Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525

Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
free
free
  English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |   
lüll The role of autophagy in mammalian development: cell makeover rather than cell death Cecconi F; Levine BDev Cell 2008[Sep]; 15 (3): 344-357Autophagy is important for the degradation of bulk cytoplasm, long-lived proteins, and entire organelles. In lower eukaryotes, autophagy functions as a cell death mechanism or as a stress response during development. However, autophagy's significance in vertebrate development, and the role (if any) of vertebrate-specific factors in its regulation, remains unexplained. Through careful analysis of the current autophagy gene mutant mouse models, we propose that in mammals, autophagy may be involved in specific cytosolic rearrangements needed for proliferation, death, and differentiation during embryogenesis and postnatal development. Thus, autophagy is a process of cytosolic "renovation," crucial in cell fate decisions.|*Morphogenesis[MESH]|Adaptor Proteins, Signal Transducing[MESH]|Animals[MESH]|Apoptosis Regulatory Proteins[MESH]|Autophagy-Related Protein 5[MESH]|Autophagy-Related Protein 7[MESH]|Autophagy-Related Proteins[MESH]|Autophagy/*physiology[MESH]|Beclin-1[MESH]|Cell Death/*physiology[MESH]|Cell Differentiation[MESH]|Cell Proliferation[MESH]|Cell Survival[MESH]|Disease Models, Animal[MESH]|Humans[MESH]|Mice[MESH]|Microtubule-Associated Proteins/genetics/metabolism[MESH]|Phagosomes/metabolism[MESH]|Protein Kinases/genetics/metabolism[MESH]|Proteins/genetics/metabolism[MESH]|Saccharomyces cerevisiae Proteins/genetics/metabolism[MESH]|Signal Transduction/physiology[MESH] |