| Structural basis for the interaction between human Npl4 and Npl4-binding motif of human Ufd1. | Structural basis for the interaction between human Npl4 and Npl4-binding motif of human Ufd1.
Nguyen TQ, My Le LT, Kim DH, Ko KS, Lee HT, Kim Nguyen YT, Kim HS, Han BW, Kang W, Yang JK. | 11/12/2022 |
| Multiple UBX proteins reduce the ubiquitin threshold of the mammalian p97-UFD1-NPL4 unfoldase. | Multiple UBX proteins reduce the ubiquitin threshold of the mammalian p97-UFD1-NPL4 unfoldase.
Fujisawa R, Polo Rivera C, Labib KPM., Free PMC Article | 08/20/2022 |
| PCBP2 Posttranscriptional Modifications Induce Breast Cancer Progression via Upregulation of UFD1 and NT5E. | PCBP2 Posttranscriptional Modifications Induce Breast Cancer Progression via Upregulation of UFD1 and NT5E.
Wang X, Guo Q, Wang H, Yuan X, Wang B, Lobie PE, Zhu T, Tan S, Wu Z. | 10/23/2021 |
| Involvement of VCP/UFD1/Nucleolin in the viral entry of Enterovirus A species. | Involvement of VCP/UFD1/Nucleolin in the viral entry of Enterovirus A species.
Yan J, Wang M, Wang M, Dun Y, Zhu L, Yi Z, Zhang S., Free PMC Article | 08/28/2021 |
| Seesaw conformations of Npl4 in the human p97 complex and the inhibitory mechanism of a disulfiram derivative. | Seesaw conformations of Npl4 in the human p97 complex and the inhibitory mechanism of a disulfiram derivative.
Pan M, Zheng Q, Yu Y, Ai H, Xie Y, Zeng X, Wang C, Liu L, Zhao M., Free PMC Article | 01/16/2021 |
| Multisystem proteinopathy mutations in VCP/p97 increase NPLOC4-UFD1L binding and substrate processing. | Multisystem Proteinopathy Mutations in VCP/p97 Increase NPLOC4·UFD1L Binding and Substrate Processing.
Blythe EE, Gates SN, Deshaies RJ, Martin A., Free PMC Article | 07/4/2020 |
| results support that Ufd1 S229 phosphorylation status mediated by PKA serves as a key regulatory point for the VCP-Ufd1 interaction and functional ERAD. | Ufd1 phosphorylation at serine 229 negatively regulates endoplasmic reticulum-associated degradation by inhibiting the interaction of Ufd1 with VCP.
Nguyen QT, Choi J, Yang JK, Lee SY. | 03/21/2020 |
| CHOP inactivation or BCL2 overexpression is sufficient to rescue tumor cell apoptosis induced by UFD1 knockdown. | UFD1 contributes to MYC-mediated leukemia aggressiveness through suppression of the proapoptotic unfolded protein response.
Huiting LN, Samaha Y, Zhang GL, Roderick JE, Li B, Anderson NM, Wang YW, Wang L, Laroche F, Choi JW, Liu CT, Kelliher MA, Feng H., Free PMC Article | 06/15/2019 |
| We demonstrate that WT p97 can unfold proteins and that this activity is dependent on the p97 adaptor NPLOC4-UFD1L, ATP hydrolysis, and substrate ubiquitination, with branched chains providing maximal stimulation. | Ubiquitin- and ATP-dependent unfoldase activity of P97/VCP•NPLOC4•UFD1L is enhanced by a mutation that causes multisystem proteinopathy.
Blythe EE, Olson KC, Chau V, Deshaies RJ., Free PMC Article | 05/12/2018 |
| The study revealed a regulatory role of the p97-Npl4-Ufd1 complex in regulating a partial degradation of the NF-kappaB subunit p100. | The Transitional Endoplasmic Reticulum ATPase p97 Regulates the Alternative Nuclear Factor NF-κB Signaling via Partial Degradation of the NF-κB Subunit p100.
