Letter to Editor
BibTex RIS Cite

Cellular Pathways In Endoplasmic Reticulum Stress And The Role Of Beta Cell Apoptosis Induced By Endoplasmic Reticulum Stress In The Pathogenesis Of Type II Diabetes

Year 2015, Volume: 16 Issue: 3, 227 - 237, 27.08.2015
https://doi.org/10.18229/ktd.19744

Abstract

It was assumed that apoptosis is the main factor in beta cell deaths in type II diabetes. Apoptosis is important owing to eradicate the damaged or harmful cells without inflammation
in various biological facts. This process is also important for homeostasis of organism. B cells are often exposed to ER stress due to excess insulin secretion. In recent years, it was showed
that endoplasmic reticulum was an important organelle in apoptotic signal conduction. Investigations including apoptosis induced ER stress will supply new approaches in to clarify the new mechanisms in diabetic pathogenesis and new treatment strategies in diabetes.

References

  • Gurzov EN, Ortis F, Bakiri L, Wagner EF, Eizirik DL. JunB Inhibits ER Stress and Apoptosis in Pancreatic Beta Cells. PLoS ONE. 2008;3(8)
  • Diabetes&Metabolism. 2008;34,56-64
  • Büyükgebiz O, Caferler JS. Apoptoz. Sendrom 2001;13:102-7.
  • Fadeel B, Orrenius S, Zhivotovsky B. Apoptosis in human disease: A new skin for the old ceremony? Biochemical and Biophysical Research Communications 1999; 266 :699-717. Klin J Med Sci. 2003;23:499-508
  • Bonner-Weir S, White MF. Disruption of IRS- 2 causes type 2 diabetes in mice. Nature. 1998; 26;391(6670):900-4. 2001;13;414(6865):792-8.
  • Eizirik DL, Poulsen TM. A choice of death-the signal-transduction of immune-mediated beta cell apoptosis, Diabetologia. 2001;44,2115-2133.
  • Kaneto H, Kajimoto Y, Miyagawa J, Matsuoka T, Fujitani Y, Umayahara Y, Hanafusa T, Matsuzawa Y, Yamasaki Y, Hori M. Beneficial effects of antioxidants in diabetes: possible protection of pancreatic short- and long-term hyperglycemia. Diabetes. beta-cells against glucose toxicity. Diabetes. 1999;48(12):2398-406.
  • Oyadomari S, Takeda K, Takiguchi M, Gotoh T, Matsumoto M, Wada I, Akira S, Araki E, Mori M. Nitric oxide-induced apoptosis in pancreatic beta cells and p21WAF1/CIP1. FEBS Lett. 1999;455(3):315-20. is mediated by the endoplasmic reticulum stress pathway. Proc Natl Acad Sci U S A. 2001;98(19):10845
  • Zhou YP, Teng D, Dralyuk F, Ostrega D, Roe Saini KS, Thompson C, Winterford CM, Walker NI, Cameron DP. Streptozotocin at low doses induces apoptosis and at high doses causes necrosis in a murine pancreatic beta cell line, INS-1. Biochem Mol Biol Int. 1996;39(6):1229-36.
  • Unger RH. Lipotoxic diseases. Annu Rev Med. 2002;53:319-36.
  • Withers DJ, Burks DJ, Towery HH, Altamuro SL, Flint CL, White MF. Irs-2 coordinates Igf-1 receptor- mediated beta-cell development and peripheral differentiation in BETA2/neuroD-deficient mice. insulin signalling. Nat Genet. 1999;23(1):32-40. Genes Dev. 1997;11(18):2323-34.
  • Withers DJ, Gutierrez JS, Towery H, Burks DJ, Ren JM, Previs S, Zhang Y, Bernal D, Pons S, Shulman GI, Bonner-Weir S, White MF. Disruption of IRS-2 causes type 2 diabetes in mice. Nature. 1998;391(6670):900
  • Miettinen PJ, Huotari M, Koivisto T, Ustinov J, Palgi J, Rasilainen S, Lehtonen E, Keski-Oja J, Otonkoski T. Impaired migration and delayed differentiation of pancreatic islet cells in mice lacking EGF-receptors. Development. 2000;127(12):2617-27.
  • Hart AW, Baeza N, Apelqvist A, Edlund H. Attenuation of FGF signalling in mouse beta-cells leads to diabetes. Nature. 2000;408(6814):864-8.
  • Rane SG, Dubus P, Mettus RV, Galbreath EJ, Boden G, Reddy EP, Barbacid M. Loss of Cdk4 expression causes insulin-deficient diabetes and Cdk4 activation results in beta-islet cell hyperplasia. Nat Genet. 1999;22(1):44-52. apoptosis, and increased sensitivity to ceramide-, but not to high glucose-induced cell death. J Biol Chem. 2002;277(8):6413.
