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CUL3 (cullin 3)-mediated ubiquitination and degradation of BECN1 (beclin 1) inhibit autophagy and promote tumor progression.
Li X, Yang KB, Chen W, Mai J, Wu XQ, Sun T, Wu RY, Jiao L, Li DD, Ji J, Zhang HL, Yu Y, Chen YH, Feng GK, Deng R, Li JD, Zhu XF. Li X, et al. Autophagy. 2021 Dec;17(12):4323-4340. doi: 10.1080/15548627.2021.1912270. Epub 2021 May 12. Autophagy. 2021. PMID: 33977871 Free PMC article.
The underlying mechanism, however, has not been fully illuminated. Here, we found that CUL3 (cullin 3), an E3 ubiquitin ligase, could interact with BECN1 and promote the K48-linked ubiquitination and degradation of this protein; In addition, CUL3 led to a decrease i …
The underlying mechanism, however, has not been fully illuminated. Here, we found that CUL3 (cullin 3), an E3 ubiquitin ligase, could …
Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development.
Morandell J, Schwarz LA, Basilico B, Tasciyan S, Dimchev G, Nicolas A, Sommer C, Kreuzinger C, Dotter CP, Knaus LS, Dobler Z, Cacci E, Schur FKM, Danzl JG, Novarino G. Morandell J, et al. Nat Commun. 2021 May 24;12(1):3058. doi: 10.1038/s41467-021-23123-x. Nat Commun. 2021. PMID: 34031387 Free PMC article.
However, induction of Cul3 haploinsufficiency later in life does not lead to ASD-relevant behaviors, pointing to an important role of Cul3 during a critical developmental window. Here we show that Cul3 is essential to regulate neuronal migration and, therefor …
However, induction of Cul3 haploinsufficiency later in life does not lead to ASD-relevant behaviors, pointing to an important role of …
Loss-of-Function Variants in CUL3 Cause a Syndromic Neurodevelopmental Disorder.
Blackburn PR, Ebstein F, Hsieh TC, Motta M, Radio FC, Herkert JC, Rinne T, Thiffault I, Rapp M, Alders M, Maas S, Gerard B, Smol T, Vincent-Delorme C, Cogné B, Isidor B, Vincent M, Bachmann-Gagescu R, Rauch A, Joset P, Ferrero GB, Ciolfi A, Husson T, Guerrot AM, Bacino C, Macmurdo C, Thompson SS, Rosenfeld JA, Faivre L, Mau-Them FT, Deb W, Vignard V, Agrawal PB, Madden JA, Goldenberg A, Lecoquierre F, Zech M, Prokisch H, Necpál J, Jech R, Winkelmann J, Koprušáková MT, Konstantopoulou V, Younce JR, Shinawi M, Mighton C, Fung C, Morel CF, Lerner-Ellis J, DiTroia S, Barth M, Bonneau D, Krapels I, Stegmann APA, van der Schoot V, Brunet T, Bußmann C, Mignot C, Zampino G, Wortmann SB, Mayr JA, Feichtinger RG, Courtin T, Ravelli C, Keren B, Ziegler A, Hasadsri L, Pichurin PN, Klee EW, Grand K, Sanchez-Lara PA, Krüger E, Bézieau S, Klinkhammer H, Krawitz PM, Eichler EE, Tartaglia M, Küry S, Wang T. Blackburn PR, et al. Ann Neurol. 2024 Sep 20:10.1002/ana.27077. doi: 10.1002/ana.27077. Online ahead of print. Ann Neurol. 2024. PMID: 39301775
Here, we aimed to collect sporadic cases carrying rare variants in CUL3, describe the genotype-phenotype correlation, and investigate the underlying pathogenic mechanism. ...Dysmorphic facial features were analyzed using GestaltMatcher. Variant effects on CUL3 prote …
Here, we aimed to collect sporadic cases carrying rare variants in CUL3, describe the genotype-phenotype correlation, and investigate …
CRL3s: The BTB-CUL3-RING E3 Ubiquitin Ligases.
Wang P, Song J, Ye D. Wang P, et al. Adv Exp Med Biol. 2020;1217:211-223. doi: 10.1007/978-981-15-1025-0_13. Adv Exp Med Biol. 2020. PMID: 31898230 Review.
Differently, a single BTB-containing adaptor molecule utilizing two protein interaction sites can link the CUL3 scaffold to the substrate, forming as many as 188 CUL3-BTB E3 ligase complexes in mammals. ...Next, we discuss the mutual exclusivity of somatic mutations …
Differently, a single BTB-containing adaptor molecule utilizing two protein interaction sites can link the CUL3 scaffold to the subst …
CUL3 E3 ligases in plant development and environmental response.
