Associated Papers
Molecular Mechanism of ATP Hydrolysis Catalyzed by p97: A QM/MM Study.
Szántó JK et al.
Journal of Chemical Theory and Computation, 2025
Targeting mitophagy in neurodegenerative diseases.
Antico O et al.
Nature Reviews. Drug Discovery, 2025
VCP activator reverses nuclear proteostasis defects and enhances TDP-43 aggregate clearance in multisystem proteinopathy models.
Phan JM et al.
The Journal of Clinical Investigation, 2024
Characterizing ATP processing by the AAA+ protein p97 at the atomic level.
Shein M et al.
Nature Chemistry, 2024
Novel VCP activator reverses multisystem proteinopathy nuclear proteostasis defects and enhances TDP-43 aggregate clearance.
Phan JM et al.
Biorxiv : the Preprint Server for Biology, 2023
Cryo-electron microscopy structures of VCP/p97 reveal a new mechanism of oligomerization regulation.
Yu G et al.
Iscience, 2021
Conserved L464 in p97 D1-D2 linker is critical for p97 cofactor regulated ATPase activity.
Zhang X et al.
The Biochemical Journal, 2021
Structural and Functional Analysis of Disease-Linked p97 ATPase Mutant Complexes.
Nandi P et al.
International Journal of Molecular Sciences, 2021
Mechanistic insight into substrate processing and allosteric inhibition of human p97.
Pan M et al.
Nature Structural & Molecular Biology, 2021
Targeting acute myeloid leukemia dependency on VCP-mediated DNA repair through a selective second-generation small-molecule inhibitor.
Roux B et al.
Science Translational Medicine, 2021
Observation of a Transient Reaction Intermediate Illuminates the Mechanochemical Cycle of the AAA-ATPase p97.
Rydzek S et al.
Journal of the American Chemical Society, 2020
Uncoupling of p97 ATPase activity has a dominant negative effect on protein extraction.
Rycenga HB et al.
Scientific Reports, 2019
VCP/p97 increases BMP signaling by accelerating ubiquitin ligase Smurf1 degradation.
Li H et al.
Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology, 2019
Adapted ATPase domain communication overcomes the cytotoxicity of p97 inhibitors.
Wei Y et al.
The Journal of Biological Chemistry, 2018
Ubiquitin- and ATP-dependent unfoldase activity of P97/VCP•NPLOC4•UFD1L is enhanced by a mutation that causes multisystem proteinopathy.
Blythe EE et al.
Proceedings of the National Academy of Sciences of the United States of America, 2017
Valosin-containing protein (VCP/p97) inhibitors relieve Mitofusin-dependent mitochondrial defects due to VCP disease mutants.
Zhang T et al.
Elife, 2017
VCP cooperates with UBXD1 to degrade mitochondrial outer membrane protein MCL1 in model of Huntington's disease.
Guo X et al.
Biochimica Et Biophysica Acta. Molecular Basis of Disease, 2017
Structure and Function of p97 and Pex1/6 Type II AAA+ Complexes.
Saffert P et al.
Frontiers in Molecular Biosciences, 2017
A Dynamic molecular basis for malfunction in disease mutants of p97/VCP.
Schuetz AK et al.
Elife, 2016
Role of the D1-D2 Linker of Human VCP/p97 in the Asymmetry and ATPase Activity of the D1-domain.
Tang WK et al.
Scientific Reports, 2016
Structural Basis of ATP Hydrolysis and Intersubunit Signaling in the AAA+ ATPase p97.
Hänzelmann P et al.
Structure (london, England : 1993), 2016
Altered cofactor regulation with disease-associated p97/VCP mutations.
Zhang X et al.
Proceedings of the National Academy of Sciences of the United States of America, 2015
Molecular pathogenesis of spondylocheirodysplastic Ehlers-Danlos syndrome caused by mutant ZIP13 proteins.
Bin BH et al.
Embo Molecular Medicine, 2014
Specific inhibition of p97/VCP ATPase and kinetic analysis demonstrate interaction between D1 and D2 ATPase domains.
Chou TF et al.
Journal of Molecular Biology, 2014
Altered intersubunit communication is the molecular basis for functional defects of pathogenic p97 mutants.
Tang WK et al.
The Journal of Biological Chemistry, 2013
VCP is essential for mitochondrial quality control by PINK1/Parkin and this function is impaired by VCP mutations.
Kim NC et al.
Neuron, 2013
Proliferating cell nuclear antigen (PCNA)-binding protein C1orf124 is a regulator of translesion synthesis.
Ghosal G et al.
The Journal of Biological Chemistry, 2012
The role of the N-domain in the ATPase activity of the mammalian AAA ATPase p97/VCP.
Niwa H et al.
The Journal of Biological Chemistry, 2012
Yeast sterol regulatory element-binding protein (SREBP) cleavage requires Cdc48 and Dsc5, a ubiquitin regulatory X domain-containing subunit of the Golgi Dsc E3 ligase.
Stewart EV et al.
The Journal of Biological Chemistry, 2012
The AAA-ATPase VCP/p97 promotes 53BP1 recruitment by removing L3MBTL1 from DNA double-strand breaks.
Acs K et al.
Nature Structural & Molecular Biology, 2011
A genome-wide screen identifies p97 as an essential regulator of DNA damage-dependent CDT1 destruction.
Raman M et al.
Molecular Cell, 2011
VCP/p97 is essential for maturation of ubiquitin-containing autophagosomes and this function is impaired by mutations that cause IBMPFD.
Tresse E et al.
Autophagy, 2010
The otubain YOD1 is a deubiquitinating enzyme that associates with p97 to facilitate protein dislocation from the ER.
Ernst R et al.
Molecular Cell, 2009
VCP mutations causing frontotemporal lobar degeneration disrupt localization of TDP-43 and induce cell death.
Gitcho MA et al.
The Journal of Biological Chemistry, 2009
Impaired protein aggregate handling and clearance underlie the pathogenesis of p97/VCP-associated disease.
Ju JS et al.
The Journal of Biological Chemistry, 2008
Inclusion body myopathy-associated mutations in p97/VCP impair endoplasmic reticulum-associated degradation.
Weihl CC et al.
Human Molecular Genetics, 2006
ATPase activity of p97-valosin-containing protein (VCP). D2 mediates the major enzyme activity, and D1 contributes to the heat-induced activity.
Song C et al.
The Journal of Biological Chemistry, 2003
Functional ATPase activity of p97/valosin-containing protein (VCP) is required for the quality control of endoplasmic reticulum in neuronally differentiated mammalian PC12 cells.
Kobayashi T et al.
The Journal of Biological Chemistry, 2002
VCP/p97 in abnormal protein aggregates, cytoplasmic vacuoles, and cell death, phenotypes relevant to neurodegeneration.
Hirabayashi M et al.
Cell Death and Differentiation, 2001