Anti-oncogenic role of the endoplasmic reticulum differentially activated by mutations in the MAPK pathway

[1]  R. Kaufman,et al.  Cytoplasmic IRE1α-mediated XBP1 mRNA Splicing in the Absence of Nuclear Processing and Endoplasmic Reticulum Stress* , 2006, Journal of Biological Chemistry.

[2]  M. Serrano,et al.  The power and the promise of oncogene-induced senescence markers , 2006, Nature Reviews Cancer.

[3]  J. Aguirre-Ghiso,et al.  Functional coupling of p38-induced up-regulation of BiP and activation of RNA-dependent protein kinase-like endoplasmic reticulum kinase to drug resistance of dormant carcinoma cells. , 2006, Cancer research.

[4]  Amy S. Lee,et al.  Stress induction of GRP78/BiP and its role in cancer. , 2006, Current molecular medicine.

[5]  D. Matallanas,et al.  Distinct Utilization of Effectors and Biological Outcomes Resulting from Site-Specific Ras Activation: Ras Functions in Lipid Rafts and Golgi Complex Are Dispensable for Proliferation and Transformation , 2006, Molecular and Cellular Biology.

[6]  M. Serrano,et al.  The Senescent Side of Tumor Suppression , 2005, Cell cycle.

[7]  John Calvin Reed,et al.  Endoplasmic reticulum stress: cell life and death decisions. , 2005, The Journal of clinical investigation.

[8]  R. Hamanaka,et al.  PERK and GCN2 contribute to eIF2alpha phosphorylation and cell cycle arrest after activation of the unfolded protein response pathway. , 2005, Molecular biology of the cell.

[9]  S. Lowe,et al.  Senescence comes of age , 2005, Nature Medicine.

[10]  J. Shay,et al.  BRAFE600-associated senescence-like cell cycle arrest of human naevi , 2005, Nature.

[11]  R. DePinho,et al.  Cancer: Crime and punishment , 2005, Nature.

[12]  H. Stein,et al.  Oncogene-induced senescence as an initial barrier in lymphoma development , 2005, Nature.

[13]  Jason A. Koutcher,et al.  Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis , 2005, Nature.

[14]  M. Philips.  Compartmentalized signalling of Ras. , 2005, Biochemical Society transactions.

[15]  D. Ron,et al.  The dynamic ER: experimental approaches and current questions. , 2005, Current opinion in cell biology.

[16]  A. Trumpp,et al.  Metastasizing melanoma formation caused by expression of activated N-RasQ61K on an INK4a-deficient background. , 2005, Cancer research.

[17]  F. Barany,et al.  Detection of the BRAF V600E mutation in melanocytic lesions using the ligase detection reaction , 2005, Journal of cutaneous pathology.

[18]  M. Martinka,et al.  Prognostic significance of activated Akt expression in melanoma: a clinicopathologic study of 292 cases. , 2005, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[19]  J. Campisi.  Senescent Cells, Tumor Suppression, and Organismal Aging: Good Citizens, Bad Neighbors , 2005, Cell.

[20]  R. Kaufman,et al.  The mammalian unfolded protein response. , 2003, Annual review of biochemistry.

[21]  B. Bastian,et al.  Genomic analysis of melanocytic neoplasia. , 2005, Advances in dermatology.

[22]  A. Jemal,et al.  Cancer Statistics, 2005 , 2005, CA: a cancer journal for clinicians.

[23]  L. Hendershot,et al.  The role of the unfolded protein response in tumour development: friend or foe? , 2004, Nature Reviews Cancer.

[24]  S. Lowe,et al.  Intrinsic tumour suppression , 2004, Nature.

[25]  K. Mori,et al.  XBP1: a link between the unfolded protein response, lipid biosynthesis, and biogenesis of the endoplasmic reticulum. , 2004, The Journal of cell biology.

[26]  D. Ron,et al.  Membrane biogenesis and the unfolded protein response , 2004, The Journal of cell biology.

[27]  Inara Strungs,et al.  Common and uncommon variants of melanocytic naevi. , 2004, Pathology.

[28]  G. Saldanha,et al.  High BRAF mutation frequency does not characterize all melanocytic tumor types , 2004, International journal of cancer.

[29]  K. Guan,et al.  Transformation Potential of Ras Isoforms Correlates with Activation of Phosphatidylinositol 3-Kinase but Not ERK* , 2004, Journal of Biological Chemistry.

