The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
ULK1 negatively regulates Wnt signaling by phosphorylating Dishevelled
Abstract
Wnt signaling pathway plays critical roles in body axes patterning, cell fate specification, cell proliferation, cell migration, stem cell maintenance, cancer development and etc. Deregulation of this pathway can be causative of cancer, metabolic disease and neurodegenerative disease such as Parkinson`s disease. Among the core components of Wnt signaling pathway, we discovered that Dishevelled (Dsh) interacts with ULK1 and is phosphorylated by ULK1. Unexpectedly, the knockdown of ULK1 elicited a marked increase in Wnt/β-catenin signaling. Multiple ULK1 phosphorylation sites existed on Dsh and many of them were located on the PDZ-DEP region. By using evolutionarily well conserved Drosophila Dsh, we found that S239, S247 and S254 in the PDZ-DEP region are involved in phosphorylation of Dsh by ULK1. Among these, S247 and S254 were conserved in human Dsh. When phospho-mimetic mutants (2D and 2E Dsh mutants) of these conserved residues were generated and expressed in the eyes of the fruit flies, the activity of Dsh was significantly decreased compared to wild type Dsh. Through additional alanine scanning, we further identified that S239, S247, S254, S266, S376, S554 and S555 on full length Dsh were phosphorylated by ULK1. In regards to the S266A mutation located in the PDZ domain among these phosphorylated residues, our results suggested that Dsh forms an SDS-resistant high molecular weight complex with β-catenin and TCF in the nucleus in an S266 phosphorylation-dependent manner.…
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Finally, there are several ULK1 substrates that exhibit no, or at least no apparent, function in autophagy, or that have additional cellular functions separate from autophagy.”
From Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1 (2021) · cites this paper as [722]
Citations
Cites
The role of the Atg1/ULK1 complex in autophagy regulation
Mizushima, N. (2010) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2009.12.004 · Cited by 1,062
Frizzled/PCP signalling: a conserved mechanism regulating cell polarity and directed motility
Seifert, J. R. K., & Mlodzik, M. (2007) · Nature Reviews Genetics · doi:10.1038/nrg2042 · Cited by 513
Flagged first, then by citations
Research works printed but not linked: 26
- van Amerongen, 2009, Towards an integrated view of Wnt signaling in development, Development, 136, 3205, 10.1242/dev.033910 · DOI
- Klaus, 2008, Wnt signalling and its impact on development and cancer, Nat. Rev. Canc., 8, 387, 10.1038/nrc2389 · DOI · Paper page
- Niehrs, 2012, The complex world of WNT receptor signalling, Nat. Rev. Mol. Cell Biol., 13, 767, 10.1038/nrm3470 · DOI
- Kim, 2013, Wnt/beta-catenin signalling: from plasma membrane to nucleus, Biochem. J., 450, 9, 10.1042/BJ20121284 · DOI
- Gao, 2010, Dishevelled: the hub of Wnt signaling, Cell. Signal., 22, 717, 10.1016/j.cellsig.2009.11.021 · DOI
- Gao, 2010, Autophagy negatively regulates Wnt signalling by promoting Dishevelled degradation, Nat. Cell Biol., 12, 10.1038/ncb2082 · DOI
- C. He, D.J. Klionsky, Regulation mechanisms and signaling pathways of autophagy, Annu. Rev. Genet., pp. 67-93. · DOI · Paper page
- Florey, 2012, Autophagy proteins in macroendocytic engulfment, Trends Cell Biol., 22, 374, 10.1016/j.tcb.2012.04.005 · DOI
- Shimizu, 2018, Biological roles of alternative autophagy, Mol. Cell., 41, 50
