title
  

Autophagy in urology (Ürolojide otofaji)

Warning The system is temporarily closed to updates for reporting purpose.

Oral, Özlem and Irmak, Ster and Ekici, Sinan and Gözüaçık, Devrim (2012) Autophagy in urology (Ürolojide otofaji). In: Türkeri, Levent and Özer, Ayşe and Narter, Fehmi, (eds.) Moleküler Üroloji. Moleküler Üroloji: Ürolojik Hastalıkların Moleküler Temeli. Üroonkoloji Derneği Yayınları, İstanbul, pp. 271-283. ISBN 978-975-01697-2-4

This is the latest version of this item.

[img]MS Word - Repository staff only
660Kb

Abstract

Autophagy is an evolutionary conserved physiological event. It regulates intracellular homeostasis through recycling of cellular organelles and long-lived proteins. Autophagy is rapidly activated under stress conditions such as starvation and growth factor deprivation and supplies necessary components for the survival of cells. Thus, autophagy plays a role as a pro-survival phenomenon under certain conditions. On the other hand in some cases, autophagy pathways are involved in a caspase-independent, non-apoptotic cell death program called “autophagic cell death”. Studies in the last decade revealed the involvement of autophagy in several physiological and pathological events, establishing it as a new and important field of research for both basic scientists and clinicians. In this chapter, the effects of autophagy and -related molecular events in the development, progress and treatment of the urinary system diseases will be discussed.

Item Type:Book Section / Chapter
Additional Information:DG is the corresponding author
Uncontrolled Keywords:Urological Disease, urinary system, autophagy, cell, stress, apoptosis, programmed cell death, survival, signal transduction.
Subjects:Q Science > Q Science (General)
R Medicine > R Medicine (General)
R Medicine > RB Pathology
Q Science > QL Zoology
Q Science > QP Physiology
ID Code:20179
Deposited By:Devrim Gözüaçık
Deposited On:30 Nov 2012 15:06
Last Modified:29 Jul 2019 12:06

Available Versions of this Item

Repository Staff Only: item control page