CFH sirna

CFH siRNA (Mouse)

Cat. Num. AAA8236980

• Gene Names: Cfh; NOM; Sas1; Mud-1; Sas-1
• Reactivity: Mouse
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: CFH; CFH siRNA (Mouse); HF1; Complement factor H; Protein beta-1-H; CFH sirna

• Host: Synthetic
• Reactivity: Mouse
• Specificity: CFH 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
• Sequence Length: 1,234

• Applicable Applications for CFH sirna: RNA Interference (RNAi)
• 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 CFH 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.

Related Product Information for CFH sirna

siRNA to inhibit CFH expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 109627652
• NCBI GeneID: 12628
• NCBI Accession #: NP_034018.2
• NCBI GenBank Nucleotide #: NM_009888.3
• UniProt Accession #: P06909; Q6NZK3
• Molecular Weight: 139,138 Da
• NCBI Official Full Name: complement factor H
• NCBI Official Synonym Full Names: complement component factor h
• NCBI Official Symbol: Cfh
• NCBI Official Synonym Symbols: NOM; Sas1; Mud-1; Sas-1
• NCBI Protein Information: complement factor H
• UniProt Protein Name: Complement factor H
• Protein Family: Complement factor
• UniProt Gene Name: Cfh
• UniProt Synonym Gene Names: Hf1
• UniProt Entry Name: CFAH_MOUSE

Uniprot Description

CFH: Factor H functions as a cofactor in the inactivation of C3b by factor I and also increases the rate of dissociation of the C3bBb complex (C3 convertase) and the (C3b)NBB complex (C5 convertase) in the alternative complement pathway. Genetic variations in CFH are associated with basal laminar drusen (BLD); also known as drusen of Bruch membrane or cuticular drusen or grouped early adult-onset drusen. Drusen are extracellular deposits that accumulate below the retinal pigment epithelium on Bruch membrane. Basal laminar drusen refers to an early adult-onset drusen phenotype that shows a pattern of uniform small, slightly raised yellow subretinal nodules randomly scattered in the macula. In later stages, these drusen often become more numerous, with clustered groups of drusen scattered throughout the retina. In time these small basal laminar drusen may expand and ultimately lead to a serous pigment epithelial detachment of the macula that may result in vision loss. Defects in CFH are the cause of complement factor H deficiency (CFHD). A disorder that can manifest as several different phenotypes, including asymptomatic, recurrent bacterial infections, and renal failure. Laboratory features usually include decreased serum levels of factor H, complement component C3, and a decrease in other terminal complement components, indicating activation of the alternative complement pathway. It is associated with a number of renal diseases with variable clinical presentation and progression, including membranoproliferative glomerulonephritis and atypical hemolytic uremic syndrome. Defects in CFH are a cause of susceptibility to hemolytic uremic syndrome atypical type 1 (AHUS1). An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype. Genetic variation in CFH is associated with age-related macular degeneration type 4 (ARMD4). ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid (known as drusen) that lie beneath the retinal pigment epithelium and within an elastin- containing structure known as Bruch membrane. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Secreted, signal peptide; Secreted

Cellular Component: extracellular space; cytoplasm; extracellular region; plasma membrane; nucleus

Molecular Function: heparin binding; heparan sulfate proteoglycan binding; complement component C3b binding

Biological Process: immune system process; complement activation, alternative pathway; regulation of complement activation; innate immune response