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Product Name
RXRB antibody
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Description
RXRB Rabbit Polyclonal antibody. Positive IP detected in MCF-7 cells. Positive WB detected in NIH/3T3 cells, MCF7 cells. Observed molecular weight by Western-blot: 57 kDa
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Tested applications
ELISA, WB, IP
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Species reactivity
Human,Mouse,Rat; other species not tested.
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Alternative names
DAUDI6 antibody; H 2RIIBP antibody; NR2B2 antibody; RCoR 1 antibody; Retinoid X receptor beta antibody; retinoid X receptor antibody; beta antibody; RXRB antibody
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Isotype
Rabbit IgG
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Preparation
This antibody was obtained by immunization of RXRB recombinant protein (Accession Number: NM_021976). Purification method: Antigen affinity purified.
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Clonality
Polyclonal
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Formulation
PBS with 0.02% sodium azide and 50% glycerol pH 7.3.
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Storage instructions
Store at -20℃. DO NOT ALIQUOT
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Applications
Recommended Dilution:
WB: 1:200-1:2000
IP: 1:200-1:2000
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Validations
NIH/3T3 cells were subjected to SDS PAGE followed by western blot with Catalog No:114947(RXRB antibody) at dilution of 1:500
IP Result of anti-RXRB (IP:Catalog No:114947, 4ug; Detection:Catalog No:114947 1:500) with MCF-7 cells lysate 1200ug.
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Background
Retinoid X receptor beta (RXRβ), like other members of the RXR subfamily, possesses a characteristic tripartite modular structure consisting of (a) a highly conserved central region containing the C4/C5 zinc-finger domain, which is responsible for DNA binding; (b) a relatively well-conserved C-terminal region, which contains the hormone binding and dimerization domains; and © a variable N-terminal domain, which has been implicated in either transactivation or repression of target genes. Variability within the N-terminal domain is thought to be the result of alternative splicing and/or differential promoter usage. The murine RXRβ was initially identified because of its ability to bind to the regulatory region II in the murine major histocompatability complex (MHC) class I promoter and is therefore also referred to as H-2RIIBP. Genetic ablation of murine Rxrb produced approximately 50% lethality in utero and males that survived had defects of spermatazoa, which resulted in sterility. Further studies revealed that expression of a Rxrb mutant with an impaired AF-2 core led to abnormal lipid metabolism in Sertoli cells, suggesting functional interactions between Rxrb and other nuclear receptors that control lipid metabolism. This antibody can recognize the RXRβprotein, and give a 58kd band.
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