Rab7 is required for the normal progression of the autophagic pathway in mammalian cells
By M. Gutierrez, Daniela B. Munafó, W. Berón, Marina Colombo. Journal of Cell Science, 2004
685 citations recorded by the source corpus.
Subfields: Cell Biology, Epidemiology, Physiology
View Paper: https://www.semanticscholar.org/paper/0b6b765822a72b46a3fb7bf9263fb99a5aa9cda6
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In Cell Biology
- D. Klionsky
- N. Mizushima
- I. Slaninová
- Beth Levine
- V. Deretic
- Guido Kroemer
- T. Johansen
- Alec C. Kimmelman
In Epidemiology
- N. Mizushima
- D. Klionsky
- Beth Levine
- Guido Kroemer
- I. Slaninová
- V. Deretic
- Alec C. Kimmelman
- Douglas R. Green
In Physiology
- N. Mizushima
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- D. Klionsky
- Beth Levine
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- Alec C. Kimmelman
- V. Deretic
- L. Galluzzi
Citations in the corpus
- Autophagy pathway: Cellular and molecular mechanisms (2018, background): “gosome-lysosome fusion, the requirement for RAB7 is well established.(54) RAB7 interacts with various tethering factors, and these interactions are likely to further enhance the specificity of autophagosome-lysosome fusion.”
- Molecular definitions of autophagy and related processes (2017, positive): “…role is mediated by the activation of the GTPase RAB7A, member RAS oncogene family (RAB7A), which is required for autophagosome maturation (Gutierrez et al , 2004; Jager et al , 2004; Liang et al , 2008), the RAB7 effector pleckstrin homology and RUN domain containing M1 (PLEKHM1) (McEwan…”
- Pancreatic cancers require autophagy for tumor growth. (2011, neutral): “2; Tanaka et al. 2000; Gutierrez et al. 2004; Radoshevich et al. 2010).”
- Starvation and ULK1-dependent cycling of mammalian Atg9 between the TGN and endosomes (2006, background): “AVis are not Rab7-positive and do not contain degradative enzymes, whereas AVds have acquired both Rab7 and degradative enzymes (Gutierrez et al., 2004; Jager et al., 2004).”
- Autophagy: cellular and molecular mechanisms (2010, background): “This aspect of the process is relatively understudied but requires the small G protein Rab7 in its GTP-bound state [46,47], and also the Presenilin protein that is implicated in Alzheimer’s disease [45].”
- Autophagy: molecular machinery for self-eating (2005, background): “is targeted to the autophagosome membrane and is involved in a late step, fusion with the lysosome, to allow maturation.(88,89) In contrast to mammalian Rab GTPase, it has not”
- Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, positive): “…by transferring the autophagosomes to lysosomal proximity for lysosomal membrane proteins LAMP1/2 and Rab7, member of Rab family GTPases and vesicular proteins, class III Vps, SNARE and ESCRT to enable fusion (Atlashkin et al., 2003; Gutierrez et al., 2004b; Lee et al., 2007; Webb et al., 2004).”
- Autophagy is a defense mechanism inhibiting BCG and Mycobacterium tuberculosis survival in infected macrophages. (2004, methodology): “was used as previously described (Gutierrez et al., 2004).”
- FYCO1 is a Rab7 effector that binds to LC3 and PI3P to mediate microtubule plus end–directed vesicle transport (2010, background): “In mammals, Rab7, the core class C Vpstethering complex and UVRAG are important for fusion of autophagosomes with lysosomes (Gutierrez et al., 2004; Jäger et al., 2004; Liang et al., 2008).”
- Role for Rab7 in maturation of late autophagic vacuoles (2004, methodology): “…to our electron microscopical data, showing that the size of autophagic vacuoles was similar in pSUPER and Rab7 RNAi cells, Gutierrez et al. (Gutierrez et al., 2004) reported that cells expressing the dominant negative Rab7 T22N accumulated larger autophagic vacuoles than cells expressing…”