DAP‐kinase‐mediated phosphorylation on the BH3 domain of beclin 1 promotes dissociation of beclin 1 from Bcl‐XL and induction of autophagy

By Einat Zalckvar, H. Berissi, Liat Mizrachy, Yulia Idelchuk, Itay Koren, M. Eisenstein, H. Sabanay, R. Pinkas-Kramarski, Adi Kimchi. EMBO Reports, 2009

612 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/f0eba05d7f7df2c6e9544693032354b2969bd018

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In Cell Biology

1. Beth Levine
2. Guido Kroemer
3. D. Klionsky
4. Douglas R. Green
5. L. Galluzzi
6. Zhifen Yang
7. V. Deretic
8. K. Guan

In Epidemiology

1. Guido Kroemer
2. Beth Levine
3. D. Klionsky
4. I. Slaninová
5. Douglas R. Green
6. L. Galluzzi
7. Alec C. Kimmelman
8. N. Mizushima

In Physiology

1. Guido Kroemer
2. Alec C. Kimmelman
3. Beth Levine
4. L. Galluzzi
5. D. Klionsky
6. Douglas R. Green
7. Zhifen Yang
8. D. Rubinsztein

Citations in the corpus

• Molecular definitions of autophagy and related processes (2017, neutral): “…autophagy and beclin 1 regulator 1 (AMBRA1, originally “activating molecule in Beclin 1-regulated autophagy”), as well as the BECN1 inhibitor BCL2, which also interacts with ATG12 (Liang et al , 1999; Pattingre et al , 2005; Fimia et al , 2007; Zalckvar et al , 2009; Rubinstein et al , 2011).”
• PAMPs and DAMPs: Signal 0s that Spur Autophagy and Immunity (2012, background): “In addition, phosphorylation by death-associated protein kinase (DAPK) of Beclin 1 on Thr 119 in the BH3 domain promotes autophagy (183).”
• Crosstalk between apoptosis, necrosis and autophagy. (2013, background): “DAPK-mediated phosphorylation of Beclin 1 on Thr119 at the BH3 domain promotes the dissociation of Beclin 1 from its inhibitor BCL-2-family members, thereby activating Beclin 1 to induce autophagy [110].”
• The Beclin 1 network regulates autophagy and apoptosis (2011, positive): “) or DAPK-mediated phosphorylation of Beclin 1 (Zalckvar et al.(23)).”
• ER stress: Autophagy induction, inhibition and selection (2015, background): “The subsequent phosphorylation of BECN1 results in diminished affinity for BCL2 and leads to the formation of a complex between the autophagy initiator BECN1 and PIK3C3.(115,116) Interestingly, genetic ablation of ATF6 causes repression of DAPK1 expression and ultimately failure of autophagy inducti”
• Cell Death Signaling. (2015, background): “Alternatively, dissociation of beclin 1 from Bcl2 and Bcl-xL can be achieved through phosphorylation of the beclin–1 BH3 domain by the death-associated protein kinase (DAPK) (Zalckvar et al. 2009a,b).”
• Differential regulation of distinct Vps34 complexes by AMPK in nutrient stress and autophagy (2013, background): “DAP-kinase andCDK1/5 are also reported to regulate Vps34-Beclin1 interaction through phosphorylation (Furuya et al., 2010; Zalckvar et al., 2009).”
• ULK1 induces autophagy by phosphorylating Beclin-1 and activating Vps34 lipid kinase (2013, methodology): “Active GST-ULK1 (1-649) and GST-ULK2 (1-478) from insect cells was purchased from CQuential Solutions (Moraga, CA).”
• Autophagy, Immunity, and Microbial Adaptations (2009, background): “Rapamycin induces autophagy by inhibiting Tor, and some immune signals that are transmitted via TLR adapters MyD88 and TRIF or DAPK downstream of IFNγ lead to activation of Beclin 1 (complexed with the phosphatidylinositol 3 kinase hVps34) by its dissociation from Bcl-2.”