  • Naya FJ, Huang HP, Qiu Y, Mutoh H, DeMayo FJ, Leiter AB, Tsai MJ. Diabetes, defective pancreatic morphogenesis, and abnormal enteroendocrine Silva JP, Köhler M, Graff C, Oldfors A, Magnuson MA, Berggren PO, Larsson NG. Impaired insulin secretion and beta-cell loss in tissue-specific knockout mice with mitochondrial diabetes. Nat Genet. 2000;26(3):336-40.
  • Harding HP, Zeng H, Zhang Y, Jungries R, Chung P, Plesken H, Sabatini DD, Ron D. Diabetes mellitus and exocrine pancreatic dysfunction in perk-/- mice reveals a role for translational control in secretory cell survival. Mol Cell. 2001;7(6):1153-63.
  • Welters HJ, Kulkarni RN. Wnt signaling: relevance to β-cel biology and diabetes. Trends in Endocrinology and metabolism, 2008;19,349-355.
  • Cauchi S, Eroguel P.TCF7L2 genetic defect and type 2 diabetes. Curr. Diab Rep. 2008;8(2), 149-155.
  • Shu L, Sauter NS, Schulthess FT, Matveyenko AV, Oberholzer J, Maedler K. Transcription factor 7-like 2 regulates beta-cell survival and function in human pancreatic islets. Diabetes. 2008;57(3):645-53.
  • Yoshida H, Haze K, Yanagi H, Yura T, Mori K. Identification of the cis-acting endoplasmic reticulum stress response element responsible 2000;5(4):729-35. for transcriptional induction of mammalian glucose-regulated proteins. Involvement of basic
  • Rajan S.S., Srinivasan V., Balasubramanyam leucine zipper transcription factors. J Biol Chem. 1998;273(50):33741-9.
  • Yoshida H, Matsui T, Yamamoto A, Okada T, Mori intact unfolded protein response pathway. Mol Cell. K. XBP1 mRNA is induced by ATF6 and spliced by proteins from the ER of S. cerevisiae requires an IRE1 in response to ER stress to produce a highly M, Zşñiga M, Brown PO, Ploegh H. Degradation of active transcription factor. Cell. 2001;107(7):881-91.
  • Yoshida H, Okada T, Haze K, Yanagi H, Yura T, Negishi M, Mori K. ATF6 activated by proteolysis binds in the presence of NF-Y (CBF) directly to the cis-acting element responsible for the mammalian unfolded protein response. Mol Cell Biol. 2000;20(18):6755-67.
  • Chen X, Shen J, Prywes R. The luminal domain CHOP, have opposing effects on the induction of G1/S arrest. Genes Dev. 1994;8(4):453-64. of ATF6 senses endoplasmic reticulum (ER) stress and causes translocation of ATF6 from the ER to the Golgi. J Biol Chem. 2002;277(15):13045-52.
  • Bertolotti A, Zhang Y, Hendershot LM, Harding HP, Ron D. Dynamic interaction of BiP and ER stress transducers in the unfolded-protein response. Nat Cell Biol. 2000;2(6):326-32.
  • Shi Y, Vattem KM, Sood R, An J, Liang J, Stramm L, Wek RC. Identification and characterization of panc- reatic eukaryotic initiation factor 2 alpha-subunit ki- nase, PEK, involved in translational control. Mol Cell Biol. 1998;18(12):7499-509.
  • Novoa I, Zeng H, Harding HP, Ron D. Feedback inhibition of the unfolded protein response by GADD34-mediated dephosphorylation of eIF2alpha. J Cell Biol. 2001;153(5):1011-22.
  • Iwawaki T, Hosoda A, Okuda T, Kamigori Y, Nomura-Furuwatari C, Kimata Y, Tsuru A, Kohno K. Translational control by the ER transmembrane kinase/ribonuclease IRE1 under ER stress. Nat Cell Biol. 2001;3(2):158-64.
  • Jakob CA, Burda P, Roth J, Aebi M. Degradati- on of misfolded endoplasmic reticulum glycopro- teins in Saccharomyces cerevisiae is determined by a specific oligosaccharide structure. J Cell Biol. 1998;142(5):1223-33.
  • M., Tatu U., Endoplasmic reticulum (ER) stres and diabetes. İndian J Med Res. 2007;125:411-424.