Ban Z, Estelle M. Ban Z, et al. Nat Plants. 2021 Jan;7(1):6-16. doi: 10.1038/s41477-020-00833-6. Epub 2021 Jan 15. Nat Plants. 2021. PMID: 33452490 Free PMC article. Review.
More recently, accumulating evidence has demonstrated the essential roles of CRL3 E3s, consisting of a CUL3 protein and a BTB/POZ substrate adaptor. In this Review, we describe the variety of CRL3s functioning in plants and the wide range of processes that they regulate. . …
More recently, accumulating evidence has demonstrated the essential roles of CRL3 E3s, consisting of a CUL3 protein and a BTB/POZ sub …
Current trends of high-risk gene Cul3 in neurodevelopmental disorders.
Lin P, Yang J, Wu S, Ye T, Zhuang W, Wang W, Tan T. Lin P, et al. Front Psychiatry. 2023 Jul 28;14:1215110. doi: 10.3389/fpsyt.2023.1215110. eCollection 2023. Front Psychiatry. 2023. PMID: 37575562 Free PMC article. Review.
Cul3 encodes Cullin-3, a core component of the ubiquitin E3 ligase that is involved in protein ubiquitination. ...Moreover, we characterized the behavioral, electrophysiological, and molecular changes in newly developed Cul3 deficiency models. This would guide furth …
Cul3 encodes Cullin-3, a core component of the ubiquitin E3 ligase that is involved in protein ubiquitination. ...Moreover, we charac …
The functions and effects of CUL3-E3 ligases mediated non-degradative ubiquitination.
Zhai F, Li J, Ye M, Jin X. Zhai F, et al. Gene. 2022 Jul 20;832:146562. doi: 10.1016/j.gene.2022.146562. Epub 2022 May 14. Gene. 2022. PMID: 35580799 Review.
Ubiquitination of substrates usually have two fates: one is degraded by 26S proteasome, and the other is non-degradative ubiquitination modification which is associated with cell cycle regulation, chromosome inactivation, protein transportation, tumorigenesis, achondroplasia, and …
Ubiquitination of substrates usually have two fates: one is degraded by 26S proteasome, and the other is non-degradative ubiquitination modi …
Mechanisms and controversies in mutant Cul3-mediated familial hyperkalemic hypertension.
Ferdaus MZ, McCormick JA. Ferdaus MZ, et al. Am J Physiol Renal Physiol. 2018 May 1;314(5):F915-F920. doi: 10.1152/ajprenal.00593.2017. Epub 2018 Jan 17. Am J Physiol Renal Physiol. 2018. PMID: 29361671 Free PMC article. Review.
Autosomal dominant mutations in cullin-3 ( Cul3) cause the most severe form of familial hyperkalemic hypertension (FHHt). Cul3 mutations cause skipping of exon 9, which results in an internal deletion of 57 amino acids from the CUL3 protein (CUL3-9). . …
Autosomal dominant mutations in cullin-3 ( Cul3) cause the most severe form of familial hyperkalemic hypertension (FHHt). Cul3 …
Insights into the diverse mechanisms and effects of variant CUL3-induced familial hyperkalemic hypertension.
Sharma P, Chatrathi HE. Sharma P, et al. Cell Commun Signal. 2023 Oct 16;21(1):286. doi: 10.1186/s12964-023-01269-z. Cell Commun Signal. 2023. PMID: 37845702 Free PMC article. Review.
The most severe form of the disease is caused by autosomal dominant variants in CUL3 (Cullin 3), a critical subunit of the multimeric CUL3-RING ubiquitin ligase complex. The recent identification of a novel FHHt disease variant of CUL3 revealed intricacies wi …
The most severe form of the disease is caused by autosomal dominant variants in CUL3 (Cullin 3), a critical subunit of the multimeric …
SPOP and CUL3 Modulate the Sonic Hedgehog Signal Response Through Controlled Degradation of GLI Family Transcription Factors.
Umberger PA, Ogden SK. Umberger PA, et al. Front Cell Dev Biol. 2021 Jul 30;9:710295. doi: 10.3389/fcell.2021.710295. eCollection 2021. Front Cell Dev Biol. 2021. PMID: 34395437 Free PMC article. Review.
The speckle-type POZ protein (SPOP) functions as a guardian of genome integrity and controls transcriptional regulation by functioning as a substrate adaptor for CUL3/RING-type E3 ubiquitin ligase complexes. SPOP-containing CUL3 complexes target a myriad of DNA-bind …
The speckle-type POZ protein (SPOP) functions as a guardian of genome integrity and controls transcriptional regulation by functioning as a …
1,078 results