Mouse Anti-VCP IgM Monoclonal Antibody (Hs-14)

specifications
Antibody Isotype	IgM
Clone	Hs-14
Applications	WB; FC; IF
Target	VCP
Host	Mouse
Clonality	Monoclonal
Antibody Type	Primary antibody
Species Reactivity	Human, Mouse
Immunogen	Freshly ejaculated human sperms were washed in PBS and extracted in 3% acetic acid, 10% glycerol, 30 mM benzaminidine. The acid extract was dialyzed against 0.2% acetic acid and subsequently used for immunization.
Format	Liquid
Buffer	TBS, pH 8.0
Storage	Store at 4° C.

specifications

Antibody Isotype

IgM

Clone

Hs-14

Applications

WB; FC; IF

Target

VCP

Host

Mouse

Clonality

Monoclonal

Antibody Type

Primary antibody

Species Reactivity

Human, Mouse

Immunogen

Freshly ejaculated human sperms were washed in PBS and extracted in 3% acetic acid, 10% glycerol, 30 mM benzaminidine. The acid extract was dialyzed against 0.2% acetic acid and subsequently used for immunization.

Format

Liquid

Buffer

TBS, pH 8.0

Storage

Store at 4° C.

Target Information
Target Name	VCP
Alternative Names	Valosin Containing Protein; Transitional Endoplasmic Reticulum ATPase; 15S Mg(2+)-ATPase P97 Subunit; Valosin-Containing Protein; TER ATPase; CDC48; TERA; P97; FTDALS6; IBMPFD
Related Disease	Inclusion Body Myopathy With Early-Onset Paget Disease With Or Without Frontotemporal Dementia 1; Frontotemporal Dementia And/Or Amyotrophic Lateral Sclerosis 6
Gene ID	7415
UniProt ID	P55072
Target Overview	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 UFD1, 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-UFD1-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. Involved in endoplasmic reticulum stress-induced pre-emptive quality control, a mechanism that selectively attenuates the translocation of newly synthesized proteins into the endoplasmic reticulum and reroutes them to the cytosol for proteasomal degradation. Plays a role in the regulation of stress granules (SGs) clearance process upon arsenite-induced response. 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. Together with SPRTN metalloprotease, involved in the repair of covalent DNA-protein cross-links (DPCs) during DNA synthesis. Involved in interstrand cross-link repair in response to replication stress by mediating unloading of the ubiquitinated CMG helicase complex. Required for cytoplasmic retrotranslocation of stressed/damaged mitochondrial outer-membrane proteins and their subsequent proteasomal degradation. Essential for the maturation of ubiquitin-containing autophagosomes and the clearance of ubiquitinated protein by autophagy. Acts as a negative regulator of type I interferon production by interacting with DDX58/RIG-I: interaction takes place when DDX58/RIG-I is ubiquitinated via 'Lys-63'-linked ubiquitin on its CARD domains, leading to recruit RNF125 and promote ubiquitination and degradation of DDX58/RIG-I. May play a role in the ubiquitin-dependent sorting of membrane proteins to lysosomes where they undergo degradation. May more particularly play a role in caveolins sorting in cells. By controlling the steady-state expression of the IGF1R receptor, indirectly regulates the insulin-like growth factor receptor signaling pathway.

Target Information

Target Name

VCP

Alternative Names

Valosin Containing Protein; Transitional Endoplasmic Reticulum ATPase; 15S Mg(2+)-ATPase P97 Subunit; Valosin-Containing Protein; TER ATPase; CDC48; TERA; P97; FTDALS6; IBMPFD

Related Disease

Inclusion Body Myopathy With Early-Onset Paget Disease With Or Without Frontotemporal Dementia 1; Frontotemporal Dementia And/Or Amyotrophic Lateral Sclerosis 6

Gene ID

7415

UniProt ID

P55072

Target Overview

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 UFD1, 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-UFD1-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. Involved in endoplasmic reticulum stress-induced pre-emptive quality control, a mechanism that selectively attenuates the translocation of newly synthesized proteins into the endoplasmic reticulum and reroutes them to the cytosol for proteasomal degradation. Plays a role in the regulation of stress granules (SGs) clearance process upon arsenite-induced response. 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. Together with SPRTN metalloprotease, involved in the repair of covalent DNA-protein cross-links (DPCs) during DNA synthesis. Involved in interstrand cross-link repair in response to replication stress by mediating unloading of the ubiquitinated CMG helicase complex. Required for cytoplasmic retrotranslocation of stressed/damaged mitochondrial outer-membrane proteins and their subsequent proteasomal degradation. Essential for the maturation of ubiquitin-containing autophagosomes and the clearance of ubiquitinated protein by autophagy. Acts as a negative regulator of type I interferon production by interacting with DDX58/RIG-I: interaction takes place when DDX58/RIG-I is ubiquitinated via 'Lys-63'-linked ubiquitin on its CARD domains, leading to recruit RNF125 and promote ubiquitination and degradation of DDX58/RIG-I. May play a role in the ubiquitin-dependent sorting of membrane proteins to lysosomes where they undergo degradation. May more particularly play a role in caveolins sorting in cells. By controlling the steady-state expression of the IGF1R receptor, indirectly regulates the insulin-like growth factor receptor signaling pathway.

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