  • Wang XZ, Lawson B, Brewer JW, Zinszner H, Sanjay A, Mi LJ, Boorstein R, Kreibich G, Hendershot LM, Ron D. Signals from the stressed endoplasmic reticulum induce C/EBP-homologous protein (CHOP/GADD153). Mol Cell Biol. 1996;16(8):4273
  • Zinszner H, Kuroda M, Wang X, Batchvarova N, Lightfoot RT, Remotti H, Stevens JL, Ron D. CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum. Genes Dev. 1998;12(7):982-95.
  • Wang XZ, Harding HP, Zhang Y, Jolicoeur EM, Kuroda M, Ron D. Cloning of mammalian Ire1 reveals diversity in the ER stress responses. EMBO J. 1998;17(19):5708-17.
  • Harding HP, Novoa I, Zhang Y, Zeng H, Wek R, Schapira M, Ron D. Regulated translation initiation controls stress-induced gene expression in mammalian cells. Mol Cell. 2000;6(5):1099-108.
  • Wang XZ, Ron D. Stress-induced phosphorylation and activation of the transcription factor CHOP (GADD153) by p38 MAP Kinase. Science. 1996;272(5266):1347-9.
  • Sok J, Wang XZ, Batchvarova N, Kuroda M, Harding H, Ron D. CHOP-Dependent stress-inducible expression of a novel form of carbonic anhydrase VI. Mol Cell Biol. 1999;19(1):495-504.
  • Antonsson B, Conti F, Ciavatta A, Montessuit S, Lewis S, Martinou I, Bernasconi L, Bernard A, Mermod JJ, Mazzei G, Maundrell K, Gambale F, Sadoul R, content in the pancreas of nondiabetic and diabetic Martinou JC. Inhibition of Bax channel-forming activity by Bcl-2. Science. 1997;277(5324):370-2.
  • Nakagawa T, Zhu H, Morishima N, Li E, Xu J, Yankner BA, Yuan J. Caspase-12 mediates endoplasmic- reticulum-specific apoptosis and cytotoxicity by (Akita) mutant mice. Diabetes. 1997;46(5):887-94. amyloid-beta. Nature. 2000;403(6765):98-103.
  • Oyadomari S, Koizumi A, Takeda K, Gotoh T, Tobiume K, Matsuzawa A, Takahashi T, Nishitoh H, Morita K, Takeda K, Minowa O, Miyazono K, Noda T, Ichijo H. ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis. EMBO Rep. 2001;2(3):222-8.
  • Nakagawa T, Yuan J.Cross-talk between two Lu D, Takata K, Koizumi A, Izumi T. A mutation in cysteine protease families. Activation of caspase-12 the insulin 2 gene induces diabetes with severe by calpain in apoptosis. J Cell Biol. 2000;150(4):887
  • Yoneda T, Imaizumi K, Oono K, Yui D, Gomi F, Katayama T, Tohyama M. Activation of caspase-12, an endoplastic reticulum (ER) resident caspase, through tumor necrosis factor receptor-associated factor 2-dependent mechanism in response to the ER stress. J Biol Chem. 2001;276(17):13935-40.
  • Rao RV, Hermel E, Castro-Obregon S, del Rio G, Ellerby LM, Ellerby HM, Bredesen DE. Coupling endoplasmic reticulum stress to the cell death program. Mechanism of caspase activation. J Biol Chem. 2001;276(36):33869-74.
  • Mauricio D, Mandrup-Poulsen T.Apoptosis and the pathogenesis of IDDM: a question of life and death. Diabetes. 1998;47(10):1537-43.
  • Chandler JM, Cohen GM, MacFarlane M. Different subcellular distribution of caspase-3 and caspase-7 following Fas-induced apoptosis in mouse liver. J Biol Chem. 1998;273(18):10815-8.
  • Yoshida H. ER stres and diseases, FEBS Journal2007;274:630-658.
  • Deprez P, Gautschi M, Helenius A. More than one glycan is needed for ER glucosidase II to allow entry of glycoproteins into the calnexin ⁄ calreticulin cycle. Mol Cell. 2005;19:183–195.
  • Stefan Y, Orci L, Malaisse-Lagae F, Perrelet A, Patel Y, Unger RH. Quantitation of endocrine cell Yoshioka M, Kayo T, Ikeda T, Koizumi A. A novel locus, Mody4, distal to D7Mit189 on chromosome 7 determines early-onset NIDDM in nonobese C57BL/6 Akira S, Araki E, Mori M. Targeted disruption of the Chop gene delays endoplasmic reticulum stress- mediated diabetes. J Clin Invest. 2002;109(4):525
  • Wang J, Takeuchi T, Tanaka S, Kubo SK, Kayo T, pancreatic beta-cell dysfunction in the Mody mouse. J Clin Invest. 1999;103(1):27-37.

