PERK Is a Haploinsufficient Tumor Suppressor: Gene Dose Determines Tumor-Suppressive Versus Tumor Promoting Properties of PERK in Melanoma
暂无分享,去创建一个
M. Herlyn | Gao Zhang | S. Fuchs | A. Yoshida | J. Diehl | D. Pytel | I. Majsterek | K. Staschke | K. Maćkiewicz | Yuliya Katlinskaya | Lawrence Wu | Shuo Qie | Yan Gao | M. Paredes | Olga S. Chajewski
[1] C. Thompson,et al. PERK-dependent regulation of lipogenesis during mouse mammary gland development and adipocyte differentiation , 2008, Proceedings of the National Academy of Sciences.
[2] C. Sherr,et al. Mammalian unfolded protein response inhibits cyclin D1 translation and cell-cycle progression. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[3] D. Wildman,et al. Proapoptotic BAX and BAK Modulate the Unfolded Protein Response by a Direct Interaction with IRE1a , 2006 .
[4] J. Cleveland,et al. A pathway distinct from the mammalian unfolded protein response regulates expression of endoplasmic reticulum chaperones in non‐stressed cells , 1997, The EMBO journal.
[5] M. Schröder. The unfolded protein response , 2006, Molecular biotechnology.
[6] P. Guldberg,et al. Disruption of the MMAC1/PTEN gene by deletion or mutation is a frequent event in malignant melanoma. , 1997, Cancer research.
[7] L. Hendershot,et al. Two distinct stress signaling pathways converge upon the CHOP promoter during the mammalian unfolded protein response. , 2002, Journal of molecular biology.
[8] L. Chin,et al. Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in mice. , 2002, Nature Reviews Cancer.
[9] Hiderou Yoshida,et al. A Serine Protease Inhibitor Prevents Endoplasmic Reticulum Stress-induced Cleavage but Not Transport of the Membrane-bound Transcription Factor ATF6* , 2003, Journal of Biological Chemistry.
[10] P. Pollock,et al. CDKN2A/p16 is inactivated in most melanoma cell lines. , 1997, Cancer research.
[11] M. Schröder. Endoplasmic reticulum stress responses , 2008, Cellular and Molecular Life Sciences.
[12] P. S. Pedersen,et al. The Sarco/Endoplasmic Reticulum Calcium-ATPase 2b Is an Endoplasmic Reticulum Stress-inducible Protein* , 2000, The Journal of Biological Chemistry.
[13] F. Visioli,et al. The unfolded protein response induces the angiogenic switch in human tumor cells through the PERK/ATF4 pathway. , 2012, Cancer research.
[14] M. Piepkorn,et al. Melanoma genetics: an update with focus on the CDKN2A(p16)/ARF tumor suppressors. , 2000, Journal of the American Academy of Dermatology.
[15] T. Fotsis,et al. VEGF Signals through ATF6 and PERK to promote endothelial cell survival and angiogenesis in the absence of ER stress. , 2014, Molecular cell.
[16] S. Natsugoe,et al. PRMT5 is required for lymphomagenesis triggered by multiple oncogenic drivers. , 2015, Cancer discovery.
[17] D. Ron,et al. Lipid-dependent regulation of the unfolded protein response , 2015, Current opinion in cell biology.
[18] J. Pelletier,et al. A Novel Function of eIF2α Kinases as Inducers of the Phosphoinositide-3 Kinase Signaling Pathway , 2007 .
[19] R. Wek,et al. Phosphorylation of the α-Subunit of the Eukaryotic Initiation Factor-2 (eIF2α) Reduces Protein Synthesis and Enhances Apoptosis in Response to Proteasome Inhibition* , 2005, Journal of Biological Chemistry.
[20] L. Chin,et al. p16(Ink4a) in melanocyte senescence and differentiation. , 2002, Journal of the National Cancer Institute.
[21] S. Gruber,et al. Anti-oncogenic role of the endoplasmic reticulum differentially activated by mutations in the MAPK pathway , 2006, Nature Cell Biology.
[22] L. Chodosh,et al. miR-211 is a prosurvival microRNA that regulates chop expression in a PERK-dependent manner. , 2012, Molecular cell.
