Regulation of Beclin 1 Protein Phosphorylation and Autophagy by Protein Phosphatase 2A (PP2A) and Death-associated Protein Kinase 3 (DAPK3)

Fujiwara, Norio; Usui, Tatsuya; Ohama, Takashi; Sato, Koichi

doi:10.1074/jbc.m115.704908

Cited by 84 publications

(76 citation statements)

References 33 publications

(34 reference statements)

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“…Beclin-1 phosphorylation could be mediated by a number of kinases. For example, DAPK3 and unc-51 like autophagy activating kinase (ULK) phosphorylate Beclin-1 at Ser 90 and Ser 14 , respectively (Fujiwara et al, 2016;Russell et al, 2013), thereby enhancing the kinase activity of VSP34. In addition, DAPK1 phosphorylates Beclin-1 at Thr 119 and inhibits the association between Beclin-1 and Bcl-2 (Zalckvar et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Adiponectin inhibits inflammatory cytokines production by Beclin‐1 phosphorylation and B‐cell lymphoma 2 mRNA destabilization: role for autophagy induction

Pun

Park

2018

British J Pharmacology

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Section: Discussionmentioning

confidence: 99%

Adiponectin inhibits inflammatory cytokines production by Beclin‐1 phosphorylation and B‐cell lymphoma 2 mRNA destabilization: role for autophagy induction

Pun

Park

2018

British J Pharmacology

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“…Upon glucose starvation, AMPK enhances autophagy by phosphorylating BECN1 at Ser90 and Ser94 (112). Ser90 phosphorylation is reversed by protein phosphatase 2A (PP2A) (113), which is upregulated by starvation (114). Ser15, Ser90, and Ser94 are all located in the flexible N-terminal portion of BENC1, and it is still unknown how these signals are communicated to the catalytic domain.…”

Section: Pi3kc3-c1 Phosphoregulationmentioning

confidence: 99%

Mechanisms of Autophagy Initiation

Hurley

Young

2017

Annu. Rev. Biochem.

527

424

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Autophagy is the process of cellular self-eating by a double-membrane organelle, the autophagosome. A range of signaling processes converge on two protein complexes to initiate autophagy: the ULK1 protein kinase complex and the PI3KC3-C1 lipid kinase complex. Some 90 % of the mass of these large protein complexes consists on non-catalytic domains and subunits, and the ULK1 complex has essential non-catalytic activities. Structural studies of these complexes have shed increasing light on the regulation of their catalytic and non-catalytic activities in autophagy initiation. The autophagosome is thought to nucleate from vesicles containing the integral membrane protein Atg9, COPII vesicles, and possibly other sources. In the wake of reconstitution and superresolution imaging studies, we are beginning to understand how the ULK1 and PI3KC3-C1 complexes might coordinate the nucleation and fusion of Atg9 and COPII vesicles at the start of autophagosome biogenesis.

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“…At first, DAPk3 was discovered as a canonical tumor suppressor gene (10). In recent years, increasing studies have verified that DAPk3 is involved in multiple cellular functions.…”

Section: Introductionmentioning

confidence: 99%

Anacardic acid induces cell apoptosis of prostatic cancer through autophagy by ER stress/DAPK3/Akt signaling pathway

et al. 2017

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Anacardic acid, which is commonly seen in plants of Anacardiaceae, is an important composition of cashew, ginkgo leaf and fruit, and it has been suggested in previous research to show antitumor activity. The main aim of the present study was to evaluate the anticancer effects of anacardic acid on cell apoptosis of prostatic cancer and molecular mechanisms of this phenomenon. In this study we found that anacardic acid inhibited cell proliferation, induced apoptosis and caspase-3/9 activities and Bax protein expression of prostatic cancer. Anacardic acid induced the ER stress inducing factors (BiP, CHOP, p-eIF2α), autophagy, LC3, Beclin-1, Atg 7 and DAPK3 protein expression, and suppressed p-Akt and p-mTOR protein expression of prostatic cancer. Si-CHOP was used to inhibit ER stress in prostatic cancer by anacardic acid, which showed that the cell proliferation was increased, apoptosis, and caspase-3/9 activities and Bax protein expression was suppressed, autophagy, LC3, Beclin-1, Atg 7 and DAPK3 protein expression was reduced, and p-Akt and p-mTOR protein expression was promoted. DAPK3 inhibited p-Akt and p-mTOR protein expression, enhanced the anticancer effects of anacardic acid on prostatic cancer through autophagy. For the first time, the present study showed that anacardic acid induces cell apoptosis of prostatic cancer through autophagy by ER stress/DAPK3/Akt signaling pathway.

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Regulation of Beclin 1 Protein Phosphorylation and Autophagy by Protein Phosphatase 2A (PP2A) and Death-associated Protein Kinase 3 (DAPK3)

Cited by 84 publications

References 33 publications

Adiponectin inhibits inflammatory cytokines production by Beclin‐1 phosphorylation and B‐cell lymphoma 2 mRNA destabilization: role for autophagy induction

Adiponectin inhibits inflammatory cytokines production by Beclin‐1 phosphorylation and B‐cell lymphoma 2 mRNA destabilization: role for autophagy induction

Mechanisms of Autophagy Initiation

Anacardic acid induces cell apoptosis of prostatic cancer through autophagy by ER stress/DAPK3/Akt signaling pathway

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