- Lee, 2018, Overview of the minireviews on autophagy, Mol. Cell., 41, 1
- Papinski, 2016, Regulation of autophagy by signaling through the atg1/ULK1 complex, J. Mol. Biol., 428, 1725, 10.1016/j.jmb.2016.03.030 · DOI
- Joo, 2016, The noncanonical role of ULK/ATG1 in ER-to-golgi trafficking is essential for cellular homeostasis, Mol. Cell, 62, 491, 10.1016/j.molcel.2016.04.020 · DOI · Paper page
- Konno, 2013, Cyclic dinucleotides trigger ULK1 (ATG1) phosphorylation of STING to prevent sustained innate immune signaling, Cell, 155, 688, 10.1016/j.cell.2013.09.049 · DOI · Paper page
- Saleiro, 2015, Central role of ULK1 in type I interferon signaling, Cell Rep., 11, 605, 10.1016/j.celrep.2015.03.056 · DOI · Paper page
- Kim, 2018, The role of autophagy in systemic metabolism and human-type diabetes, Mol. Cell., 41, 11
- Zhou, 2007, Unc-51-like kinase 1/2-mediated endocytic processes regulate filopodia extension and branching of sensory axons, Proc. Natl. Acad. Sci. U. S. A., 104, 5842, 10.1073/pnas.0701402104 · DOI · Paper page
- Jung, 2009, ULK-Atg13-FIP200 complexes mediate mTOR signaling to the autophagy machinery, Mol. Biol. Cell, 20, 1992, 10.1091/mbc.e08-12-1249 · DOI · Paper page
- Kim, 2011, AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1, Nat. Cell Biol., 13, 132, 10.1038/ncb2152 · DOI · Paper page
- Chan, 2009, Kinase-inactivated ULK proteins inhibit autophagy via their conserved C- terminal domains using an atg13-independent mechanism, Mol. Cell Biol., 29, 157, 10.1128/MCB.01082-08 · DOI · Paper page
- Papinski, 2014, Early steps in autophagy depend on direct phosphorylation of Atg9 by the Atg1 kinase, Mol. Cell, 53, 471, 10.1016/j.molcel.2013.12.011 · DOI
- MacDonald, 2009, Wnt/beta-Catenin signaling: components, mechanisms, and diseases, Dev. Cell, 17, 9, 10.1016/j.devcel.2009.06.016 · DOI · Paper page
- Penton, 2002, A mutational analysis of dishevelled in Drosophila defines novel domains in the dishevelled protein as well as novel suppressing alleles of axin, Genetics, 161, 747, 10.1093/genetics/161.2.747 · DOI
- Gan, 2008, Nuclear Dvl, c-Jun, beta-catenin, and TCF form a complex leading to stabilization of beta-catenin-TCF interaction, JCB (J. Cell Biol.), 180, 1087, 10.1083/jcb.200710050 · DOI
- Buendia, 2002, Genetic alterations in hepatoblastoma and hepatocellular carcinoma: common and distinctive aspects, Med. Pediatr. Oncol., 39, 530, 10.1002/mpo.10180 · DOI
- Mathew, 2007, Role of autophagy in cancer, Nat. Rev. Canc., 7, 961, 10.1038/nrc2254 · DOI · Paper page
- Kim, 2015, mTOR: a pharmacologic target for autophagy regulation, J. Clin. Invest., 125, 25, 10.1172/JCI73939 · DOI · Paper page
Cited by
Sorted by citations
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1
Klionsky, D. J., Abdel-Aziz, A. K., Abdelfatah, S., Abdellatif, M., Abdoli, A., Abel, S., Abeliovich, H., Abildgaard, M. H., Abudu, Y. P., Acevedo-Arozena, A., et al. (2021) · Autophagy · doi:10.1080/15548627.2020.1797280 · Cited by 2,897
Self-citation
Metadata
- Authors
- Hwang, S.-H., Bang, S., Kang, K. S., Kang, D., & Chung, J.
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2019-01
- Volume
- 508
- Issue
- 1
- Pages
- 308-313
- ISSN
- 0006-291X
- Cited by
- 13
- References
- 2
- Language
- en
- Funders
- Ministry of Education
- National Research Foundation of Korea
- Ministry of Science, ICT and Future Planning
- Ministry of Health and Welfare
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review