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, 11 bp deletion in exon 2 and Insertion of the selection cassette in exon 2
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-AKAP1, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
A-kinase anchoring protein 1 (AKAP1) also known as AKAP121 or D-AKAP1 is a protein that serves as an anchor point for signaling molecules. AKAP1 is approximately 121 kDa in mass. It is an important player in coordinating cellular processes by anchoring protein kinase A (PKA) to specific cellular compartments such as mitochondria. The protein is mainly expressed in the heart liver and brain but also found in other tissues indicating its broad role in cellular function.
Biological function summary
AKAP1 connects with several components to influence cellular signaling pathways and energy metabolism. It is a part of a complex network that involves mitochondrial targeting sequences which guide proteins to correct mitochondrial compartments. AKAP1 helps regulate processes like mitochondrial dynamics apoptosis and oxidative phosphorylation. These functions ensure efficient cellular energy production and maintenance of cellular health.
Pathways
AKAP1 engages in both the cAMP-dependent and mitochondrial signaling pathways. In the cAMP-dependent pathway AKAP1 interacts with PKA to modulate phosphorylation events that alter cellular responses to external signals. The mitochondrial pathway involves communication with proteins like Drp1 influencing mitochondrial fission and fusion processes. These interactions highlight AKAP1's central role in maintaining cellular energy balance and integrity.
Certain pathways involving AKAP1 link closely with neurodegenerative diseases such as Alzheimer's and cardiac disorders. During neurodegeneration AKAP1-related mitochondrial dysfunction can lead to energy deficits and increased oxidative stress contributing to disease progression. Additionally in cardiac health dysregulation of AKAP1 interactions with PKA can affect heart muscle contractility and lead to cardiac anomalies. Understanding these connections offers insights into potential therapeutic avenues for targeting such diseases.