Endoplasmik Retikulum Stresine Cevap Yolakları ve Tip 2 Diyabet Patogenezinde Endoplasmik Retikulum Stres Aracılı Beta Hücre Apoptosisinin Rolü

Year 2015, Volume: 16 Issue: 3, 227 - 237, 27.08.2015
https://doi.org/10.18229/ktd.19744

Abstract

Tip 2 Diabetes Mellitus (T2DM) hastalarındaki beta hücre kayıplarının temel nedeninin apoptosis olduğu düşünülmektedir. Apoptosisin önemi; çeşitli biyolojik olaylarda gereksiz, hasarlı ya da zararlı hücrelerin inflamatuvar yanıt olmaksızın yok edilişini sağlamasından ve organizmanın iç dengesinin devamlılığına katkıda bulunmasından ileri gelmektedir. β hücreleri yoğun olarak insülin sentezlemesi ve salgılaması nedeniyle sıklıkla ER stresine maruz kalmaktadır. Son yıllardaki çalışmalarda β hücrelerinde Endoplazmik Retikulum (ER)’un apoptotik ölüm sinyallerinin iletilmesinde önemli bir organel olduğu gösterilmiştir. β-hücrelerinde ER stresi aracılı apoptosis üzerine yapılacak çalışmalar diyabet patogenezinde yeni mekanizmaların aydınlatılmasına ve tedavi hedeflerinin iyi belirlenmesine ışık tutacaktır.

