Abcam, ab265971, Human SENP5 knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
SENP5 KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, 2 bp insertion in exon 2 and Insertion of the selection cassette in exon 2. To order both knockout and wild-type control cells: select 2 x 1000000Cells/vial. To order only knockout cells: select 1000000Cells/vial.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 2 bp insertion in exon 2 and Insertion of the selection cassette in exon 2,
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-SENP5, 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.
SENP5 also known as SUMO-specific protease 5 is an enzyme involved in the processing and deconjugation of SUMO proteins. It has an approximate mass of 82 kDa. SENP5 is expressed mainly in the heart skeletal muscle and to a lesser extent in the testis. This enzyme functions by cleaving SUMO from target proteins enabling the regulation of protein function and localization. It plays a significant role in maintaining cellular homeostasis by reversing the small ubiquitin-like modifier (SUMO) modification cycle.
Biological function summary
SENP5 removes SUMO modifications from proteins involved in cellular processes such as mitotic progression and mitochondrial dynamics. It is not part of a complex but interacts with various cellular proteins to facilitate its role in SUMOylation regulation. By controlling the SUMOylation status SENP5 influences cell cycle progression and cellular stress responses. SENP5 also contributes to mitochondrial morphology by modifying proteins related to mitochondrial fission and fusion processes.
Pathways
SENP5 interacts within the SUMOylation pathway and the mitochondrial pathway. In the SUMOylation pathway SENP5 works alongside other SENP family proteins such as SENP1 and SENP2 which share similar functional roles in SUMO processing. In the mitochondrial pathway SENP5 is linked to the regulation of proteins like DRP1 which is essential for mitochondrial fission. The interactions in these pathways demonstrate SENP5's significant role in cellular homeostasis and energy metabolism.
SENP5's dysregulation has been associated with cardiomyopathy and certain types of cancer. In cardiomyopathy altered SENP5 activity can lead to disrupted mitochondrial dynamics and impaired cardiac function. Its interaction with mitochondrial proteins such as DRP1 illustrates its importance in cardiac cell health. In cancer SENP5's role in cell cycle regulation is important as alterations can lead to uncontrolled cell proliferation. SENP5's interaction with proteins involved in the cell cycle highlights its potential impact on tumor growth and development.