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VCP (8C1) Monoclonal Antibody

Applications

  • WB
  • FCM
  • IHC-P
  • IF(ICC)
  • IHC

Reactivity

  • Human
  • Mouse
  • Rat
  • Zebrafish
Overview
Catalog # bsm-52931R
Product Name VCP (8C1) Monoclonal Antibody
Applications WB, FCM, IHC-P, IF(ICC), IHC
Reactivity Human, Mouse, Rat, Zebrafish
Specifications
Conjugation Unconjugated
Host Rabbit
Source Human VCP between 1-100 amino acids
Clonality Monoclonal
Clone # 8C1
Isotype IgG
Concentration 1ug/ul
Purification Purified by Protein A.
Storage Buffer Aqueous buffered solution containing 1xTBS (pH7.4), 1%BSA, 40%Glycerol and 0.05% Sodium Azide.
Storage Condition Store at -20°C for 12 months.
Target
Gene ID 7415
Swiss Prot P55072
Synonyms Transitional endoplasmic reticulum ATPase, 15S Mg(2+)-ATPase p97 subunit, Valosin-containing protein, TER ATPase, VCP
Background 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.
Application Dilution
WB 1:300-5000
FCM 1:20-100
IHC-P 1:200-400
IF(ICC) 1:50-200
IHC