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Human Polyclonal vcp Primary Antibody for ICC, IF - ABIN151102
Clemen, Tangavelou, Strucksberg, Just, Gaertner, Regus-Leidig, Stumpf, Reimann, Coras, Morgan, Fernandez, Hofmann, Müller, Schoser, Hanisch, Rottbauer, Blümcke, von Hörsten, Eichinger, Schröder: Strumpellin is a novel valosin-containing protein binding partner linking hereditary spastic paraplegia to protein aggregation diseases. in Brain : a journal of neurology 2010
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Human Polyclonal vcp Primary Antibody for ICC, IF - ABIN151101
Dong, Bridges, Apsley, Xu, Weaver: ERdj4 and ERdj5 are required for endoplasmic reticulum-associated protein degradation of misfolded surfactant protein C. in Molecular biology of the cell 2008
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Xenopus laevis Monoclonal vcp Primary Antibody for WB - ABIN284668
Baron, Pedrioli, Tyagi, Johnson, Wood, Fountaine, Wightman, Alexandru: VAPB/ALS8 interacts with FFAT-like proteins including the p97 cofactor FAF1 and the ASNA1 ATPase. in BMC biology 2014
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Human Monoclonal vcp Primary Antibody for ICC, FACS - ABIN302102
Pavlásek, Peknicová, Ulcová-Gallová, Nováková, Reischig, Micanová, Rokyta: [Significance of determination of intra-acrosomal proteins and sperm antibodies in human reproduction]. in Ceská gynekologie / Ceská lékarská spolecnost J. Ev. Purkyne 2004
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Human Monoclonal vcp Primary Antibody for ICC, FACS - ABIN1302844
Peknicová, Kyselová, Buckiová, Boubelík: Effect of an endocrine disruptor on mammalian fertility. Application of monoclonal antibodies against sperm proteins as markers for testing sperm damage. in American journal of reproductive immunology (New York, N.Y. : 1989) 2002
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Xenopus laevis Monoclonal vcp Primary Antibody for WB - ABIN933553
Ernst, Mueller, Ploegh, Schlieker: The otubain YOD1 is a deubiquitinating enzyme that associates with p97 to facilitate protein dislocation from the ER. in Molecular cell 2009
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Human Monoclonal vcp Primary Antibody for FACS, ICC - ABIN265891
Sullivan, Funk, Shan, Haroutunian, McCullumsmith: Decreased chloride channel expression in the dorsolateral prefrontal cortex in schizophrenia. in PLoS ONE 2015
Human Monoclonal vcp Primary Antibody for ICC, FACS - ABIN269087
Greenhalgh, Griffith, Wald: The use of immunofluorescence in microdissection testicular sperm extraction. in Journal of andrology 2009
Human Monoclonal vcp Primary Antibody for WB - ABIN1944899
Hu, Han, Song, Peng, Huang, Ren, Gu, Huang, Li, Jiang, Fu, Zhang, Gu, Dai, Mao, Gao, Rong, Ye, Zhou, Xu, Gu, Shi, Jin, Zhang, Wu, Huang, Chen, Chen, Chen: Gene expression profiling in the human hypothalamus-pituitary-adrenal axis and full-length cDNA cloning. in Proceedings of the National Academy of Sciences of the United States of America 2000
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Human Polyclonal vcp Primary Antibody for FACS, IHC (p) - ABIN390907
Rush, Moritz, Lee, Guo, Goss, Spek, Zhang, Zha, Polakiewicz, Comb: Immunoaffinity profiling of tyrosine phosphorylation in cancer cells. in Nature biotechnology 2005
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The heterozygous R155C VCP mutation is toxic in humans and harmless in mice because of a low lever expression.
These results indicate that the outer membrane protein MCL1 is degraded by the VCP-UBXD1 complex and that the process is promoted by the presence of mutant Huntingtin.
Study results suggest that VCP recruitment to mitochondria by mtHtt is a crucial step in the initiation of neuropathology in Huntington's disease.
ASPL efficiently promotes p97 hexamer disassembly, resulting in the formation of stable p97:ASPL. Overproduction of ASPL disrupts p97 hexamer function in endoplasmic reticulum-associated protein degradation.
Data indicate that approximately 9% of patients with valosin-containing protein (VCP) mutations had an amyotrophic lateral sclerosis (ALS) phenotype, 4% had been diagnosed with Parkinson's disease (PD), and 2% had been diagnosed with Alzheimer's disease (AD).
CB-5083 decreases viability in multiple myeloma cell lines and patient-derived multiple myeloma cells, including those with background proteasome inhibitor (PI) resistance. CB-5083 has a unique mechanism of action that combines well with PIs, which is likely owing to the p97-dependent retro-translocation of the transcription factor, Nrf1, which transcribes proteasome subunit genes following exposure to a PI
a p97 mutant that causes inclusion body myopathy, Paget's disease of bone, and frontotemporal dementia unfolds substrate faster, suggesting that excess activity may underlie pathogenesis
Results report that VCP/p97 promotes the degradation of ubiquitylated GS, resulting in its accumulation in cells with compromised p97 function. Notably, p97 is also required for the degradation of all four known CRBN neo-substrates [IKZF1, IKZF3, CK1alpha, and GSPT1] whose ubiquitylation is induced by immunomodulatory drugs.
non-cell-autonomous effects of VCP-mutant astrocytes on both control and mutant Motor neurons, were examined.
AAA-ATPase p97 suppresses apoptotic and autophagy-associated cell death in rheumatoid arthritis synovial fibroblasts.
