Otofaji: Programlı Hücre Ölümü

Cilt: 15 Sayı: 2 24 Haziran 2016
Aynur Karadağ
PDF İndir
EN TR

Öz

Working as a quality control system, autophagy is a physiological phenomenon responsible for the degradation of long lived proteins, dysfunctional organelles, cytosolic fragments, damaged marcomolecules and pathogens in cells. In addition to its biological recycling function, autophagy plays a significant role in the pathogenesis of metabolic syndromes such as obesity and diabetes. Since the energy required to maintain cell function is high, disturbances in the balance between anabolic and catabolic metabolism possibly contribute to various disorders.Dysfunction of autophagy leads to the initiation and progression of multiple diseases. Autophagy contributes to cell death depending on the cellular contents especially under conditions associated with impaired apoptosis. Therefore, there has been increasing research on the molecular mechanisms and metabolic regulation of autophagy. Basal autophagy may function as a tumor suppressive mechanism during tumorigenesis; however, excessive autophagy works as a pro-survival pathway in some cancer types. Research in this area is critical for the development of novel therapeutics in health problems such as cancer, infections, neurodegenerative and metabolic diseases

Anahtar Kelimeler

Autophagy, apoptosis, programmed cell death

Kaynakça

  1. Anding, Al., Baehrecke, E. H. (2015) Autophagy İn Cell Life And Cell Death. Apoptosis And Development. Volume 114, Pages 67–91.
  2. Galluzzi, L., Vitale, I., Abrams, J. M., Alnemri, E. S., Baehrecke, E. H., Blagosklonny, M.V. (2012). Molecular Definitions Of Cell Death Subroutines: Recommendations Of The Nomenclature Committee On Cell Death . Cell Death And Differentiation, 19(1), 107–120.
  3. Gözuacik, D., Kimchi, A. (2006) Dapk Protein Family And Cancer. Autophagy. 2(2):74-9.
  4. Gözuacik, D., Kimchi, A. (2007). Autophagy And Cell Death. Curr Top Dev Biol. 78:217-45.
  5. Hansen, M., Taubert, S., Crawford, D., Libina, N., Lee, S. J., Kenyon, C. (2007). Lifespan Extension By Conditions That İnhibit Translation İn Caenorhabditis Elegans. Aging Cell 6, 95-110.
  6. Hars, E. S., Qi, H., Ryazanov, A. G., Jin, S., Cai, L., Hu, C., Liu, L. F. (2007). Autophagy Regulates Ageing İn C. Elegans. Autophagy 3, 93-95.
  7. Juhasz, G., Hill, J. H., Yan, Y., Sass, M., Baehrecke, E. H., Backer, J. M., Et Al. (2008). The Class Iii Pi(3)K Vps34 Promotes Autophagy And Endocytosis But Not Tor Signaling İn Drosophila. The Journal Of Cell Biology, 181(4), 655–666.
  8. Kroemer, G., Marino, G., Levine, B. (2010). Autophagy And İntegrated Stress Response. Mol Cell 40(2):280- 293.
  9. Lee, J., Giordano, S., Zhang, J. (2012) Autophagy, Mitochondria And Oxidative Stress: Cross-Talk And Redox Signalling. Biochem J. 15;441(2):523-40.
  10. Levine, B. Yuan, J. (2005). Autophagy İn Cell Death: An İnnocent Convict?. The Journal Of Clinical Investigation, 115; 2679- 2688.

Kaynak Göster

APA
Karadağ, A. (2016). Otofaji: Programlı Hücre Ölümü. Ankara Sağlık Hizmetleri Dergisi, 15(2), 19-26. https://doi.org/10.1501/Ashd_0000000117
AMA
1.Karadağ A. Otofaji: Programlı Hücre Ölümü. ASHD. 2016;15(2):19-26. doi:10.1501/Ashd_0000000117
Chicago
Karadağ, Aynur. 2016. “Otofaji: Programlı Hücre Ölümü”. Ankara Sağlık Hizmetleri Dergisi 15 (2): 19-26. https://doi.org/10.1501/Ashd_0000000117.
EndNote
Karadağ A (01 Haziran 2016) Otofaji: Programlı Hücre Ölümü. Ankara Sağlık Hizmetleri Dergisi 15 2 19–26.
IEEE
[1]A. Karadağ, “Otofaji: Programlı Hücre Ölümü”, ASHD, c. 15, sy 2, ss. 19–26, Haz. 2016, doi: 10.1501/Ashd_0000000117.
ISNAD
Karadağ, Aynur. “Otofaji: Programlı Hücre Ölümü”. Ankara Sağlık Hizmetleri Dergisi 15/2 (01 Haziran 2016): 19-26. https://doi.org/10.1501/Ashd_0000000117.
JAMA
1.Karadağ A. Otofaji: Programlı Hücre Ölümü. ASHD. 2016;15:19–26.
MLA
Karadağ, Aynur. “Otofaji: Programlı Hücre Ölümü”. Ankara Sağlık Hizmetleri Dergisi, c. 15, sy 2, Haziran 2016, ss. 19-26, doi:10.1501/Ashd_0000000117.
Vancouver
1.Aynur Karadağ. Otofaji: Programlı Hücre Ölümü. ASHD. 01 Haziran 2016;15(2):19-26. doi:10.1501/Ashd_0000000117