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SRP5125

Sigma-Aldrich

Rel B, His tagged human

recombinant, expressed in baculovirus infected Sf9 cells, ≥70% (SDS-PAGE), buffered aqueous glycerol solution

Sinónimos:

I-REL, IREL

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About This Item

UNSPSC Code:
12352202
NACRES:
NA.32

recombinant

expressed in baculovirus infected Sf9 cells

assay

≥70% (SDS-PAGE)

form

buffered aqueous glycerol solution

mol wt

~68 kDa

NCBI accession no.

NM_006509

shipped in

dry ice

storage temp.

−70°C

Gene Information

human ... RELB(5971)

General description

Rel B is part of the NFκB complex and forms heterodimeric complexes with p50 (NFKB1) and p52 (NFKB2). The homodimeric complexes of Rel B alone do not show DNA-binding activity. IHC analysis has shown that Rel B expression correlated with dendritic cell activation. NFκB-inducing kinase NIK is required for osteoclastogenesis in response to pathologic stimuli and overexpression of Rel B rescues differentiation of mouse NIK -/- osteoclast precursors. Rel B is required for RANKL-induced osteoclastogenesis in vitro and for TNF -induced bone resorption in vivo. This indicates that the alternative NFκB pathway, via Rel B, plays an essential and unique role in RANKL signaling toward osteoclast development.

Physical form

Supplied in 50mM sodium phosphate, pH 7.0, 300mM NaCl, 150mM imidazole, 0.1mM PMSF, 0.25mM DTT, 25% glycerol.

Preparation Note

after opening, aliquot into smaller quantities and store at -70 °C. Avoid repeating handling and multiple freeze/thaw cycles

pictograms

Health hazardExclamation mark
GHS08,GHS07

signalword

Danger

Hazard Classifications

Eye Irrit. 2 - Repr. 1B - Skin Irrit. 2

Storage Class

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

wgk_germany

WGK 1

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V Bours et al.
Oncogene, 9(6), 1699-1702 (1994-06-01)
RelB belongs to the family of Rel-related proteins, dimers of which determine NF-kappa B activity. The murine RelB protein has been reported to be a dimerizing partner in kappa B-binding complexes which are capable of transactivation. On the other hand
Sergio Vaira et al.
Proceedings of the National Academy of Sciences of the United States of America, 105(10), 3897-3902 (2008-03-07)
NF-kappaB inducing kinase (NIK) is required for osteoclastogenesis in response to pathologic stimuli, and its loss leads to functional blockade of both alternative and classical NF-kappaB caused by cytoplasmic retention by p100. We now show that deletion of p100 restores

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