Zhang Z, Wang Y, Li C, Shi Z, Hao Q, Wang W, Song X, Zhao Y, Jiao S, Zhou Z., Free PMC Article | 11/7/2015 |
| p97-Ufd1-Npl4 is an integral part of G2/M checkpoint signaling and thereby suppresses chromosome instability. | The p97-Ufd1-Npl4 ATPase complex ensures robustness of the G2/M checkpoint by facilitating CDC25A degradation.
Riemer A, Dobrynin G, Dressler A, Bremer S, Soni A, Iliakis G, Meyer H., Free PMC Article | 10/25/2014 |
| Data indicate that the p97-UFD1L-NPL4 protein complex specifically associates with ubiquitinated IkappaBalpha via the interactions between p97 and the SCF(beta-TRCP) ubiquitin ligase. | The p97-UFD1L-NPL4 protein complex mediates cytokine-induced IκBα proteolysis.
Li JM, Wu H, Zhang W, Blackburn MR, Jin J., Free PMC Article | 03/22/2014 |
| This study demonistrated that UFD1L may participate in the core cognitive deficits observed in schizophrenia. | Polymorphisms in schizophrenia candidate gene UFD1L may contribute to cognitive deficits.
Ota VK, Berberian AA, Gadelha A, Santoro ML, Ottoni GL, Matsuzaka CT, Mari JJ, Melaragno MI, Lara DR, Smith MA, Belangero SI, Bressan RA. | 03/22/2014 |
| In coordination with the P97-UFD1-NPL4 complex (P97(UFD1/NPL4)), NUB1L promotes transfer of NEDD8 to proteasome for degradation. | NEDD8 ultimate buster-1 long (NUB1L) protein promotes transfer of NEDD8 to proteasome for degradation through the P97UFD1/NPL4 complex.
Liu S, Yang H, Zhao J, Zhang YH, Song AX, Hu HY., Free PMC Article | 01/4/2014 |
| increased corpus callosum volume in children with 22q11DS is associated with UFD1L polymorphism. | Increased corpus callosum volume in children with chromosome 22q11.2 deletion syndrome is associated with neurocognitive deficits and genetic polymorphisms.
Shashi V, Francis A, Hooper SR, Kranz PG, Zapadka M, Schoch K, Ip E, Tandon N, Howard TD, Keshavan MS., Free PMC Article | 06/22/2013 |
| Data indicate that Npl4-Ufd1 heterodimer is required for VCP-FAF1 interaction. | Complex of Fas-associated factor 1 (FAF1) with valosin-containing protein (VCP)-Npl4-Ufd1 and polyubiquitinated proteins promotes endoplasmic reticulum-associated degradation (ERAD).
Lee JJ, Park JK, Jeong J, Jeon H, Yoon JB, Kim EE, Lee KJ., Free PMC Article | 05/4/2013 |
| Data establish Cdc48/p97-Ufd1-Npl4 as a crucial negative regulator of Aurora B early in mitosis of human somatic cells and suggest that the activity of Aurora B on chromosomes needs to be restrained to ensure faithful chromosome segregation. | Cdc48/p97-Ufd1-Npl4 antagonizes Aurora B during chromosome segregation in HeLa cells.
Dobrynin G, Popp O, Romer T, Bremer S, Schmitz MH, Gerlich DW, Meyer H. | 09/24/2011 |
| Ubiquitin-recognition protein Ufd1 couples the endoplasmic reticulum (ER) stress response to cell cycle control | Ubiquitin-recognition protein Ufd1 couples the endoplasmic reticulum (ER) stress response to cell cycle control.
Chen M, Gutierrez GJ, Ronai ZA., Free PMC Article | 08/27/2011 |
| This study suggested that AA genotype of UFD1L gene, which is involved in neurodevelopmental processes, may contribute to early-onset schizophrenia. Therefore, rs5992403 polymorphism may not be a risk factor for schizophrenia. | The UFD1L rs5992403 polymorphism is associated with age at onset of schizophrenia.
