated Ca2+ entry , 2009, Proceedings of the National Academy of Sciences.
[23] Xin-Yun Huang,et al. Orai1 and STIM1 are critical for breast tumor cell migration and metastasis. , 2009, Cancer cell.
[24] P. Martiat,et al. Mesenchymal stromal cells promote or suppress the proliferation of T lymphocytes from cord blood and peripheral blood: the importance of low cell ratio and role of interleukin-6. , 2009, Cytotherapy.
[25] R A Kyle,et al. Criteria for diagnosis, staging, risk stratification and response assessment of multiple myeloma , 2009, Leukemia.
[26] L. Galluzzi,et al. Necroptosis: A Specialized Pathway of Programmed Necrosis , 2008, Cell.
[27] G. Peters,et al. Molecular basis of bortezomib resistance: proteasome subunit beta5 (PSMB5) gene mutation and overexpression of PSMB5 protein. , 2008, Blood.
[28] Jianmin Yang,et al. Point Mutation of the Proteasome β5 Subunit Gene Is an Important Mechanism of Bortezomib Resistance in Bortezomib-Selected Variants of Jurkat T Cell Lymphoblastic Lymphoma/Leukemia Line , 2008, Journal of Pharmacology and Experimental Therapeutics.
[29] H. Llewelyn Roderick,et al. Ca2+ signalling checkpoints in cancer: remodelling Ca2+ for cancer cell proliferation and survival , 2008, Nature Reviews Cancer.
[30] L. Zitvogel,et al. Cell death modalities: classification and pathophysiological implications , 2007, Cell Death and Differentiation.
[31] Ting-Chao Chou,et al. Theoretical Basis, Experimental Design, and Computerized Simulation of Synergism and Antagonism in Drug Combination Studies , 2006, Pharmacological Reviews.
[32] L. Boise,et al. Proteasome inhibitors induce a terminal unfolded protein response in multiple myeloma cells. , 2006, Blood.
[33] E. Terpos,et al. No evidence of mutations of the PSMB5 (beta-5 subunit of proteasome) in a case of myeloma with clinical resistance to Bortezomib. , 2006, Leukemia research.
[34] Kevin D. Nullmeyer,et al. Mitochondrial-mediated disregulation of Ca2+ is a critical determinant of Velcade (PS-341/bortezomib) cytotoxicity in myeloma cell lines. , 2005, Cancer research.
[35] Tetsuya Watanabe,et al. Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death , 2005, Nature.
[36] J. Putney,et al. Capacitative calcium entry , 1997, The Journal of cell biology.
[37] R. Kyle,et al. Drug therapy: Multiple myeloma , 2004 .
[38] J. Cuevas,et al. VPAC Receptor Modulation of Neuroexcitability in Intracardiac Neurons , 2004, Journal of Biological Chemistry.
[39] T. Yamashima. Ca2+-dependent proteases in ischemic neuronal death: a conserved 'calpain-cathepsin cascade' from nematodes to primates. , 2004, Cell calcium.
[40] Patrick A Singleton,et al. Hyaluronan-CD44 Interaction with Rac1-dependent Protein Kinase N-γ Promotes Phospholipase Cγ1 Activation, Ca2+ Signaling, and Cortactin-Cytoskeleton Function Leading to Keratinocyte Adhesion and Differentiation* , 2004, Journal of Biological Chemistry.
[41] C. Beam,et al. Genotypic and phenotypic comparisons of de novo and acquired melphalan resistance in an isogenic multiple myeloma cell line model. , 2003, Cancer research.
[42] H. Ouyang,et al. Role of Phospholipase C-β in the Modulation of Epithelial Tight Junction Permeability , 2003, Journal of Pharmacology and Experimental Therapeutics.
[43] Lauren Mackenzie,et al. 2‐Aminoethoxydiphenyl borate (2‐APB) is a reliable blocker of store‐operated Ca2+ entry but an inconsistent inhibitor of InsP3‐induced Ca2+ release , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[44] P. Elliott,et al. The proteasome inhibitor PS-341 inhibits growth, induces apoptosis, and overcomes drug resistance in human multiple myeloma cells. , 2001, Cancer research.
[45] B. Herman,et al. The mitochondrial permeability transition mediates both necrotic and apoptotic death of hepatocytes exposed to Br-A23187. , 1999, Toxicology and applied pharmacology.
[46] S. Orrenius,et al. The role of calcium in the regulation of apoptosis. , 1996, Journal of leukocyte biology.
[47] M. Berridge. Inositol trisphosphate and calcium signalling , 1993, Nature.
[48] O. Cope,et al. Multiple myeloma. , 1948, The New England journal of medicine.
[49] HighWire Press,et al. The journal of pharmacology and experimental therapeutics , 1909 .