Zobrazeno 1 - 8
of 8
pro vyhledávání: '"Kumsal Ayse, Tekirdag"'
Autor:
Gozde Korkmaz, Kumsal Ayse Tekirdag, Deniz Gulfem Ozturk, Ali Kosar, Osman Ugur Sezerman, Devrim Gozuacik
Publikováno v:
PLoS ONE, Vol 8, Iss 12, p e82556 (2013)
Autophagy is a vesicular trafficking process responsible for the degradation of long-lived, misfolded or abnormal proteins, as well as damaged or surplus organelles. Abnormalities of the autophagic activity may result in the accumulation of protein a
Externí odkaz:
https://doaj.org/article/37fd8c84c7634049bc20dd529c33560a
Autor:
Kumsal Ayse Tekirdag, Ana Maria Cuervo
A variety of mechanisms deliver cytosolic materials to the lysosomal compartment for degradation through autophagy. Here, we focus on two autophagic pathways, the chaperone-mediated autophagy and the endosomal microautophagy that rely on the cytosoli
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5d5972618ae7bcd5aecc9aea68d823bc
https://europepmc.org/articles/PMC5900761/
https://europepmc.org/articles/PMC5900761/
Publikováno v:
Current Pathobiology Reports. 1:247-261
Macroautophagy (hereafter referred to as autophagy) is an evolutionary conserved degradation pathway that targets cytoplasmic substrates, including long-lived proteins, protein aggregates and damaged organelles, and leads to their degradation in lyso
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::874836b93b111342e83f88d404fb1fc7
https://doi.org/10.1007/s40139-013-0031-x
https://doi.org/10.1007/s40139-013-0031-x
Publikováno v:
Histology and histopathology. 31(8)
MicroRNAs (miRNAs) are endogenous non-coding small RNAs that negatively regulate gene expression at the post-transcriptional level. They have been implicated in several fundamental biological processes including development, differentiation, apoptosi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::0b49e94ce3f0f0918c3c7407ff86aecd
https://pubmed.ncbi.nlm.nih.gov/26940843
https://pubmed.ncbi.nlm.nih.gov/26940843
To cope with stress factors including nutrient deprivation, toxins, abnormal protein accumulation, cells developed mechanisms to repair damage caused by stress or, in cases where the damage is irrepairable, cell death responses. Autophagy and apoptos
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5dd6e51fb7a890fc8f3bb76018c39576
http://store.elsevier.com/product.jsp?isbn=9780128010327&pagename=search
http://store.elsevier.com/product.jsp?isbn=9780128010327&pagename=search
Publikováno v:
Autophagy
Macroautophagy (autophagy herein) is a cellular catabolic mechanism activated in response to stress conditions including starvation, hypoxia and misfolded protein accumulation. Abnormalities in autophagy were associated with pathologies including can
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ae382430233ac699d7fc469db9b6316e
https://pubmed.ncbi.nlm.nih.gov/23322078
https://pubmed.ncbi.nlm.nih.gov/23322078
Publikováno v:
Autophagy
Scopus-Elsevier
Scopus-Elsevier
Macroautophagy (autophagy) is the major intracellular degradation pathway for long-lived proteins and organelles. It helps the cell to survive a spectrum of stressful conditions including starvation, growth factor deprivation and misfolded protein ac
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::adb4fce20a99b4c994bef3aa066a9e43
Autor:
Osman Ugur Sezerman, Kumsal Ayse Tekirdag, Ali Koşar, Deniz Gulfem Ozturk, Devrim Gozuacik, Gozde Korkmaz
Publikováno v:
PLoS ONE
PLoS ONE, Vol 8, Iss 12, p e82556 (2013)
PLoS ONE, Vol 8, Iss 12, p e82556 (2013)
Background: Autophagy is a vesicular trafficking process responsible for the degradation of long-lived, misfolded or abnormal proteins, as well as damaged or surplus organelles. Abnormalities of the autophagic activity may result in the accumulation
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9935bbffa6f89ec8b7fbb513659a0d67
https://doi.org/10.1371/journal.pone.0082556
https://doi.org/10.1371/journal.pone.0082556