Ambra1 at a glance

Cianfanelli, Valentina; Zio, Daniela De; Bartolomeo, Sabrina Di; Nazio, Francesca; Strappazzon, Flavie; Cecconi, Francesco

doi:10.1242/jcs.168153

Cited by 83 publications

(69 citation statements)

References 49 publications

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“…AMBRA1 can operate as a scaffold protein that regulates the stability of some autophagy-related complexes such as mTOR complex 1 and the ULK1 complex, and can also be partially localized to the mitochondria where it can act as a mitophagy receptor by binding directly to LC3 via its LIR motif (Cianfanelli et al, 2015; Strappazzon et al, 2015). …”

Section: Mitophagymentioning

confidence: 99%

Neuronal Mitophagy in Neurodegenerative Diseases

Martínez-Vicente

2017

Front. Mol. Neurosci.

158

115

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Neuronal homeostasis depends on the proper functioning of different quality control systems. All intracellular components are subjected to continuous turnover through the coordinated synthesis, degradation and recycling of their constituent elements. Autophagy is the catabolic mechanism by which intracellular cytosolic components, including proteins, organelles, aggregates and any other intracellular materials, are delivered to lysosomes for degradation. Among the different types of selective autophagy described to date, the process of mitophagy involves the selective autophagic degradation of mitochondria. In this way, mitophagy is responsible for basal mitochondrial turnover, but can also be induced under certain physiological or pathogenic conditions to eliminate unwanted or damaged mitochondria. Dysfunctional cellular proteolytic systems have been linked extensively to neurodegenerative diseases (ND) like Alzheimer’s disease (AD), Parkinson’s disease (PD), or Huntington’s disease (HD), with autophagic failure being one of the main factors contributing to neuronal cell death in these diseases. Neurons are particularly vulnerable to autophagic impairment as well as to mitochondrial dysfunction, due mostly to their particular high energy dependence and to their post-mitotic nature. The accurate and proper degradation of dysfunctional mitochondria by mitophagy is essential for maintaining control over mitochondrial quality and quantity in neurons. In this report, I will review the role of mitophagy in neuronal homeostasis and the consequences of its dysfunction in ND.

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Section: Mitophagymentioning

confidence: 99%

Neuronal Mitophagy in Neurodegenerative Diseases

Martínez-Vicente

2017

Front. Mol. Neurosci.

158

115

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“…Autophagy participates in recycling of organelles such as mitochondria (mitophagy), 16,17 endoplasmic reticulum (ER), and peroxisomes 7,[18][19][20][21][22] ; the clearance of polyubiquitinated proteins aggregates 23 ; and lipid degradation (lipophagy). 24 Dysregulation of autophagy is involved in the pathogenesis of a variety of metabolic and age-related diseases.…”

Section: Autophagy Functions Of Autophagymentioning

confidence: 99%

Autophagy in kidney disease and aging: lessons from rodent models

Lenoir¹,

Tharaux²,

Huber³

2016

Kidney International

120

110

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Autophagy is a highly regulated lysosomal protein degradation pathway that removes protein aggregates and damaged or excess organelles to maintain intracellular homeostasis and cell integrity. Dysregulation of autophagy is involved in the pathogenesis of a variety of metabolic and age-related diseases. Growing evidence suggests that autophagy is implicated in cell injury during renal diseases, both in the tubulointerstitial compartment and in glomeruli. Nevertheless, the impact of autophagy on renal disease progression and aging is still not fully understood. This review summarizes the recent advances in understanding the role of autophagy for kidney disease and aging.

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“…The AMBRA1 gene encodes the activating molecule in beclin1regulated autophagy (Ambra1) protein, which has roles in autophagy, cell growth, cell death, embryonic development and carcinogenesis [96] . AMBRA1 is mutated in a subset of colorectal neoplasms [97] .…”

Section: Ambra1 Genementioning

confidence: 99%

Autophagy in colorectal cancer: An important switch from physiology to pathology

Burada

Nicoli

Ciurea

et al. 2015

WJGO

134

131

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Colorectal cancer (CRC) remains a leading cause of cancer death in both men and women worldwide. Among the factors and mechanisms that are involved in the multifactorial etiology of CRC, autophagy is an important transformational switch that occurs when a cell shifts from normal to malignant. In recent years, multiple hypotheses have been considered regarding the autophagy mechanisms that are involved in cancer. The currently accepted hypothesis is that autophagy has dual and contradictory roles in carcinogenesis, but the precise mechanisms leading to autophagy in cancer are not yet fully defined and seem to be context dependent. Autophagy is a surveillance mechanism used by normal cells that protects them from the transformation to malignancy by removing damaged organelles and aggregated proteins and by reducing reactive oxygen species, mitochondrial abnormalities and DNA damage. However, autophagy also supports tumor formation by promoting access to nutrients that are critical to the metabolism and growth of tumor cells and by inhibiting cellular death and increasing drug resistance. Autophagy studies in CRC have focused on several molecules, mainly microtubule-associated protein 1 light chain 3, beclin 1, and autophagy related 5, with conflicting results. Beneficial effects were observed for some agents that modulate autophagy in CRC either alone or, more often, in combination with other agents. More extensive studies are needed in the future to clarify the roles of Core tip: This review describes the role of autophagy in cancer, focusing on the involvement of autophagy in colorectal cancer (CRC). Initially, we describe the steps and components of autophagy, and we then further highlight the dual role of autophagy in cancer, where it can potentially act as both a promoter and an inhibitor during the transformation from normal to malignant cell. In particular, we emphasize the major autophagy genes involved in CRC pathogenesis along with autophagymodulating agents and their modes of action in the context of CRC therapy. TOPIC HIGHLIGHT

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Ambra1 at a glance

Cited by 83 publications

References 49 publications

Neuronal Mitophagy in Neurodegenerative Diseases

Neuronal Mitophagy in Neurodegenerative Diseases

Autophagy in kidney disease and aging: lessons from rodent models

Autophagy in colorectal cancer: An important switch from physiology to pathology

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