Autophagy regulation: RNF2 targets AMBRA1

Morel, Étienne; Dupont, Nicolas; Codogno, Patrice

doi:10.1038/cr.2014.105

Cited by 6 publications

(4 citation statements)

References 10 publications

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“…CUL4 can re-associate with AMBRA1 to promote its proteolysis when autophagy terminates, thus regulating autophagy response [ 55 ]. What’s more, E3 ligase RNF2 can also catalyze K48-linked ubiquitination and proteolysis of AMBRA1, thus downregulating autophagy [ 246 ]. Therefore, all the components of the Class III PI3K complex can be regulated by ubiquitination, which exerts important effects on autophagy.…”

Section: Ubiquitination and Autophagymentioning

confidence: 99%

The role of ubiquitination and deubiquitination in cancer metabolism

Sun¹,

Liu²,

Yang³

2020

Mol Cancer

274

178

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Metabolic reprogramming, including enhanced biosynthesis of macromolecules, altered energy metabolism, and maintenance of redox homeostasis, is considered a hallmark of cancer, sustaining cancer cell growth. Multiple signaling pathways, transcription factors and metabolic enzymes participate in the modulation of cancer metabolism and thus, metabolic reprogramming is a highly complex process. Recent studies have observed that ubiquitination and deubiquitination are involved in the regulation of metabolic reprogramming in cancer cells. As one of the most important type of post-translational modifications, ubiquitination is a multistep enzymatic process, involved in diverse cellular biological activities. Dysregulation of ubiquitination and deubiquitination contributes to various disease, including cancer. Here, we discuss the role of ubiquitination and deubiquitination in the regulation of cancer metabolism, which is aimed at highlighting the importance of this post-translational modification in metabolic reprogramming and supporting the development of new therapeutic approaches for cancer treatment.

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Section: Ubiquitination and Autophagymentioning

confidence: 99%

The role of ubiquitination and deubiquitination in cancer metabolism

Sun¹,

Liu²,

Yang³

2020

Mol Cancer

274

178

View full text Add to dashboard Cite

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“…WASH recruits the RING-type E3 ligase RNF2 ( ring finger protein 2/Ring1b ), which ubiquitinates the residue Lys45 within AMBRA 1 with a Lys48-linked polyubiquitin chain. This modification primes AMBRA 1 for the degradation by the 26S proteasome and finally results in the down-regulation of autophagy [ 75 , 76 ].…”

Section: Regulation Of Beclin 1 Via Distinct Ubiquitination Machinmentioning

confidence: 99%

Regulation of the Tumor-Suppressor BECLIN 1 by Distinct Ubiquitination Cascades

Boutouja

Brinkmeier

Mastalski

et al. 2017

IJMS

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Autophagy contributes to cellular homeostasis through the degradation of various intracellular targets such as proteins, organelles and microbes. This relates autophagy to various diseases such as infections, neurodegenerative diseases and cancer. A central component of the autophagy machinery is the class III phosphatidylinositol 3-kinase (PI3K-III) complex, which generates the signaling lipid phosphatidylinositol 3-phosphate (PtdIns3P). The catalytic subunit of this complex is the lipid-kinase VPS34, which associates with the membrane-targeting factor VPS15 as well as the multivalent adaptor protein BECLIN 1. A growing list of regulatory proteins binds to BECLIN 1 and modulates the activity of the PI3K-III complex. Here we discuss the regulation of BECLIN 1 by several different types of ubiquitination, resulting in distinct polyubiquitin chain linkages catalyzed by a set of E3 ligases. This contribution is part of the Special Issue “Ubiquitin System”.

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“…Huang et al indicated that miR-200b inhibits autophagy and triggers apoptosis by directly targeting the autophagy-related gene Ambra1 (autophagy/Be-clin1 regulatory factor 1) [26]. The phosphatidylinositol 3-kinase complex I (PI3K complex I) is a crucial regulator of autophagy, which contains Beclin 1, a long ATG14 isoform of autophagy-related gene 14 (ATG14L), vacuolar protein sorting 34 (VPS34), and Ambra1, and controls autophagosome formation [27].…”

Section: Original Papermentioning

confidence: 99%

sh- Ambra1 inhibits IRS-1/PI3K/Akt signalling pathway to reduce autophagy in gestational diabetes

Qu,

Li,

Feng

et al. 2024

Endokrynol Pol

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velop diabetes [3]. During normal pregnancy, IR begins in mid-pregnancy and develops mainly in late gestation [4]. Among other things, hormones and adipokines secreted by the placenta (including human placental lactogen and human placental growth hormone) may be responsible for the development of IR in women during pregnancy. In addition, the increase in oestrogen, progesterone, and cortisol during pregnancy leads to a disruption of glucose insulin homeostasis [5]. To compensate for peripheral IR during pregnancy, insulin secretion in the female pancreas increases, and GDM occurs when the insulin secreted by the female pancreas is not sufficient to compensate for the metabolic stress of IR.Insulin substrate receptor 1 (IRS-1) plays an important role in insulin resistance by activating 2 major pathways [phosphatidylinositol 3 kinase (PI3K) and mitogen-activated protein kinase (MAPK)] to deliver insulin signals in cells. Of these, PI3K is primarily involved in metabolic signalling, and it catalyses

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Autophagy regulation: RNF2 targets AMBRA1

Cited by 6 publications

References 10 publications

The role of ubiquitination and deubiquitination in cancer metabolism

The role of ubiquitination and deubiquitination in cancer metabolism

Regulation of the Tumor-Suppressor BECLIN 1 by Distinct Ubiquitination Cascades

sh- Ambra1 inhibits IRS-1/PI3K/Akt signalling pathway to reduce autophagy in gestational diabetes

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