Mouse VCP peptide (ab39788)
Key features and details
- Purity: > 90% SDS-PAGE
- Suitable for: Blocking, Neutralising
Description
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Product name
Mouse VCP peptide
See all VCP proteins and peptides -
Purity
> 90 % SDS-PAGE. -
Animal free
No -
Nature
Synthetic -
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Species
Mouse -
Sequence
GGSVYTEDNDDDLYG -
Amino acids
792 to 806
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Specifications
Our Abpromise guarantee covers the use of ab39788 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
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Applications
Blocking
Neutralising
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Form
Lyophilized -
Concentration information loading...
Preparation and Storage
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Stability and Storage
Shipped at 4°C. Store at -20°C. Avoid freeze / thaw cycle.
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ReconstitutionPlease reconstitute this product using 100ul distilled water.
General Info
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Alternative names
- 15S Mg(2+) ATPase p97 subunit
- 15S Mg(2+)-ATPase p97 subunit
- ALS14
see all -
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 (By similarity). Regulates E3 ubiquitin-protein ligase activity of RNF19A. -
Involvement in disease
Defects in VCP are the cause of inclusion body myopathy with early-onset Paget disease and frontotemporal dementia (IBMPFD) [MIM:167320]; also known as muscular dystrophy, limb-girdle, with Paget disease of bone or pagetoid amyotrophic lateral sclerosis or pagetoid neuroskeletal syndrome or lower motor neuron degeneration with Paget-like bone disease. IBMPFD features adult-onset proximal and distal muscle weakness (clinically resembling limb girdle muscular dystrophy), early-onset Paget disease of bone in most cases and premature frontotemporal dementia. -
Sequence similarities
Belongs to the AAA ATPase family. -
Post-translational
modificationsPhosphorylated by tyrosine kinases in response to T-cell antigen receptor activation (By similarity). Phosphorylated upon DNA damage, probably by ATM or ATR.
ISGylated. -
Cellular localization
Cytoplasm > cytosol. Nucleus. Present in the neuronal hyaline inclusion bodies specifically found in motor neurons from amyotrophic lateral sclerosis patients. Present in the Lewy bodies specifically found in neurons from Parkinson disease patients. - Information by UniProt
Protocols
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
Datasheets and documents
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Datasheet download
References (2)
ab39788 has been referenced in 2 publications.
- Wiederstein JL et al. Skeletal Muscle-Specific Methyltransferase METTL21C Trimethylates p97 and Regulates Autophagy-Associated Protein Breakdown. Cell Rep 23:1342-1356 (2018). PubMed: 29719249
- Nadeau MÈ et al. Pharmacological targeting of valosin containing protein (VCP) induces DNA damage and selectively kills canine lymphoma cells. BMC Cancer 15:479 (2015). PubMed: 26104798