Rabbit Polyclonal Phospho-VCP (S352) antibody (STJ90640)


Reactivity: Human, Mouse, Rat
Applications: WB, ELISA
Conjugation: Unconjugated
Supplier: St John’s Laboratory Ltd.

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Rabbit Polyclonal Phospho-VCP (S352) antibody (STJ90640)

Supplier: St John’s Laboratory Ltd.

Recommended applications: WB, ELISA

Recommended dilution: WB 1:500-1:2000; ELISA 1:5000;

Recommended protocols: check protocols

Image descriptions:

Click or hover above images to see image description for VCP (phospho Ser352) Polyclonal Antibody.

Alternative names:

Check alternative names for the antibody


VCP antibody,|15S Mg(2+) ATPase p97 subunit antibody|15S Mg(2+)-ATPase p97 subunit antibody|ALS14 antibody|ATPase p97 antibody|CDC48 antibody|IBMPFD antibody|MGC131997 antibody|MGC148092 antibody|MGC8560 antibody|p97 antibody|TER ATPase antibody|TERA antibody|TERA_HUMAN antibody|Transitional endoplasmic reticulum ATPase antibody|Valosin containing protein antibody|Valosin-containing protein antibody|VCP antibody|Yeast Cdc48p homolog antibody|Anti-VCP antibody [5] (ab11433)
SCBT cat No: To be updated



VCP (phospho Ser352) Polyclonal Antibody

Catalogue No.



Human, Mouse, Rat


Phospho-VCP (S352) Polyclonal Antibody detects endogenous levels of VCP protein only when phosphorylated at S352.


Synthesized phospho-peptide derived from VCP (phospho Ser352) at AA range 290-370





Recommended dilution

WB 1:500-1:2000; ELISA 1:5000;







Molecular weight

85 kDa


VCP (phospho Ser352) Antibody was tube-contained. Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.


1 mg/ml


VCP (phospho Ser352) Antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.


-20 Celsius degree. Avoid repeated freeze/thaw cycles.

Alternative antibody names

Transitional endoplasmic reticulum ATPase antibody, TER ATPase antibody, 15S Mgantibody, 2+ antibody,-ATPase p97 subunit antibody, Valosin-containing protein antibody, VCP antibody

Database links

Human UniProt/Swiss-Prot:P55072;Mouse UniPort/Swiss-Prot: Q01853;Rat UniProt/Swiss-Port: P46462;Human Entrez Gene: 7415;Mouse Entrez Gene: 269523;Rat Entrez Gene: Rn.98891

Protein names

Transitional endoplasmic reticulum ATPase , TER ATPase , 15S Mg, 2+ ,-ATPase p97 subunit , Valosin-containing protein , VCP

Protein function

Necessary for the fragmentation of Golgi stacks during mitosis and for their reassembly after mitosis. Involved in the formation of the transitional endoplasmic reticulum (tER). The transfer of membranes from the endoplasmic reticulum to the Golgi apparatus occurs via 50-70 nm transition vesicles which derive from part-rough, part-smooth transitional elements of the endoplasmic reticulum (tER). Vesicle budding from the tER is an ATP-dependent process. The ternary complex containing UFD1L, VCP and NPLOC4 binds ubiquitinated proteins and is necessary for the export of misfolded proteins from the ER to the cytoplasm, where they are degraded by the proteasome. The NPLOC4-UFD1L-VCP complex regulates spindle disassembly at the end of mitosis and is necessary for the formation of a closed nuclear envelope. Regulates E3 ubiquitin-protein ligase activity of RNF19A. Component of the VCP/p97-AMFR/gp78 complex that participates in the final step of the sterol-mediated ubiquitination and endoplasmic reticulum-associated degradation (ERAD) of HMGCR. Also involved in DNA damage response: recruited to double-strand breaks (DSBs) sites in a RNF8- and RNF168-dependent manner and promotes the recruitment of TP53BP1 at DNA damage sites. Recruited to stalled replication forks by SPRTN: may act by mediating extraction of DNA polymerase eta (POLH) to prevent excessive translesion DNA synthesis and limit the incidence of mutations induced by DNA damage. Required for cytoplasmic retrotranslocation of stressed/damaged mitochondrial outer-membrane proteins and their subsequent proteasomal degradation. / ATP + H2O = ADP + phosphate.

Involvement in disease

Inclusion body myopathy with early-onset Paget disease with or without frontotemporal dementia 1 (IBMPFD1) [MIM:167320]: An autosomal dominant disease characterized by disabling muscle weakness clinically resembling to limb girdle muscular dystrophy, osteolytic bone lesions consistent with Paget disease, and premature frontotemporal dementia. Clinical features show incomplete penetrance. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Amyotrophic lateral sclerosis 14, with or without frontotemporal dementia (ALS14) [MIM:613954]: A neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. Patients with ALS14 may develop frontotemporal dementia. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Charcot-Marie-Tooth disease 2Y (CMT2Y) [MIM:616687]: An autosomal dominant, axonal form of Charcot-Marie-Tooth disease, a disorder of the peripheral nervous system, characterized by progressive weakness and atrophy, initially of the peroneal muscles and later of the distal muscles of the arms. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathies (designated CMT1 when they are dominantly inherited) and primary peripheral axonal neuropathies (CMT2). Neuropathies of the CMT2 group are characterized by signs of axonal degeneration in the absence of obvious myelin alterations, normal or slightly reduced nerve conduction velocities, and progressive distal muscle weakness and atrophy. . Note: The disease is caused by mutations affecting the gene represented in this entry.

Protein sequence and domain

Belongs to the AAA ATPase family.

Protein post-translational modifications

Phosphorylated by tyrosine kinases in response to T-cell antigen receptor activation. / ISGylated. / Methylation at Lys-315 catalyzed by VCPKMT is increased in the presence of ASPSCR1. Lys-315 methylation may decrease ATPase activity.

Protein cellular localization

Cytoplasm > cytosol / Endoplasmic reticulum / Nucleus

Research area

All research areas>Cell Cycle Proteins>VCP
(View all antibody categories related to Cell Cycle Proteins)


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St John’s Laboratory Ltd.

Product type

Primary antibody


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