Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: Insertion of the selection cassette in exon 1,
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-FADD, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Zygosity-Homozygous, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
FADD also known as Fas-Associated protein with Death Domain is an adaptor molecule with a molecular weight of approximately 23 kDa. It plays a critical role in the transmission of apoptotic signals. FADD is widely expressed in various tissues particularly in the thymus and immune system cells. This protein serves as a bridge linking death receptors like Fas and TNFR-1 with caspase activation pathways.
Biological function summary
FADD is essential in apoptosis where it assists in the assembly of the death-inducing signaling complex (DISC). Upon receptor activation FADD recruits procaspase-8 or -10 to DISC promoting their autocatalytic cleavage and activation. This leads to the subsequent cascade that results in cell apoptosis. FADD also plays a role in necroptosis and is involved in the immune response regulation highlighting its multifunctional nature in cellular processes.
Pathways
FADD integrates into the apoptotic and necroptotic pathways. In the apoptotic pathway it interacts closely with Fas a death receptor to promote caspase-8 activation. Additionally in the necroptotic pathway FADD associates with RIP1 and RIP3 contributing to an alternative form of programmed cell death. These interactions underline its significant role in controlling cell fate decisions.
Aberrations in FADD function are associated with cancer and autoimmune diseases. Overexpression or mutation of FADD can lead to unchecked cell proliferation or defective apoptosis contributing to cancer development. In autoimmune disorders improper regulation of FADD may disrupt immune tolerance and lead to systemic inflammation. Key proteins involved in these disease processes include caspase-8 and RIPK1 which interact with FADD in regulating cell death and survival mechanisms.
