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Knockdown of the host ubiquitin-dependent segregase VCP/p97, results in loss of IE2 expression, subsequent suppression of early and late gene expression and, ultimately, failure in virus replication. NMS (show NMS ELISA Kits)-873, a small molecule inhibitor of VCP, is a potent HCMV antiviral with potential as a novel host targeting therapeutic for HCMV infection.
VCP removes sterically trapped Ku70/80 rings from DNA in double-strand break repair.
Data suggest that AAA+ (ATPases associated with diverse cellular activities) ATPase p97 is essential to wide range of cellular functions, including endoplasmic reticulum-associated degradation, membrane fusion, NFkappaB (nuclear factor kappa-light-chain-enhancer of activated B cells) activation, and chromatin-associated processes, which are regulated by ubiquitination. [REVIEW]
Upon damage, p97 (show EIF4G2 ELISA Kits) translocates to lysosomes and there cooperates with a distinct set of cofactors including UBXD1 (show UBXN6 ELISA Kits), PLAA (show PLAA ELISA Kits), and the deubiquitinating enzyme YOD1 (show YOD1 ELISA Kits), which we term ELDR components for Endo-Lysosomal Damage Response.
Data show that inhibition of VCP/p97, or siRNA-mediated ablation of VCP/p97 impairs ultraviolet radiation (UVR)-induced RNA polymerase II (RNAPII) degradation.
p97 (show EIF4G2 ELISA Kits) negatively regulates NRF2 (show GABPA ELISA Kits) through the canonical pathway by extracting ubiquitylated NRF2 (show GABPA ELISA Kits) from the KEAP1 (show KEAP1 ELISA Kits)-CUL3 (show CUL3 ELISA Kits) E3 complex.
Data suggest that dimerization of UBX domain protein 7 (UBXD7) could affect the formation of the p97 ATPase-UBXD7 complex.
a VCP mutation/knockdown-induced dysregulation in the adenine nucleotide translocase, which results in a slower rate of ADP or ATP translocation across the mitochondrial membranes.
The functional motions of p97 (show EIF4G2 ELISA Kits) using symmetric normal modes have been predicted.
insights into the interactions between other SHP (show LAMC1 ELISA Kits)-containing proteins and p97N
Together, these results suggested that mouse mammary tumor virus Rem (show REM1 ELISA Kits) uses a novel p97 (show EIF4G2 ELISA Kits)-dependent, Derlin-independent retrotranslocation mechanism distinct from other pathogens to avoid signal peptide ubiquitylation and proteasomal degradation.
cellular phenotypes caused by P137L mutant expression were not isolated observations, and some other IBMPFD disease-related VCP/p97 mutations could lead to similar outcomes
results suggest that (i) NLRP3 inflammasome and local IL-1beta((+))F4/80((+))Ly6C((+)) inflammatory macrophages contribute to pathogenesis of VCP-associated myopathy
VCP (valosin-containing protein), together with its cofactor P47 (show MFGE8 ELISA Kits) and the endoplasmic reticulum (ER) morphology regulator ATL1 (Atlastin-1 (show ATL1 ELISA Kits)), regulates tubular ER formation
Lysine Methylation of the Valosin-Containing Protein (VCP) Is Dispensable for Development and Survival of Mice
Global expression profiling of VCP(R155H/+) mice identified key dysregulated signaling pathways including genes involved in the physiological system development and function, diseases and disorders, and molecular and cellular functions.
The results reveal an unexpected, crucial role of ATP consumption by VCP in determining cell fate in retinitis pigmentosa, and point to a promising new neuroprotective strategy for this currently incurable disease.
Pro(178) and Pro(183) of SelS (show SELS ELISA Kits) play important roles in the translocation of p97(VCP) to the ER membrane and protect cells from ER stress
Knockdown or chemical inhibition of p97 (show EIF4G2 ELISA Kits) causes robust accumulation of USP33 (show USP33 ELISA Kits) due to inhibition of its degradation
Findings indicate that p97 plays a conserved role in dismantling the CMG (show CASK ELISA Kits) helicase (show DNA2 ELISA Kits) complex during different cellular events, but that distinct regulatory signals ultimately control when and where unloading takes place.
p97 is an essential regulator of DNA damage-dependent CDT1 (show CDT1 ELISA Kits) destruction
CDC-48/p97 coordinates CDT-1 (show CDT1 ELISA Kits) degradation with GINS chromatin dissociation to ensure faithful DNA replication
data reveal an essential pathway that regulates reformation of the nucleus after mitosis and defines ubiquitin-dependent protein extraction as a common mechanism of Cdc48/p97 activity also during nucleus formation
results suggest that VCP plays a mechanistic role in releasing WRNp from the nucleolus
When we introduced CDC48 antisense morpholino oligonucleotides into zebrafish embryos, the morphant embryos were lethal and showed defects in neuronal outgrowth and neurodegeneration.
CDC48 may promote cell cycling and cell proliferation via C-terminal tyrosine phosphorylation during cold acclimation in fish cells
The protein encoded by this gene is a member of a family that includes putative ATP-binding proteins involved in vesicle transport and fusion, 26S proteasome function, and assembly of peroxisomes. This protein, as a structural protein, is associated with clathrin, and heat-shock protein Hsc70, to form a complex. It has been implicated in a number of cellular events that are regulated during mitosis, including homotypic membrane fusion, spindle pole body function, and ubiquitin-dependent protein degradation.
transitional endoplasmic reticulum ATPase
, valosin-containing protein
, valosin containing protein
, 15S Mg(2+)-ATPase p97 subunit
, TER ATPase
, yeast Cdc48p homolog
, AAA ATPase p97
, Inv protein
, homolog of yeast cdc48
, p97 ATPase