Abcam, ab265649, Human SERTAD3 knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
SERTAD3 KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, 17 bp deletion in exon 2 and 1 bp insertion 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, 17 bp deletion in exon 2 and 1 bp insertion 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-SERTAD3, 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.
The SERTAD3 protein also known as SEI1 or TRIP-Br1 acts mechanically by serving as a transcriptional regulator. It has a mass of approximately 33 kDa. SERTAD3 is expressed in various human tissues with increased levels in the heart brain and skeletal muscle. It engages in interactions with other transcription factors which modulate cell cycle progression and proliferation.
Biological function summary
SERTAD3 plays a role in cellular growth and division processes. As a part of multi-protein complexes it interacts with cyclin-dependent kinase 4 (CDK4) and cyclin D1. This interaction helps regulate the cell cycle particularly influencing the transition from the G1 to the S phase. SERTAD3 contributes significantly to controlling cell division making it important for maintaining normal cellular homeostasis.
Pathways
Several aspects of cell cycle regulation involve SERTAD3. It is an important participant in the cyclin D-CDK4/6 signaling pathway which is necessary for cell cycle progression. SERTAD3 interacts with retinoblastoma protein (pRB) through this pathway impacting its phosphorylation status and thereby influencing cell cycle control. The interaction helps facilitate proper DNA synthesis and replication.
SERTAD3 has connections to certain cancers and cardiovascular diseases. Overexpression of SERTAD3 has been observed in some cancers such as breast cancer which suggests its role in facilitating uncontrolled cellular proliferation. In this context it interacts closely with proteins like pRB affecting pathways that lead to tumorigenesis. Additionally its regulation of cell cycle processes implies potential involvement in heart diseases where abnormal cell cycle re-entry is a concern.