[30]  A. Koong,et al.  XBP1 Is Essential for Survival under Hypoxic Conditions and Is Required for Tumor Growth , 2004, Cancer Research.

[31]  B. Wouters,et al.  Activating Transcription Factor 4 Is Translationally Regulated by Hypoxic Stress , 2004, Molecular and Cellular Biology.

[32]  J. Fridlyand,et al.  Mechanisms of cell-cycle arrest in Spitz nevi with constitutive activation of the MAP-kinase pathway. , 2004, The American journal of pathology.

[33]  J. Shay,et al.  Hallmarks of senescence in carcinogenesis and cancer therapy , 2004, Oncogene.

[34]  D. Galloway,et al.  Normal Human Fibroblasts Are Resistant to RAS-Induced Senescence , 2004, Molecular and Cellular Biology.

[35]  I. Komuro,et al.  Akt negatively regulates the in vitro lifespan of human endothelial cells via a p53/p21‐dependent pathway , 2004, The EMBO journal.

[36]  Frédérick A. Mallette,et al.  Human fibroblasts require the Rb family of tumor suppressors, but not p53, for PML-induced senescence , 2004, Oncogene.

[37]  M. Flaig,et al.  Mutations of the BRAF gene in benign and malignant melanocytic lesions. , 2003, The Journal of investigative dermatology.

[38]  Manuel Serrano,et al.  Tumor induction by an endogenous K-ras oncogene is highly dependent on cellular context. , 2003, Cancer cell.

[39]  S. Lowe,et al.  Rb-Mediated Heterochromatin Formation and Silencing of E2F Target Genes during Cellular Senescence , 2003, Cell.

[40]  M. Barbacid,et al.  RAS oncogenes: the first 30 years , 2003, Nature Reviews Cancer.

[41]  R. Paules,et al.  An integrated stress response regulates amino acid metabolism and resistance to oxidative stress. , 2003, Molecular cell.

[42]  P. Meltzer,et al.  High frequency of BRAF mutations in nevi , 2003, Nature Genetics.

[43]  A. Nicholson,et al.  Mutations of the BRAF gene in human cancer , 2002, Nature.

[44]  R. Bernards,et al.  A System for Stable Expression of Short Interfering RNAs in Mammalian Cells , 2002, Science.

[45]  S. Joel,et al.  DNA damage is able to induce senescence in tumor cells in vitro and in vivo. , 2002, Cancer research.

[46]  Amy S. Lee,et al.  The glucose-regulated proteins: stress induction and clinical applications. , 2001, Trends in biochemical sciences.

[47]  Tsonwin Hai,et al.  ATF4 Degradation Relies on a Phosphorylation-Dependent Interaction with the SCFβTrCPUbiquitin Ligase , 2001, Molecular and Cellular Biology.

[48]  M. Schapira,et al.  Regulated translation initiation controls stress-induced gene expression in mammalian cells. , 2000, Molecular cell.

[49]  D. Pinkel,et al.  Mutations and copy number increase of HRAS in Spitz nevi with distinctive histopathological features. , 2000, The American journal of pathology.

[50]  R. Kaufman,et al.  Activation of ATF6 and an ATF6 DNA binding site by the endoplasmic reticulum stress response. , 2000, The Journal of biological chemistry.

[51]  D. Weiss,et al.  Mutational analysis of the N-ras,p53,p16INK4a ,CDK4, and MC1R genes in human congenital melanocytic naevi , 1999, Journal of medical genetics.

[52]  M. Mihm,et al.  Atypical Spitz nevi/tumors: lack of consensus for diagnosis, discrimination from melanoma, and prediction of outcome. , 1999, Human pathology.

[53]  S. Lowe,et al.  Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling. , 1998, Genes & development.

[54]  P. Cohen,et al.  Role of Translocation in the Activation and Function of Protein Kinase B* , 1997, The Journal of Biological Chemistry.

[55]  Amy S. Lee,et al.  Inhibition of tumor progression by suppression of stress protein GRP78/BiP induction in fibrosarcoma B/C10ME. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[56]  D. Ron,et al.  C/ATF, a member of the activating transcription factor family of DNA-binding proteins, dimerizes with CAAT/enhancer-binding proteins and directs their binding to cAMP response elements. , 1993, Proceedings of the National Academy of Sciences of the United States of America.