[23] D. Ron,et al. Diabetes mellitus and exocrine pancreatic dysfunction in perk-/- mice reveals a role for translational control in secretory cell survival. , 2001, Molecular cell.
[24] J. Reis-Filho,et al. Oncogenic Braf induces melanocyte senescence and melanoma in mice. , 2009, Cancer cell.
[25] A. Hassell,et al. Discovery of GSK2656157: An Optimized PERK Inhibitor Selected for Preclinical Development. , 2013, ACS medicinal chemistry letters.
[26] T. McCormick,et al. Mouse Lymphoma Cells Destined to Undergo Apoptosis in Response to Thapsigargin Treatment Fail to Generate a Calcium-mediated grp78/grp94 Stress Response* , 1997, The Journal of Biological Chemistry.
[27] J. Debnath,et al. PERK Integrates Autophagy and Oxidative Stress Responses To Promote Survival during Extracellular Matrix Detachment , 2011, Molecular and Cellular Biology.
[28] Nicholas,et al. CDKN 2 A / p 16 Is Inactivated in Most Melanoma Cell Lines ' , 2006 .
[29] S. Korsmeyer,et al. Proapoptotic BAX and BAK Modulate the Unfolded Protein Response by a Direct Interaction with IRE1α , 2006, Science.
[30] R. DePinho,et al. BRafV600E cooperates with Pten silencing to elicit metastatic melanoma , 2009, Nature Genetics.
[31] L. Insabato,et al. Endoplasmic Reticulum Stress in Endometrial Cancer , 2014, Front. Med..
[32] L. Chin,et al. Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[33] R. Kaufman,et al. A stress response pathway from the endoplasmic reticulum to the nucleus requires a novel bifunctional protein kinase/endoribonuclease (Ire1p) in mammalian cells. , 1998, Genes & development.
[34] K. Mori,et al. XBP1 mRNA Is Induced by ATF6 and Spliced by IRE1 in Response to ER Stress to Produce a Highly Active Transcription Factor , 2001, Cell.
[35] R. Wek,et al. Dimerization and Release of Molecular Chaperone Inhibition Facilitate Activation of Eukaryotic Initiation Factor-2 Kinase in Response to Endoplasmic Reticulum Stress* , 2002, The Journal of Biological Chemistry.
[36] L. Shewchuk,et al. Discovery of 7-methyl-5-(1-{[3-(trifluoromethyl)phenyl]acetyl}-2,3-dihydro-1H-indol-5-yl)-7H-pyrrolo[2,3-d]pyrimidin-4-amine (GSK2606414), a potent and selective first-in-class inhibitor of protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK). , 2012, Journal of medicinal chemistry.
[37] Jiangbin Ye,et al. PERK promotes cancer cell proliferation and tumor growth by limiting oxidative DNA damage , 2010, Oncogene.
[38] Brian F. Teskea,et al. The eIF 2 kinase PERK and the integrated stress response facilitate activation of ATF 6 during endoplasmic reticulum stress , 2011 .
[39] K. Mori,et al. Mammalian transcription factor ATF6 is synthesized as a transmembrane protein and activated by proteolysis in response to endoplasmic reticulum stress. , 1999, Molecular biology of the cell.
[40] M. Herlyn,et al. The FBXO4 Tumor Suppressor Functions as a Barrier to BrafV600E-Dependent Metastatic Melanoma , 2013, Molecular and Cellular Biology.
[41] C. Koumenis,et al. PERK-ing up autophagy during MYC-induced tumorigenesis , 2013, Autophagy.
[42] D. Scheuner,et al. ER stress‐regulated translation increases tolerance to extreme hypoxia and promotes tumor growth , 2005, The EMBO journal.
[43] Hong Zhang,et al. Deletion in p16INK4a and loss of p16 expression in human skin primary and metastatic melanoma cells. , 2004, International journal of oncology.
[44] A. Rustgi,et al. Nuclear accumulation of cyclin D1 during S phase inhibits Cul4-dependent Cdt1 proteolysis and triggers p53-dependent DNA rereplication. , 2007, Genes & development.