References

  • Gurzov EN, Ortis F, Bakiri L, Wagner EF, Eizirik DL. JunB Inhibits ER Stress and Apoptosis in Pancreatic Beta Cells. PLoS ONE. 2008;3(8)
  • Diabetes&Metabolism. 2008;34,56-64
  • Büyükgebiz O, Caferler JS. Apoptoz. Sendrom 2001;13:102-7.
  • Fadeel B, Orrenius S, Zhivotovsky B. Apoptosis in human disease: A new skin for the old ceremony? Biochemical and Biophysical Research Communications 1999; 266 :699-717. Klin J Med Sci. 2003;23:499-508
  • Bonner-Weir S, White MF. Disruption of IRS- 2 causes type 2 diabetes in mice. Nature. 1998; 26;391(6670):900-4. 2001;13;414(6865):792-8.
  • Eizirik DL, Poulsen TM. A choice of death-the signal-transduction of immune-mediated beta cell apoptosis, Diabetologia. 2001;44,2115-2133.
  • Kaneto H, Kajimoto Y, Miyagawa J, Matsuoka T, Fujitani Y, Umayahara Y, Hanafusa T, Matsuzawa Y, Yamasaki Y, Hori M. Beneficial effects of antioxidants in diabetes: possible protection of pancreatic short- and long-term hyperglycemia. Diabetes. beta-cells against glucose toxicity. Diabetes. 1999;48(12):2398-406.
  • Oyadomari S, Takeda K, Takiguchi M, Gotoh T, Matsumoto M, Wada I, Akira S, Araki E, Mori M. Nitric oxide-induced apoptosis in pancreatic beta cells and p21WAF1/CIP1. FEBS Lett. 1999;455(3):315-20. is mediated by the endoplasmic reticulum stress pathway. Proc Natl Acad Sci U S A. 2001;98(19):10845
  • Zhou YP, Teng D, Dralyuk F, Ostrega D, Roe Saini KS, Thompson C, Winterford CM, Walker NI, Cameron DP. Streptozotocin at low doses induces apoptosis and at high doses causes necrosis in a murine pancreatic beta cell line, INS-1. Biochem Mol Biol Int. 1996;39(6):1229-36.
  • Unger RH. Lipotoxic diseases. Annu Rev Med. 2002;53:319-36.
  • Withers DJ, Burks DJ, Towery HH, Altamuro SL, Flint CL, White MF. Irs-2 coordinates Igf-1 receptor- mediated beta-cell development and peripheral differentiation in BETA2/neuroD-deficient mice. insulin signalling. Nat Genet. 1999;23(1):32-40. Genes Dev. 1997;11(18):2323-34.
  • Withers DJ, Gutierrez JS, Towery H, Burks DJ, Ren JM, Previs S, Zhang Y, Bernal D, Pons S, Shulman GI, Bonner-Weir S, White MF. Disruption of IRS-2 causes type 2 diabetes in mice. Nature. 1998;391(6670):900
  • Miettinen PJ, Huotari M, Koivisto T, Ustinov J, Palgi J, Rasilainen S, Lehtonen E, Keski-Oja J, Otonkoski T. Impaired migration and delayed differentiation of pancreatic islet cells in mice lacking EGF-receptors. Development. 2000;127(12):2617-27.
  • Hart AW, Baeza N, Apelqvist A, Edlund H. Attenuation of FGF signalling in mouse beta-cells leads to diabetes. Nature. 2000;408(6814):864-8.
  • Rane SG, Dubus P, Mettus RV, Galbreath EJ, Boden G, Reddy EP, Barbacid M. Loss of Cdk4 expression causes insulin-deficient diabetes and Cdk4 activation results in beta-islet cell hyperplasia. Nat Genet. 1999;22(1):44-52. apoptosis, and increased sensitivity to ceramide-, but not to high glucose-induced cell death. J Biol Chem. 2002;277(8):6413.
  • Naya FJ, Huang HP, Qiu Y, Mutoh H, DeMayo FJ, Leiter AB, Tsai MJ. Diabetes, defective pancreatic morphogenesis, and abnormal enteroendocrine Silva JP, Köhler M, Graff C, Oldfors A, Magnuson MA, Berggren PO, Larsson NG. Impaired insulin secretion and beta-cell loss in tissue-specific knockout mice with mitochondrial diabetes. Nat Genet. 2000;26(3):336-40.
