MTI-101 treatment inducing activation of Stim1 and TRPC1 expression is a determinant of response in multiple myeloma

[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 .