[45] R. Sood,et al. Translational Control -subunit Kinase, Pek, Involved in Α Pancreatic Eukaryotic Initiation Factor 2 Identification and Characterization Of , 1998 .
[46] J. Diehl,et al. Tumor progression and the Different Faces of the PERK kinase , 2015, Oncogene.
[47] L. P. Vaites,et al. PERK Utilizes Intrinsic Lipid Kinase Activity To Generate Phosphatidic Acid, Mediate Akt Activation, and Promote Adipocyte Differentiation , 2012, Molecular and Cellular Biology.
[48] L. Glimcher,et al. XBP-1 Regulates a Subset of Endoplasmic Reticulum Resident Chaperone Genes in the Unfolded Protein Response , 2003, Molecular and Cellular Biology.
[49] B. Wouters,et al. Activating Transcription Factor 4 Is Translationally Regulated by Hypoxic Stress , 2004, Molecular and Cellular Biology.
[50] P. Hersey,et al. Oncogenic activation of MEK/ERK primes melanoma cells for adaptation to endoplasmic reticulum stress. , 2014, The Journal of investigative dermatology.
[51] R. Wek,et al. Phosphorylation of the alpha-subunit of the eukaryotic initiation factor-2 (eIF2alpha) reduces protein synthesis and enhances apoptosis in response to proteasome inhibition. , 2005, The Journal of biological chemistry.
[52] S. Fuchs,et al. The cell biology of the unfolded protein response. , 2011, Gastroenterology.
[53] F. Haluska,et al. Identification of PTEN/MMAC1 alterations in uncultured melanomas and melanoma cell lines , 1998, Oncogene.
[54] T. Jahnke,et al. IRE 1 Signaling Affects Cell Fate During the Unfolded Protein Response , 2008 .
[55] Hiderou Yoshida,et al. Identification of the cis-Acting Endoplasmic Reticulum Stress Response Element Responsible for Transcriptional Induction of Mammalian Glucose-regulated Proteins , 1998, The Journal of Biological Chemistry.
[56] Z. Zhou,et al. IRE1 Phosphatase PP2Ce Regulates Adaptive ER Stress Response in the Postpartum Mammary Gland , 2014, PloS one.
[57] Stevan R. Hubbard,et al. IRE1 couples endoplasmic reticulum load to secretory capacity by processing the XBP-1 mRNA , 2002, Nature.
[58] J. Diehl,et al. UPR-inducible miRNAs contribute to stressful situations. , 2013, Trends in biochemical sciences.
[59] C. Bassing,et al. ATM deficiency augments constitutively nuclear cyclin D1-driven genomic instability and lymphomagenesis , 2014, Oncogene.
[60] W. Doerrler,et al. Regulation of the dolichol pathway in human fibroblasts by the endoplasmic reticulum unfolded protein response. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[61] T. W. Fawcett,et al. Complexes containing activating transcription factor (ATF)/cAMP-responsive-element-binding protein (CREB) interact with the CCAAT/enhancer-binding protein (C/EBP)-ATF composite site to regulate Gadd153 expression during the stress response. , 1999, The Biochemical journal.
[62] Xiaozhong Wang,et al. CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum. , 1998, Genes & development.
[63] 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.
[64] H. Yi,et al. Suppression of tumorigenicity and metastasis in B16F10 cells by PTEN/MMAC1/TEP1 gene. , 2001, Cancer letters.
[65] S. Elledge,et al. The DNA damage response: putting checkpoints in perspective , 2000, Nature.
[66] Xi Chen,et al. ER stress regulation of ATF6 localization by dissociation of BiP/GRP78 binding and unmasking of Golgi localization signals. , 2002, Developmental cell.
[67] D. Ron,et al. Perk-Dependent Translational Regulation Promotes Tumor Cell Adaptation and Angiogenesis in Response to Hypoxic Stress , 2006, Molecular and Cellular Biology.
[68] David M. Stern,et al. Stress-Associated Endoplasmic Reticulum Protein 1 (Serp1)/Ribosome-Associated Membrane Protein 4 (Ramp4) Stabilizes Membrane Proteins during Stress and Facilitates Subsequent Glycosylation , 1999, The Journal of cell biology.
