GABARAPL1 (GEC1): Original or copycat?

Grand, Jaclyn Nicole Le; Chakrama, Fatima Zahra; Seguin-Py, Stéphanie; Fraîchard, Annick; Delage-Mourroux, Régis; Jouvenot, Michèle; Boyer-Guittaut, Michaël

doi:10.4161/auto.7.10.15904

Cited by 74 publications

(75 citation statements)

References 80 publications

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“…Gabarapl1 was involved in the formation of autophagic vesicles especially in later stages of the formation of autophagosome [12,13]. Gabarapl1 was also participated in various events such as tumor progression [14]. Gabarapl1 was found to be a good indicator of the risk of recurrence in breast tumors [15].…”

Section: Discussionmentioning

confidence: 98%

Gabarapl1 mediates androgen-regulated autophagy in prostate cancer

et al. 2015

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Autophagy plays an important role in prostate cancer development. It promotes tumor cell survival and was found to be associated with androgen pathway. In the present study, we found that GABA(A) receptor-associated protein like 1 (Gabarapl1), a ubiquitin-like modifier, participates in the regulation of autophagy. Gabarapl1 is transcriptionally regulated by androgen receptor (AR) and has a repressive role in autophagy. Androgen deprivation downregulates Gabarapl1 in an AR dependent manner, resulting in the increase of autophagy flux. Elevated Gabarapl1 also represses the proliferation of prostate cancer cells. In summary, our study provides evidence to show that Gabarapl1 is a mediator involved in androgen-regulated autophagy process.

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Section: Discussionmentioning

confidence: 98%

Gabarapl1 mediates androgen-regulated autophagy in prostate cancer

et al. 2015

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“…The products are subsequently lipidated by phosphatidylethanolamine and inserted into autophagosomes. [27][28][29] It has been shown that phosphatidylethanolamine conjugated to LC3B, which is LC3B-II, migrates at a different protein size compared with the unconjugated LC3B-I on sodium dodecyl sulfatepolyacrylamide gel electrophoresis and that the levels of LC3B-II are proportional to the amount of autophagosomes, as assessed by TEM studies. 30 In our study, we showed that the expression of LC3B-II and the number of autophagosomes were both induced by Ang II and LC3B cDNA overexpression strategies.…”

Section: Discussionmentioning

confidence: 99%

LC3B, a Protein That Serves as an Autophagic Marker, Modulates Angiotensin II-induced Myocardial Hypertrophy

Huang¹,

Pan

et al. 2015

Journal of Cardiovascular Pharmacology

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LC3B is a marker of autophagic activity, and growing evidence supports its importance in myocardial hypertrophy. Thus, regulating LC3B expression may provide an important avenue to inhibit autophagy and protect against or inhibit pathological myocardial hypertrophy. To address this question, we investigated the effects of altering LC3B mRNA expression and autophagic activity in the setting of cardiomyocyte hypertrophy. In an in vitro angiotensin II (Ang II)-induced cardiomyocyte hypertrophy model, LC3B mRNA and protein expression was increased and there was activation of cardiomyocyte autophagy, which was assessed by transmission electron microscopy and flow cytometry. LC3B cDNA transfection also resulted in an upregulation of autophagic activity, whereas downregulation of autophagic activity was observed with knockdown of LC3B expression. Induction of LC3B expression was shown to further exacerbate Ang II-stimulated cardiomyocyte hypertrophy, whereas inhibition of LC3B expression inhibited the Ang II-stimulated cardiomyocyte hypertrophy (as assessed through cardiomyocyte morphology and expression of ANP and β-MHC). This study demonstrated that LC3B modulates the Ang II-induced cardiomyocyte hypertrophy in cultured neonatal rat ventricular cardiomyocytes.

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“…109,146 Certain types of mitophagy induced by BNIP3L/NIX are highly dependent on GABARAP and less dependent on LC3 proteins. 147 Furthermore, commercial antibodies for GABARAPL1 also recognize GABARAP, 108 which might lead to misinterpretation of experiments, in particular those using immunohistochemical techniques. The problem with cross-reactivity of the anti-GABARAPL1 antibody can be overcome when analyzing these proteins by western blot because they can be resolved during SDS-PAGE using high concentration (15%) gels, with GABARAP migrating faster than GABARAPL1 (Boyer-Guittaut M, personal communication).…”

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confidence: 99%

“…108 The nonlipidated and lipidated forms are usually referred to as LC3-I and LC3-II, or GABARAP and GABARAP-PE, etc. The positions of both Atg8/LC3-I (approximately 18 kDa) and Atg8-PE/LC3-II (approximately 16 kDa) should be indicated on western blots whenever both are detectable.…”

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confidence: 99%

Guidelines for the use and interpretation of assays for monitoring autophagy

Klionsky¹,

Abdalla²,

Abeliovich³

et al. 2012

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In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

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GABARAPL1 (GEC1): Original or copycat?

Cited by 74 publications

References 80 publications

Gabarapl1 mediates androgen-regulated autophagy in prostate cancer

Gabarapl1 mediates androgen-regulated autophagy in prostate cancer

LC3B, a Protein That Serves as an Autophagic Marker, Modulates Angiotensin II-induced Myocardial Hypertrophy

Guidelines for the use and interpretation of assays for monitoring autophagy

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