RSK2 (D21B2) XP® Rabbit mAb (BSA and Azide Free) #99402
- WB
- IHC
- IF
- F
Supporting Data
REACTIVITY | H M R Mk B Pg |
SENSITIVITY | Endogenous |
MW (kDa) | 90 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
- B-Bovine
- Pg-Pig
Product Information
Product Usage Information
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.
Formulation
For standard formulation of this product see product #5528
Storage
Specificity / Sensitivity
Species Reactivity:
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Source / Purification
Background
Stimulation by various growth factors leads to activation of RSK2, which is a critical downstream effector kinase in several pathways. EGF stimulation leads to phosphorylation of CREB at Ser133 and phosphorylation of histone H3 in vivo by RSK2 (4,5). RSK2 phosphorylation of p53 may help regulate chromatin structure and cell cycle (6). RSK2 is prominently expressed in the brain and is essential for cognitive function and learning. During development, RSK2 regulates the differentiation of osteoblasts and skeletal muscle cells (7,8). Mutations in the corresponding gene are associated with Coffin-Lowry syndrome (CLS), an X-linked disorder characterized by mental retardation and the presence of characteristic facial anomalies (9).
- Fisher, T.L. and Blenis, J. (1996) Mol Cell Biol 16, 1212-9.
- Smith, J.A. et al. (1999) J Biol Chem 274, 2893-8.
- Dalby, K.N. et al. (1998) J Biol Chem 273, 1496-505.
- De Cesare, D. et al. (1998) Proc Natl Acad Sci U S A 95, 12202-7.
- Sassone-Corsi, P. et al. (1999) Science 285, 886-91.
- Cho, Y.Y. et al. (2005) Cancer Res 65, 3596-603.
- Yang, X. et al. (2004) Cell 117, 387-98.
- Cho, Y.Y. et al. (2007) J Biol Chem 282, 8380-92.
- Delaunoy, J.P. et al. (2006) Clin Genet 70, 161-6.
Limited Uses
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