Ota VK, Belangero SI, Gadelha A, Bellucco FT, Christofolini DM, Mancini TI, Ribeiro-dos-Santos AK, Santos SE, Mari Jde J, Bressan RA, Melaragno MI, Smith Mde A, Ota VK, Belangero SI, Gadelha A, Bellucco FT, Christofolini DM, Mancini TI, Ribeiro-dos-Santos AK, Santos SE, Mari Jde J, Bressan RA, Melaragno MI, Smith Mde A. | 02/26/2011 |
| Data suggest that the human cytomegalovirus dislocation reaction in US2 cells is independent of the p97 cofactor Ufd1-Npl4, and different retrotranslocation mechanisms can employ distinct p97 ATPase complexes to dislocate substrates. | The p97 ATPase dislocates MHC class I heavy chain in US2-expressing cells via a Ufd1-Npl4-independent mechanism.
Soetandyo N, Ye Y., Free PMC Article | 12/11/2010 |
| allelic associations of the UFD1L locus identified; 4-SNP haplotype analysis showed strong association with schizophrenia; possibility that a disease-resistant variant may be carried by two or more haplotypes due to frequent recombination during meiosis. | A family- and population-based study of the UFD1L gene for schizophrenia.
Xie L, Ye L, Ju G, Xu Q, Zhang X, Liu S, Shi J, Yu Y, Wang Z, Shen Y, Wei J, Xie L, Ye L, Ju G, Xu Q, Zhang X, Liu S, Shi J, Yu Y, Wang Z, Shen Y, Wei J. | 01/21/2010 |
| This favors the model where the Ufd1-Npl4 dimer forms a regulatory gate at the exit from the retrotranslocone, rather than actively promoting retrotranslocation like the p97VCP ATPase. | Analysis of Npl4 deletion mutants in mammalian cells unravels new Ufd1-interacting motifs and suggests a regulatory role of Npl4 in ERAD.
Lass A, McConnell E, Fleck K, Palamarchuk A, Wójcik C. | 01/21/2010 |
| Observational study of gene-disease association. (HuGE Navigator) | See all PubMed (3) articlesMaternal genes and facial clefts in offspring: a comprehensive search for genetic associations in two population-based cleft studies from Scandinavia.
Jugessur A, Shi M, Gjessing HK, Lie RT, Wilcox AJ, Weinberg CR, Christensen K, Boyles AL, Daack-Hirsch S, Nguyen TT, Christiansen L, Lidral AC, Murray JC. The UFD1L rs5992403 polymorphism is associated with age at onset of schizophrenia.
Ota VK, Belangero SI, Gadelha A, Bellucco FT, Christofolini DM, Mancini TI, Ribeiro-dos-Santos AK, Santos SE, Mari Jde J, Bressan RA, Melaragno MI, Smith Mde A, Ota VK, Belangero SI, Gadelha A, Bellucco FT, Christofolini DM, Mancini TI, Ribeiro-dos-Santos AK, Santos SE, Mari Jde J, Bressan RA, Melaragno MI, Smith Mde A. A family- and population-based study of the UFD1L gene for schizophrenia.
Xie L, Ye L, Ju G, Xu Q, Zhang X, Liu S, Shi J, Yu Y, Wang Z, Shen Y, Wei J, Xie L, Ye L, Ju G, Xu Q, Zhang X, Liu S, Shi J, Yu Y, Wang Z, Shen Y, Wei J. | 04/3/2008 |
| This study identifies Ufd1 as a cofactor of gp78, reveals an unappreciated function of Ufd1 in the ubiquitination reaction during endoplasmic reticulum -associated degradation, and illustrates that Ufd1 plays a critical role in cholesterol metabolism. | Ufd1 is a cofactor of gp78 and plays a key role in cholesterol metabolism by regulating the stability of HMG-CoA reductase.
Cao J, Wang J, Qi W, Miao HH, Wang J, Ge L, DeBose-Boyd RA, Tang JJ, Li BL, Song BL. | 01/21/2010 |
| Ufd1l is localized around the nucleus and it does not interfere with Fas-and ceramide-mediated apoptosis. | Analysis of intracellular distribution and apoptosis involvement of the Ufd1l gene product by over-expression studies.
Amati F, Condò I, Conti E, Sangiuolo F, Dallapiccola B, Testi R, Novelli G. | 01/21/2010 |