Description
Key facts
Cell type:SW480,
Species or organism:Human,
Tissue:Colon,
Form:LiquidSee storage information,
Knockout validation:Next Generation Sequencing,
Mutation description:Knockout achieved by CRISPR/Cas9 X = 16 bp deletion Frameshift = 100%,
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-BID, 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.
Bid also known as BH3-interacting domain death agonist or BID protein functions as a pro-apoptotic member of the Bcl-2 protein family. This protein plays a significant role in the apoptotic process by helping to mediate the release of cytochrome c from mitochondria an important step in this cell death pathway. Bid exists in cells as an inactive uncleaved form but upon activation a caspase cleaves it into a truncated form tBID. The molecular weight of Bid is approximately 22 kDa. It is commonly expressed in numerous tissues throughout the body contributing to its various apoptotic regulatory roles.
Biological function summary
Bid induces mitochondria-mediated apoptosis that significantly affects cellular homeostasis. Bid is not considered to be part of a permanent protein complex; instead it acts as a mobile activator bridging interactions between different proteins within the apoptotic pathway. Upon activation tBID interacts with other Bcl-2 family members like Bax and Bak which leads to mitochondrial membrane permeabilization and subsequent release of cytochrome c.
Pathways
Bid significantly influences apoptotic signaling under different cellular stress conditions. It plays important functions in both intrinsic and extrinsic pathways of apoptosis. Within the intrinsic pathway Bid links the external death receptor signals to the mitochondria-mediated apoptotic pathway. In addition to interacting with Bax and Bak Bid indirectly connects to the apoptosome complex facilitating caspase activation which ultimately results in cellular apoptosis.
Bid has strong associations with conditions characterized by deregulated apoptosis such as cancer and neurodegenerative diseases. For instance downregulation or dysfunction of Bid is noted in certain cancer types contributing to the evasion of apoptosis a hallmark of cancer. Moreover in neurodegenerative diseases where excess apoptosis leads to loss of neuronal cells Bid activity has shown to connect with the regulation of apoptosis through its interactions with key apoptotic proteins such as Bcl-2 and Bax. Understanding Bid's role provides potential therapeutic targets to either promote or inhibit apoptotic processes in disease treatment.