[69] R. Kaufman,et al. Ligand-independent Dimerization Activates the Stress Response Kinases IRE1 and PERK in the Lumen of the Endoplasmic Reticulum* , 2000, The Journal of Biological Chemistry.
[70] Jiangbin Ye,et al. The GCN2‐ATF4 pathway is critical for tumour cell survival and proliferation in response to nutrient deprivation , 2010, The EMBO journal.
[71] P. Hu,et al. Critical Role of Endogenous Akt/IAPs and MEK1/ERK Pathways in Counteracting Endoplasmic Reticulum Stress-induced Cell Death* , 2004, Journal of Biological Chemistry.
[72] N. Bardeesy,et al. mTORC1 activation blocks BrafV600E-induced growth arrest but is insufficient for melanoma formation. , 2015, Cancer cell.
[73] R. Hamanaka,et al. PERK-dependent regulation of IAP translation during ER stress , 2008, Oncogene.
[74] Brent M. Sanders,et al. Characterization of a novel PERK kinase inhibitor with antitumor and antiangiogenic activity. , 2013, Cancer research.
[75] J. W. Brewer,et al. PERK mediates cell-cycle exit during the mammalian unfolded protein response. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[76] T. Aw,et al. Gadd153 Sensitizes Cells to Endoplasmic Reticulum Stress by Down-Regulating Bcl2 and Perturbing the Cellular Redox State , 2001, Molecular and Cellular Biology.
[77] D. Rutkowski,et al. C/EBP Homologous Protein (CHOP) Contributes to Suppression of Metabolic Genes during Endoplasmic Reticulum Stress in the Liver* , 2012, The Journal of Biological Chemistry.
[78] D. Rutkowski,et al. The Stress-Regulated Transcription Factor CHOP Promotes Hepatic Inflammatory Gene Expression, Fibrosis, and Oncogenesis , 2013, PLoS genetics.
[79] N. Socci,et al. MDM2 turnover and expression of ATRX determine the choice between quiescence and senescence in response to CDK4 inhibition , 2015, Oncotarget.
[80] Sharon J. Sequeira,et al. Inhibition of Proliferation by PERK Regulates Mammary Acinar Morphogenesis and Tumor Formation , 2007, PloS one.
[81] J. McClintick,et al. The eIF2 kinase PERK and the integrated stress response facilitate activation of ATF6 during endoplasmic reticulum stress , 2011, Molecular biology of the cell.
[82] M. Schapira,et al. Regulated translation initiation controls stress-induced gene expression in mammalian cells. , 2000, Molecular cell.
[83] N. Lowndes,et al. DNA Repair: The Importance of Phosphorylating Histone H2AX , 2005, Current Biology.
[84] J. Kushner,et al. PERK Is Required in the Adult Pancreas and Is Essential for Maintenance of Glucose Homeostasis , 2012, Molecular and Cellular Biology.
[85] D. Ron,et al. Protein translation and folding are coupled by an endoplasmic-reticulum-resident kinase , 1999, Nature.
[86] Chao Zhang,et al. IRE1 Signaling Affects Cell Fate During the Unfolded Protein Response , 2007, Science.
[87] P. Hersey,et al. Ets-1 mediates upregulation of Mcl-1 downstream of XBP-1 in human melanoma cells upon ER stress , 2011, Oncogene.
[88] J. Pelletier,et al. A Novel Function of eIF 2 Kinases as Inducers of the Phosphoinositide-3 Kinase Signaling Pathway , 2007 .
[89] A. Yoshida,et al. Induction of Therapeutic Senescence in Vemurafenib-Resistant Melanoma by Extended Inhibition of CDK4/6. , 2016, Cancer research.
[90] Peichuan Zhang,et al. The PERK Eukaryotic Initiation Factor 2α Kinase Is Required for the Development of the Skeletal System, Postnatal Growth, and the Function and Viability of the Pancreas , 2002, Molecular and Cellular Biology.
[91] K. Seyb,et al. Enzymatic Characterization of ER Stress-Dependent Kinase, PERK, and Development of a High-Throughput Assay for Identification of PERK Inhibitors , 2014, Journal of biomolecular screening.