Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

RIP140, Mouse anti-Mouse, Rat, Human, Clone: 6D7, Millipore Sigma™

Catalog No. MABS191725 Shop All MilliporeSigma Products
Change view
Click to view available options
Quantity:
25 μg
1 product options available for selection
Product selection table with 1 available options. Use arrow keys to navigate and Enter or Space to select.
Catalog No. Quantity
MABS191725 25 μg
Use arrow keys to navigate between rows. Press Enter or Space to select a product option. 1 options available.
1 options
Catalog No. MABS191725 Supplier MilliporeSigma Supplier No. MABS191725UG
Add to Cart
Add to Cart

Mouse Monoclonal Antibody

Anti-RIP140, clone 6D7, Cat. No. MABS1917, is a mouse monocloanl antibody that detects RIP140 and has been tested for use in Chromatin Immunoprecipitation (ChIP) and Western Blotting.

Nuclear receptor-interacting protein 1 (UniProt: P48552; also known as Nuclear factor RIP140, Receptor-interacting protein 140) is encoded by the NRIP1 gene (Gene ID: 8204) in human. RIP140 is a nuclear protein that is localized to discrete foci and redistributes to larger nuclear domains upon binding to ligand-bound NR3C1. It is expressed in liver in a circadian manner. RIP140 contains 9 Leu-Xaa-Xaa-Leu-Leu (LXXLL) motifs, which have different affinities for nuclear receptors. The C-terminal LTKTNPILYYMLQK motif is required for ligand-dependent interaction with retinoic acid (RA) receptor-alpha (RARA) and retinoid X receptor beta (RXRB) homodimers and heterodimers, for the corepressor activity, and for the formation of an HDAC3 complex with RARA/RXRB. It also contains at least four autonomous repression domains (RD1-4). RD1 functions via a histone deacetylase (HDAC)-independent mechanism, whereas RD2, RD3 and RD4 can function by HDAC-dependent or independent mechanisms, depending on cell type. RIP140 Acetylation regulates its nuclear translocation and co-repressive activity of RIP140 is regulated by its acetylation, which is shown to abolish its interaction with C-terminal-binding protein 1 (CTBP1). Several glucocorticoid responses are shown to be deregulated by RIP140 possibly via an interaction between the glucocorticoid receptor (GR), which prevents binding of true co-activator with GR. (Ref.: Subramaniam N, et al. (1999). J. Biol. Chem. 274(25):18121-7).
TRUSTED_SUSTAINABILITY

Specifications

Antigen RIP140
Applications ChIP Assay, Western Blot
Classification Monoclonal
Clone 6D7
Conjugate Unconjugated
Dilution Western Blotting Analysis: A representative lot detected RIP140 in Western Blotting applications (Kiskinis, E., et. al. (2007). EMBO J. 26(23):4831-40; Hallberg, M., et. al. (2008). Mol Cell Biol. 28(22):6785-95).Chromatin Immunoprecipitation Analysis: A representative lot detected RIP140 in Chromatin Immunoprecitpiation applications (Hallberg, M., et. al. (2008). Mol Cell Biol. 28(22):6785-95).
Formulation Purified mouse monoclonal antibody IgG1 in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Gene Alias Nuclear receptor-interacting protein 1;Nuclear factor RIP140;Receptor-interacting protein 140
Gene Symbols NRIP1
Host Species Mouse
Immunogen GST-tagged recombinant fragment corresponding to 178 amino acids from the N-terminal half of human Nuclear receptor-interacting protein 1 (RIP140).
Purification Method Protein G purified
Quantity 25 μg
Regulatory Status RUO
Research Discipline Signaling
Primary or Secondary Primary
Test Specificity Clone 6D7 detects Nuclear receptor-interacting protein 1 (RIP140) in human, mouse, and rat cells. It targets an epitope with in 178 amino acids from the N-terminal half.
Target Species Mouse, Rat, Human
Content And Storage Stable for 1 year at 2-8°C from date of receipt.
Form Purified
Isotype IgG1
Show More Show Less
Product Title
Select an issue

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.