Upstream / Downstream

Explore pathways related to this product.

Antibody Guarantee

CST Antibody Performance Guarantee

LEARN MORE  

To Purchase # 7062S

7062S 300 µl (3 nmol) $249.00
$ 0. 00

Questions?

Find answers on our FAQs page.

ANSWERS  

Visit PhosphoSitePlus®

PTM information and tools available.

LEARN MORE

REACTIVITY
H

Western blot analysis of extracts from 293T cells, transfected with 100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-), SignalSilence® JMJD2B siRNA I #7435 (+), or SignalSilence® JMJD2B siRNA II (+), using JMJD2B (D7E6) Rabbit mAb #8639 (upper) or GAPDH (D16H11) XP® Rabbit mAb #5174 (lower). The JMJD2B (D7E6) Rabbit mAb confirms silencing of JMJD2B expression, while the GAPDH (D16H11) XP® Rabbit mAb is used as a loading control.

Learn more about how we got this image
Image

Order Details

Custom Ordering Details: This item is packaged to order. Please allow two to three days for your order to be processed and shipped.

Product Usage Information

CST recommends transfection with 100 nM SignalSilence® JMJD2B siRNA II 48 to 72 hours prior to cell lysis. For transfection procedure, follow protocol provided by the transfection reagent manufacturer. Please feel free to contact CST with any questions on use.

Each vial contains the equivalent of 100 transfections, which corresponds to a final siRNA concentration of 100 nM per transfection in a 24-well plate with a total volume of 300 μl per well.


Storage: SignalSilence® siRNA is supplied in RNAse-free water. Aliquot and store at -20ºC.

Product Description

SignalSilence® JMJD2B siRNA II from Cell Signaling Technology (CST) allows the researcher to specifically inhibit JMJD2B expression using RNA interference, a method whereby gene expression can be selectively silenced through the delivery of double stranded RNA molecules into the cell. All SignalSilence® siRNA products from CST are rigorously tested in-house and have been shown to reduce target protein expression by western analysis.


Quality Control

Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.

The methylation state of lysine residues in histone proteins is a major determinant of the formation of active and inactive regions of the genome and is crucial for proper programming of the genome during development (1,2). Jumonji C (JmjC) domain-containing proteins represent the largest class of potential histone demethylase proteins (3). The JmjC domain can catalyze the demethylation of mono-, di-, and tri-methyl lysine residues via an oxidative reaction that requires iron and α-ketoglutarate (3). Based on homology, both humans and mice contain at least 30 such proteins, which can be divided into 7 separate families (3). The jumonji domain-containing protein 2 (JMJD2) family, also known as the JmjC domain-containing histone demethylation protein 3 (JHDM3) family, contains four members: JMJD2A/JHDM3A, JMJD2B/JHDM3B, JMJD2C/JHDM3C, and JMJD2D/JHDM3D. In addition to the JmjC domain, these proteins also contain JmjN, PHD, and tudor domains, the latter of which has been shown to bind to methylated histone H3 at Lys4 and Lys9, and methylated histone H4 at Lys20 (4,5). JMJD2 proteins have been shown to demethylate di- and tri-methyl histone H3 at Lys9 and Lys36 and function as both activators and repressors of transcription (6-11). JMJD2A, JMJD2C, and JMJD2D function as coactivators of the androgen receptor in prostate tumor cells (7). In contrast, JMJD2A also associates with Rb and NCoR corepressor complexes and is necessary for transcriptional repression of target genes (8,9). JMJD2B antagonizes histone H3 Lys9 tri-methylation at pericentric heterochromatin (10). JMJD2C, also known as GASC1, is amplified in squamous cell carcinomas and metastatic lung carcinoma and inhibition of JMJD2C expression decreases cell proliferation (11,12). JMJD2C has also been identified as a downstream target of Oct-4 and is critical for the regulation of self-renewal in embryonic stem cells (13).


1.  Kubicek, S. et al. (2006) Ernst Schering Res. Found Workshop, 1-27.

2.  Klose, R.J. et al. (2006) Nat Rev Genet 7, 715-27.

3.  Lin, W. and Dent, S.Y. (2006) Curr. Opin. Genet. Dev. 16, 137-142.

4.  Chen, Z. et al. (2007) Proc Natl Acad Sci USA 104, 10818-23.

5.  Lee, J. et al. (2008) Nat Struct Mol Biol 15, 109-11.

6.  Whetstine, J.R. et al. (2006) Cell 125, 467-81.

7.  Shin, S. and Janknecht, R. (2007) Biochem Biophys Res Commun 359, 742-6.

8.  Gray, S.G. et al. (2005) J Biol Chem 280, 28507-18.

9.  Zhang, D. et al. (2005) Mol Cell Biol 25, 6404-14.

10.  Fodor, B.D. et al. (2006) Genes Dev 20, 1557-62.

11.  Cloos, P.A. et al. (2006) Nature 442, 307-11.

12.  Italiano, A. et al. (2006) Cancer Genet Cytogenet 167, 122-30.

13.  Loh, Y.H. et al. (2007) Genes Dev 21, 2545-57.


Entrez-Gene Id 23030
Swiss-Prot Acc. O94953


For Research Use Only. Not For Use In Diagnostic Procedures.
Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.
SignalSilence® is a trademark of Cell Signaling Technology, Inc.