  • Harding HP, Zeng H, Zhang Y, Jungries R, Chung P, Plesken H, Sabatini DD, Ron D. Diabetes mellitus and exocrine pancreatic dysfunction in perk-/- mice reveals a role for translational control in secretory cell survival. Mol Cell. 2001;7(6):1153-63.
  • Welters HJ, Kulkarni RN. Wnt signaling: relevance to β-cel biology and diabetes. Trends in Endocrinology and metabolism, 2008;19,349-355.
  • Cauchi S, Eroguel P.TCF7L2 genetic defect and type 2 diabetes. Curr. Diab Rep. 2008;8(2), 149-155.
  • Shu L, Sauter NS, Schulthess FT, Matveyenko AV, Oberholzer J, Maedler K. Transcription factor 7-like 2 regulates beta-cell survival and function in human pancreatic islets. Diabetes. 2008;57(3):645-53.
  • Yoshida H, Haze K, Yanagi H, Yura T, Mori K. Identification of the cis-acting endoplasmic reticulum stress response element responsible 2000;5(4):729-35. for transcriptional induction of mammalian glucose-regulated proteins. Involvement of basic
  • Rajan S.S., Srinivasan V., Balasubramanyam leucine zipper transcription factors. J Biol Chem. 1998;273(50):33741-9.
  • Yoshida H, Matsui T, Yamamoto A, Okada T, Mori intact unfolded protein response pathway. Mol Cell. K. XBP1 mRNA is induced by ATF6 and spliced by proteins from the ER of S. cerevisiae requires an IRE1 in response to ER stress to produce a highly M, Zşñiga M, Brown PO, Ploegh H. Degradation of active transcription factor. Cell. 2001;107(7):881-91.
  • Yoshida H, Okada T, Haze K, Yanagi H, Yura T, Negishi M, Mori K. ATF6 activated by proteolysis binds in the presence of NF-Y (CBF) directly to the cis-acting element responsible for the mammalian unfolded protein response. Mol Cell Biol. 2000;20(18):6755-67.
  • Chen X, Shen J, Prywes R. The luminal domain CHOP, have opposing effects on the induction of G1/S arrest. Genes Dev. 1994;8(4):453-64. of ATF6 senses endoplasmic reticulum (ER) stress and causes translocation of ATF6 from the ER to the Golgi. J Biol Chem. 2002;277(15):13045-52.
  • Bertolotti A, Zhang Y, Hendershot LM, Harding HP, Ron D. Dynamic interaction of BiP and ER stress transducers in the unfolded-protein response. Nat Cell Biol. 2000;2(6):326-32.
  • Shi Y, Vattem KM, Sood R, An J, Liang J, Stramm L, Wek RC. Identification and characterization of panc- reatic eukaryotic initiation factor 2 alpha-subunit ki- nase, PEK, involved in translational control. Mol Cell Biol. 1998;18(12):7499-509.
  • Novoa I, Zeng H, Harding HP, Ron D. Feedback inhibition of the unfolded protein response by GADD34-mediated dephosphorylation of eIF2alpha. J Cell Biol. 2001;153(5):1011-22.
  • Iwawaki T, Hosoda A, Okuda T, Kamigori Y, Nomura-Furuwatari C, Kimata Y, Tsuru A, Kohno K. Translational control by the ER transmembrane kinase/ribonuclease IRE1 under ER stress. Nat Cell Biol. 2001;3(2):158-64.
  • Jakob CA, Burda P, Roth J, Aebi M. Degradati- on of misfolded endoplasmic reticulum glycopro- teins in Saccharomyces cerevisiae is determined by a specific oligosaccharide structure. J Cell Biol. 1998;142(5):1223-33.
  • M., Tatu U., Endoplasmic reticulum (ER) stres and diabetes. İndian J Med Res. 2007;125:411-424.
  • Wang XZ, Lawson B, Brewer JW, Zinszner H, Sanjay A, Mi LJ, Boorstein R, Kreibich G, Hendershot LM, Ron D. Signals from the stressed endoplasmic reticulum induce C/EBP-homologous protein (CHOP/GADD153). Mol Cell Biol. 1996;16(8):4273
  • Zinszner H, Kuroda M, Wang X, Batchvarova N, Lightfoot RT, Remotti H, Stevens JL, Ron D. CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum. Genes Dev. 1998;12(7):982-95.
