Full Product Name
CCM2 siRNA (Mouse)
Product Synonym Names
OSM; Malcavernin; Cerebral cavernous malformations protein 2 homolog; Osmosensing scaffold for MEKK3
Product Gene Name
CCM2 sirna
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Research Use Only
For Research Use Only. Not for use in diagnostic procedures.
3D Structure
ModBase 3D Structure for Q8K2Y9
Specificity
CCM2 siRNA (Mouse) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
Purity/Purification
> 97%
Form/Format
Lyophilized powder
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.
Directions for Use
We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
Components
We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of mouse CCM2 gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
Preparation and Storage
Shipped at 4 degree C. Store at -20 degree C for one year.
Negative Control
siRNA Negative Control (Catalog# MBS8241404) is a non-targeting 21 nt siRNA recommended as a negative control for experiments using targeted siRNA transfection.
Other Notes
Small volumes of CCM2 sirna vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.
Related Product Information for
CCM2 sirna
siRNA to inhibit CCM2 expression using RNA interference
Applications Tested/Suitable for CCM2 sirna
RNA Interference (RNAi)
NCBI/Uniprot data below describe general gene information for CCM2. It may not necessarily be applicable to this product.
NCBI Accession #
NP_666126.1
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NCBI GenBank Nucleotide #
NM_146014.3
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UniProt Primary Accession #
Q8K2Y9
[Other Products]
UniProt Secondary Accession #
Q5SUA3[Other Products]
UniProt Related Accession #
Q8K2Y9[Other Products]
Molecular Weight
48,248 Da
NCBI Official Full Name
cerebral cavernous malformations protein 2 homolog isoform 1
NCBI Official Synonym Full Names
cerebral cavernous malformation 2
NCBI Official Symbol
Ccm2??[Similar Products]
NCBI Official Synonym Symbols
BC029157
??[Similar Products]
NCBI Protein Information
cerebral cavernous malformations protein 2 homolog
UniProt Protein Name
Cerebral cavernous malformations protein 2 homolog
UniProt Synonym Protein Names
Malcavernin
Protein Family
Cerebral cavernous malformations protein
UniProt Gene Name
Ccm2??[Similar Products]
UniProt Synonym Gene Names
Osm??[Similar Products]
UniProt Entry Name
CCM2_MOUSE
UniProt Comments for CCM2
CCM2: Component of the CCM signaling pathway which is a crucial regulator of heart and vessel formation and integrity. May act through the stabilization of endothelial cell junctions. May function as a scaffold protein for MAP2K3-MAP3K3 signaling. Seems to play a major role in the modulation of MAP3K3- dependent p38 activation induced by hyperosmotic shock. Defects in CCM2 are the cause of cerebral cavernous malformations type 2 (CCM2). Cerebral cavernous malformations (CCMs) are congenital vascular anomalies of the central nervous system that can result in hemorrhagic stroke, seizures, recurrent headaches, and focal neurologic deficits. CCMs have an incidence of 0.1%-0.5% in the general population and are usually present clinically during the 3rd to 5th decades of life. The lesions are characterized by grossly enlarged blood vessels consisting of a single layer of endothelium and without any intervening neural tissue, ranging in diameter from a few millimeters to several centimeters. 2 isoforms of the human protein are produced by alternative splicing.
Protein type: Adaptor/scaffold; Motility/polarity/chemotaxis
Cellular Component: protein complex; cytoplasm
Molecular Function: protein binding
Biological Process: blood vessel development; pericardium development; intercellular junction assembly and maintenance; venous blood vessel morphogenesis; vasculature development; in utero embryonic development; multicellular organism growth; heart development; vasculogenesis; inner ear development; endothelial cell development
Research Articles on CCM2
1. Down-modulation of STK25, but not STK24, rescued medulloblastoma cells from NGF-induced TrkA-dependent cell death, suggesting that STK25 is part of the death-signaling pathway initiated by TrkA and CCM2.
Precautions
All of MyBioSource's Products are for scientific laboratory research purposes and are not for diagnostic, therapeutics, prophylactic or in vivo use. Through your purchase, you expressly represent and warrant to MyBioSource that you will properly test and use any Products purchased from MyBioSource in accordance with industry standards. MyBioSource and its authorized distributors reserve the right to refuse to process any order where we reasonably believe that the intended use will fall outside of our acceptable guidelines.
Disclaimer
While every efforts were made to ensure the accuracy of the information provided in this datasheet, MyBioSource will not be liable for any omissions or errors contained herein. MyBioSource reserves the right to make changes to this datasheet at any time without prior notice.
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