Data suggest ATXN3 binds with low-micromolar affinity to both wild-type p97/VCP and mutants linked to proteostasis deficiency multisystem proteinopathy 1 (MSP1; also called hereditary inclusion body myopathy); stoichiometry of binding is one ATXN3 molecule per p97/VCP hexamer in presence of ATP; MSP1 mutants of p97/VCP bind ATXN3 irrespective of nucleotide state. (VCP = valosin-containing protein/ATPase; ATXN3 = ataxin-3)
a substantial proportion of the beta2AR produced is non-functional and VCP plays a key role in the maturation and trafficking of the beta2AR.
Its mutation is not found in a cohort of German patients with sporadic amyotrophic lateral sclerosis and frontotemporal lobar degeneration comorbidity.
When HEK293T cells were co-transfected with IQGAP1 and VCP, an immunoprecipitation assay revealed that binding of IQGAP1 with disease-related mutant (R155H or A232E) VCP was markedly reduced compared to wild-type VCP. This suggests that reduction of IQGAP1 and VCP interaction may be associated with the pathophysiology of inclusion body myopathy with Paget's disease of bone and frontotemporal dementia (IBMPFD).
Rare variants in VCP genes are risk for sporadic inclusion body myositis.
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-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 translocates to lysosomes and there cooperates with a distinct set of cofactors including UBXD1, PLAA, and the deubiquitinating enzyme YOD1, 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.
Findings indicate that p97 plays a conserved role in dismantling the CMG helicase 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 destruction
CDC-48/p97 coordinates CDT-1 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
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
Both the mRNA and protein levels of Valosin-Containing Protein were regulated by Bap31 in vivo and in vitro.
The valosin-containing protein is a novel mediator of mitochondrial respiration and cell survival in the heart in vivo
Study reports for the first time that VCP is aberrantly translocated to the mitochondria and bound to mutant Huntingtin in a variety of Huntington's disease models.
Valosin-containing protein is a novel repressor of cardiomyocyte hypertrophy induced by pressure overload.
Together, these results suggested that mouse mammary tumor virus Rem uses a novel p97-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
The functional motions of p97 using symmetric normal modes have been predicted.
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 and the endoplasmic reticulum (ER) morphology regulator ATL1 (Atlastin-1), 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 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 causes robust accumulation of USP33 due to inhibition of its degradation
conclude that the Akt substrate, VCP, mediates the increased expression of iNOS downstream from Hsp22 through an NF-kappaB-dependent mechanism
Molecular dynamics simulations are used to probe energetic requirements of substrate protein translocation through the p97 pore and mechanisms of substrate binding and release from p97 subunits during the allosteric cycle.
Data indicate that genetic ablation or chemical inhibition of p97 does not diminish DRiP antigen presentation nor does it alter the levels of MHC class I molecules on the cell surface.
Cav-1 may be a cofactor in the interaction of Derlin-1 and N-glycosylated COX-2 and may facilitate Derlin-1- and p97 complex-mediated COX-2 ubiquitination, retrotranslocation, and degradation.
results suggest that VCP plays a mechanistic role in releasing WRNp from the nucleolus
rescue experiments with a lethal mfap1 mutant show that the VCP binding region is not essential for Mfap1 function, but may act to increase its stability or activity
Clu is upstream of and binds to VCP in vivo and promotes VCP-dependent Marf degradation in vitro Marf accumulates in whole muscle lysates of clu-deficient flies and is destabilized upon Clu overexpression. Thus, Clu is essential for mitochondrial homeostasis and functions in concert with Parkin and VCP for Marf degradation to promote damaged mitochondrial clearance.
results have revealed SUMOylation as a molecular signaling switch to regulate the distribution and functions of VCP during stress response, and suggest that deficiency in VCP SUMOylation caused by pathogenic mutations will render cells vulnerable to stress insults.
The authors propose that VCP sustains sarcoplasmic proteostasis, in part, by controlling the integrity of a dynamic tubular lysosomal network.
Ter94/VCP appears to be an evolutionarily conserved component that regulates BMP-Smad1/5/8 signaling.
Data identifies that ter94, Drosophila VCP, as a strong modulator of motor neuron degeneration induced by knockdown of Caz, Drosophila FUS
Valosin-Containing Protein has an essential role in dendrite pruning through regulating mRNA metabolism
VCP was validated as an atlastin-interacting protein.
Ter94 ATPase and K11-linked ubiquitination in Ci contribute to the selectivity by proteasomes for partial degradation.
VCP binds to DIAP1 in a ubiquitin- and BIR domain-dependent manner and facilitates its degradation, therefore, establishing a new link between ubiquitin, dendrite pruning and the apoptosis machinery.
Subcellular localization and ATPase activity of VCP clearly influenced the localization of the aggregates throughout the cells.
Genetic inactivation of ter94 increased the levels of misfolded Rh1 in retina.
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.
15S Mg(2+)-ATPase p97 subunit
, TER ATPase
, transitional endoplasmic reticulum ATPase
, valosin-containing protein
, yeast Cdc48p homolog
, p97 ATPase
, AAA ATPase p97
, Inv protein
, homolog of yeast cdc48
, valosin containing protein
, CG2331 gene product from transcript CG2331-RA
, TRANSITIONAL ENDOPLASMIC RETICULUM ATPASE TER94
, Valosin-Containing protein
, Valosin-containing protein homolog
, complementation group I
, transitional endoplasmic reticulum 94
, Fanconi anemia group G protein
, Fanconi anemia, complementation group G