  • Wang XZ, Harding HP, Zhang Y, Jolicoeur EM, Kuroda M, Ron D. Cloning of mammalian Ire1 reveals diversity in the ER stress responses. EMBO J. 1998;17(19):5708-17.
  • Harding HP, Novoa I, Zhang Y, Zeng H, Wek R, Schapira M, Ron D. Regulated translation initiation controls stress-induced gene expression in mammalian cells. Mol Cell. 2000;6(5):1099-108.
  • Wang XZ, Ron D. Stress-induced phosphorylation and activation of the transcription factor CHOP (GADD153) by p38 MAP Kinase. Science. 1996;272(5266):1347-9.
  • Sok J, Wang XZ, Batchvarova N, Kuroda M, Harding H, Ron D. CHOP-Dependent stress-inducible expression of a novel form of carbonic anhydrase VI. Mol Cell Biol. 1999;19(1):495-504.
  • Antonsson B, Conti F, Ciavatta A, Montessuit S, Lewis S, Martinou I, Bernasconi L, Bernard A, Mermod JJ, Mazzei G, Maundrell K, Gambale F, Sadoul R, content in the pancreas of nondiabetic and diabetic Martinou JC. Inhibition of Bax channel-forming activity by Bcl-2. Science. 1997;277(5324):370-2.
  • Nakagawa T, Zhu H, Morishima N, Li E, Xu J, Yankner BA, Yuan J. Caspase-12 mediates endoplasmic- reticulum-specific apoptosis and cytotoxicity by (Akita) mutant mice. Diabetes. 1997;46(5):887-94. amyloid-beta. Nature. 2000;403(6765):98-103.
  • Oyadomari S, Koizumi A, Takeda K, Gotoh T, Tobiume K, Matsuzawa A, Takahashi T, Nishitoh H, Morita K, Takeda K, Minowa O, Miyazono K, Noda T, Ichijo H. ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis. EMBO Rep. 2001;2(3):222-8.
  • Nakagawa T, Yuan J.Cross-talk between two Lu D, Takata K, Koizumi A, Izumi T. A mutation in cysteine protease families. Activation of caspase-12 the insulin 2 gene induces diabetes with severe by calpain in apoptosis. J Cell Biol. 2000;150(4):887
  • Yoneda T, Imaizumi K, Oono K, Yui D, Gomi F, Katayama T, Tohyama M. Activation of caspase-12, an endoplastic reticulum (ER) resident caspase, through tumor necrosis factor receptor-associated factor 2-dependent mechanism in response to the ER stress. J Biol Chem. 2001;276(17):13935-40.
  • Rao RV, Hermel E, Castro-Obregon S, del Rio G, Ellerby LM, Ellerby HM, Bredesen DE. Coupling endoplasmic reticulum stress to the cell death program. Mechanism of caspase activation. J Biol Chem. 2001;276(36):33869-74.
  • Mauricio D, Mandrup-Poulsen T.Apoptosis and the pathogenesis of IDDM: a question of life and death. Diabetes. 1998;47(10):1537-43.
  • Chandler JM, Cohen GM, MacFarlane M. Different subcellular distribution of caspase-3 and caspase-7 following Fas-induced apoptosis in mouse liver. J Biol Chem. 1998;273(18):10815-8.
  • Yoshida H. ER stres and diseases, FEBS Journal2007;274:630-658.
  • Deprez P, Gautschi M, Helenius A. More than one glycan is needed for ER glucosidase II to allow entry of glycoproteins into the calnexin ⁄ calreticulin cycle. Mol Cell. 2005;19:183–195.
  • Stefan Y, Orci L, Malaisse-Lagae F, Perrelet A, Patel Y, Unger RH. Quantitation of endocrine cell Yoshioka M, Kayo T, Ikeda T, Koizumi A. A novel locus, Mody4, distal to D7Mit189 on chromosome 7 determines early-onset NIDDM in nonobese C57BL/6 Akira S, Araki E, Mori M. Targeted disruption of the Chop gene delays endoplasmic reticulum stress- mediated diabetes. J Clin Invest. 2002;109(4):525
  • Wang J, Takeuchi T, Tanaka S, Kubo SK, Kayo T, pancreatic beta-cell dysfunction in the Mody mouse. J Clin Invest. 1999;103(1):27-37.
There are 49 citations in total.

