Autophagy: cellular and molecular mechanisms

By Danielle Glick, Sandra Barth, Kay F Macleod. Journal of Pathology, 2010

3,549 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/03cac8cbabf29f6cc6ab94ac512b2eab548d01de

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Kay F Macleod
2. Xiaohua Li
3. D. Hong
4. Danielle Glick
5. Binyun Ma
6. Shi-kun He
7. Sandra Barth
8. F. Janku

In Molecular Biology

1. Kay F Macleod
2. P. Lei
3. Xiaohua Li
4. Shu-ting Zhang
5. A. Kabanov
6. Danielle Glick
7. Binyun Ma
8. Shi-kun He

In Physiology

1. Kay F Macleod
2. Xiaohua Li
3. Danielle Glick
4. Binyun Ma
5. Shi-kun He
6. Sandra Barth

Citations in the corpus

• Autophagy: assays and artifacts (2010, background): “The role of autophagy in preventing human diseases [1], including cancer, neurodegenerative disorders and inflammatory bowel disease, has also made it important to examine autophagy in situ in human tissue sections.”
• Brief update on endocytosis of nanomedicines (2019, background): “Induction of autophagy leads to the capture of cytosolic materials by autophagosomes, which subsequently fuse with lysosomes for degradation or exocytosis [60].”
• Autophagy and autophagy-related proteins in cancer (2020, background): “There are three morphologically and mechanistically distinct types of autophagy in cells: macroautophagy, microautophagy and chaperone mediated autophagy [3], and usually macroautophagy is referred to as autophagy [4].”
• Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications (2021, background): “BNIP3 is also a competitive substrate of Bcl‐2 and Beclin‐1 and therefore leads to the release of Beclin‐1 and the activation of autophagy.(157,158) It was observed that the Beclin‐1 protein level increased as early as 4 h and peaked at 24–72 h after a rat model of severe neonatal cerebral hypoxia‐i”
• Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, neutral): “steps with subsequent fusion with lysosomes to form autolysosome or amphisome (Alavian et al., 2011; Glick et al., 2010).”
• Autophagy and chemotherapy resistance: a promising therapeutic target for cancer treatment (2013, background): “Several of the known tumor-suppressor genes (p53, PTEN, TSC1/TSC2) and tumor-associated genes (p21, AKT) also respectively stimulate or inhibit autophagy.(10,15) Autophagy is also induced by a variety of metabolic stresses such as endoplasmic reticulum (ER) stress, hypoxia, oxidative stress, express”
• Autophagy as a target for anticancer therapy (2011, background): “Such an adaptive response to hypoxia would prevent wasteful ATP consumption at the endoplasmic reticulum, allow the cell to generate ATP from catabolism, and limit production of reactive oxygen species at the mitochondria”