The late stages of autophagy: how does the end begin?

Noda, Tetsuji; Fujita, Naonobu; Yoshimori, Tamotsu

doi:10.1038/cdd.2009.54

Cited by 153 publications

(129 citation statements)

References 52 publications

Supporting

Mentioning

124

Contrasting

Order By: Relevance

“…Autophagy requires the clearance of autophagosomes and their cargo upon fusion with lysosomes. 5,6 It is suggested that this fusion is regulated by several Rab proteins and soluble N-ethylmaleimidine-sensitive factor attachment protein receptors (SNAREs). 4,6,7 Similarly in case of bi-directional ER-Golgi transport the tethering of the COPII-coated vesicles at Golgi membrane takes place in anterograde transport, when in retrograde transport COPIcoated vesicles are tethered at ER membrane.…”

mentioning

confidence: 99%

Rint1 inactivation triggers genomic instability, ER stress and autophagy inhibition in the brain

et al. 2015

View full text Add to dashboard Cite

Endoplasmic reticulum (ER) stress, defective autophagy and genomic instability in the central nervous system are often associated with severe developmental defects and neurodegeneration. Here, we reveal the role played by Rint1 in these different biological pathways to ensure normal development of the central nervous system and to prevent neurodegeneration. We found that inactivation of Rint1 in neuroprogenitors led to death at birth. Depletion of Rint1 caused genomic instability due to chromosome fusion in dividing cells. Furthermore, Rint1 deletion in developing brain promotes the disruption of ER and Cis/Trans Golgi homeostasis in neurons, followed by ER-stress increase. Interestingly, Rint1 deficiency was also associated with the inhibition of the autophagosome clearance. Altogether, our findings highlight the crucial roles of Rint1 in vivo in genomic stability maintenance, as well as in prevention of ER stress and autophagy.

show abstract

mentioning

confidence: 99%

Rint1 inactivation triggers genomic instability, ER stress and autophagy inhibition in the brain

et al. 2015

View full text Add to dashboard Cite

show abstract

“…13 Subsequently, by fusing with endosomal/lysosomal compartments, the autophagosome matures into the autophagolysosome, wherein the substrate is degraded by acid hydrolases. 14 Autophagy is triggered by the so-called beclin-1/PI3kIII interactome, a macro-complex participated by several other proteins, which locates in the proximity of the trans Golgi network. 12 The autophagy process is finely tuned by sensors of nutrients and energy available.…”

mentioning

confidence: 99%

Autophagy-active beclin-1 correlates with favourable clinical outcome in non-Hodgkin lymphomas

Nicotra

Mercalli

Peracchio³

et al. 2010

Modern Pathology

View full text Add to dashboard Cite

The expression of beclin-1, an oncosuppressor monoallelically deleted in 460% epithelial cancers, has been shown to be developmentally regulated in T and B lymphocytes. By interacting with either bcl-2 or class III phosphatidyl-inositol-3-phosphate kinase, beclin-1 regulates apoptosis and autophagy, two processes crucial for lymphatic tissue homeostasis. We analyzed the potential link between beclin-1-mediated autophagy and the malignant behaviour of lymphomas. The tissue expression of beclin-1 was analyzed in a large series of nonHodgkin lymphomas and correlated with patient's clinical outcome. By immunofluorescence, beclin-1 staining showed faintly detectable and diffusely distributed in the cytoplasm (regarded as negative) or confined to the perinuclear region as large and brilliant puncta suggestive of macro-aggregate reactivity (regarded as positive). The positive expression of beclin-1 well correlated with the presence of LC3-positive autophagic vacuoles and was inversely correlated with the expression of bcl-2. Non-Hodgkin lymphomas in which X20% of tumour cells expressed high level of beclin-1 aggregates were associated with a complete (57%) or partial (35%) remission. The 5-year overall survival probability, calculated by the Kaplan-Meier method, was 92% and 42% in beclin-1-expressing non-Hodgkin lymphomas with X20% and o20% positive cells, respectively (log-rank test, Po0.000.1). In Cox multivariate analysis, the level of beclin-1 expression, adjusted for patient's age and pathologic stage, revealed to be significantly correlated with patient's survival (Po0.0001). This is the first demonstration of the involvement of beclin-1 and autophagy in the clinical behaviour of non-Hodgkin lymphomas. The present data are compatible with the hypothesis that non-Hodgkin lymphomas with upregulated autophagy are more responsive to chemotherapy and indicate that beclin-1 could be a valuable independent prognostic factor in this heterogeneous group of tumours. Modern Pathology (2010) 23, 937-950;

show abstract

“…to function in the later phase (Fujita et al, 2008a;Noda et al, 2009). To determine whether Atg14L is involved in the initial phase of autophagosome formation or at a later phase, we observed the GFP-DFCP1 distribution pattern before and after autophagy-inducing nutrient starvation conditions.…”

Section: Introductionmentioning

confidence: 99%

Autophagy requires endoplasmic reticulum targeting of the PI3-kinase complex via Atg14L

Matsunaga¹,

Morita²,

Saitoh³

et al. 2010

J Exp Med

View full text Add to dashboard Cite

The late stages of autophagy: how does the end begin?

Cited by 153 publications

References 52 publications

Rint1 inactivation triggers genomic instability, ER stress and autophagy inhibition in the brain

Rint1 inactivation triggers genomic instability, ER stress and autophagy inhibition in the brain

Autophagy-active beclin-1 correlates with favourable clinical outcome in non-Hodgkin lymphomas

Autophagy requires endoplasmic reticulum targeting of the PI3-kinase complex via Atg14L

Contact Info

Product

Resources

About