Details

Primary Language Turkish
Subjects Clinical Sciences
Journal Section Review
Authors

Sefa Çelik This is me

Serkan Şen

Ömer Hazman This is me

Publication Date August 27, 2015
Published in Issue Year 2015 Volume: 16 Issue: 3

Cite

APA Çelik, S., Şen, S., & Hazman, Ö. (2015). Endoplasmik Retikulum Stresine Cevap Yolakları ve Tip 2 Diyabet Patogenezinde Endoplasmik Retikulum Stres Aracılı Beta Hücre Apoptosisinin Rolü. Kocatepe Tıp Dergisi, 16(3), 227-237. https://doi.org/10.18229/ktd.19744
AMA Çelik S, Şen S, Hazman Ö. Endoplasmik Retikulum Stresine Cevap Yolakları ve Tip 2 Diyabet Patogenezinde Endoplasmik Retikulum Stres Aracılı Beta Hücre Apoptosisinin Rolü. KTD. August 2015;16(3):227-237. doi:10.18229/ktd.19744
Chicago Çelik, Sefa, Serkan Şen, and Ömer Hazman. “Endoplasmik Retikulum Stresine Cevap Yolakları Ve Tip 2 Diyabet Patogenezinde Endoplasmik Retikulum Stres Aracılı Beta Hücre Apoptosisinin Rolü”. Kocatepe Tıp Dergisi 16, no. 3 (August 2015): 227-37. https://doi.org/10.18229/ktd.19744.
EndNote Çelik S, Şen S, Hazman Ö (August 1, 2015) Endoplasmik Retikulum Stresine Cevap Yolakları ve Tip 2 Diyabet Patogenezinde Endoplasmik Retikulum Stres Aracılı Beta Hücre Apoptosisinin Rolü. Kocatepe Tıp Dergisi 16 3 227–237.
IEEE S. Çelik, S. Şen, and Ö. Hazman, “Endoplasmik Retikulum Stresine Cevap Yolakları ve Tip 2 Diyabet Patogenezinde Endoplasmik Retikulum Stres Aracılı Beta Hücre Apoptosisinin Rolü”, KTD, vol. 16, no. 3, pp. 227–237, 2015, doi: 10.18229/ktd.19744.
ISNAD Çelik, Sefa et al. “Endoplasmik Retikulum Stresine Cevap Yolakları Ve Tip 2 Diyabet Patogenezinde Endoplasmik Retikulum Stres Aracılı Beta Hücre Apoptosisinin Rolü”. Kocatepe Tıp Dergisi 16/3 (August 2015), 227-237. https://doi.org/10.18229/ktd.19744.
JAMA Çelik S, Şen S, Hazman Ö. Endoplasmik Retikulum Stresine Cevap Yolakları ve Tip 2 Diyabet Patogenezinde Endoplasmik Retikulum Stres Aracılı Beta Hücre Apoptosisinin Rolü. KTD. 2015;16:227–237.
MLA Çelik, Sefa et al. “Endoplasmik Retikulum Stresine Cevap Yolakları Ve Tip 2 Diyabet Patogenezinde Endoplasmik Retikulum Stres Aracılı Beta Hücre Apoptosisinin Rolü”. Kocatepe Tıp Dergisi, vol. 16, no. 3, 2015, pp. 227-3, doi:10.18229/ktd.19744.
Vancouver Çelik S, Şen S, Hazman Ö. Endoplasmik Retikulum Stresine Cevap Yolakları ve Tip 2 Diyabet Patogenezinde Endoplasmik Retikulum Stres Aracılı Beta Hücre Apoptosisinin Rolü. KTD. 2015;16(3):227-3.

88x31.png
Bu Dergi Creative Commons Atıf-GayriTicari-AynıLisanslaPaylaş 4.0 Uluslararası Lisansı ile lisanslanmıştır.