Description
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 2 bp deletion in exon 1
Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-FAM162A, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
FAM162A also known as protein family with sequence similarity 162 member A is a mitochondrial protein that plays a role in cellular apoptosis. It has a molecular mass of approximately 16-20 kDa. This protein is widely expressed in various tissues with notable expression in the heart brain and liver. FAM162A is an integral part of the mitochondrial inner membrane suggesting its involvement in mitochondrial-related processes.
Biological function summary
FAM162A is involved in promoting apoptosis through the intrinsic mitochondrial pathway. It assists in the release of cytochrome c from mitochondria which then activates caspase cascades. FAM162A does not appear to function as part of a larger protein complex; rather it operates independently to exert its pro-apoptotic effects. Its expression levels increase in response to hypoxic conditions indicating a specific role in hypoxia-induced apoptosis.
Pathways
FAM162A significantly impacts the apoptosis and hypoxia response pathways. In these pathways it interacts with proteins like cytochrome c and apoptosome components. Its action in the mitochondrial pathway suggests its role in regulating cell death in response to cellular stress making it an important component of the intrinsic apoptotic signaling pathway. FAM162A might also interplay with anti-apoptotic proteins such as Bcl-2 influencing the balance between cell survival and death.
FAM162A is linked to neurodegenerative diseases like Alzheimer's and ischemic stroke. Its role in apoptosis especially under hypoxic conditions leads to neuronal cell death in these disorders. For instance FAM162A overexpression under hypoxia can worsen cellular damage in stroke by promoting unnecessary apoptosis. It is also connected with other apoptotic proteins such as caspase-3 an executor caspase which highlights its role in exacerbating neuronal death during pathologies associated with excessive apoptosis.
