Description
Key facts
Cell type:MCF7,
Species or organism:Human,
Tissue:Breast,
Form:LiquidSee storage information,
Knockout validation:Next Generation Sequencing,
Mutation description:Knockout achieved by CRISPR/Cas9; X = 1 bp insertion; Frameshift: 98%,
Disease:Adenocarcinoma
Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-CD55, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Next Generation Sequencing, Shipped at conditions-Dry Ice, Appropriate short-term storage duration-1-2 weeks, Appropriate short-term storage conditions--196°C, -80°C, Appropriate long-term storage conditions--196°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
CD55 also known as Decay-Accelerating Factor (DAF) is a glycoprotein that regulates the complement cascade. This protein typically weighs around 70 kDa. It is expressed in many cells including epithelial and endothelial cells and is often present on the surface of blood cells. CD55 plays an important role in protecting cells against lysis by inhibiting the formation and stability of C3 and C5 convertases which ultimately prevent cell destruction by the complement system.
Biological function summary
CD55 helps maintain immune homeostasis by preventing the complement-mediated damage to host tissues. It functions as a member of the regulators of complement activation (RCA) family. While not necessarily part of a larger protein complex its function is related to other regulatory proteins such as CD46 and CD59 which cooperate to regulate complement activity. The DAF protein's immunology function is instrumental in ensuring that self-cells are not inadvertently attacked by the body's immune system.
Pathways
CD55 significantly impacts the complement pathway which is a central component of the innate immune system. It directly interacts with complement components C3 and C5 accelerating their decay and disassembly. Through this pathway CD55 has a working relationship with other complement regulatory proteins like Factor H which also aids in controlling complement activation on the cell surface.
A dysfunctional CD55 can relate to conditions such as paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS). In PNH the absence or insufficiency of CD55 (and CD59) on red blood cells leads to complement-mediated lysis causing hemolytic anemia. In aHUS impaired regulation of the complement system including abnormalities in CD55 function exacerbates symptoms. CD55's role is therefore important in preventing these complement-related disorders and preserving cellular integrity in the human body.
