Abcam, ab266326, Human SMAD9 knockout HEK-293T cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
SMAD9 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 8 bp deletion 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:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 17 bp deletion in exon 2 and 8 bp deletion 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 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-SMAD9, 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.
SMAD9 also known as Mothers against decapentaplegic homolog 9 or MADH9 is a transcription factor involved in signal transduction and transcriptional activity. It has a molecular mass of approximately 50 kDa. SMAD9 is widely expressed in various tissues including the heart brain and skeletal muscle. In its mechanical function SMAD9 becomes activated through phosphorylation by type I receptor serine/threonine kinases and forms part of the SMAD protein family that transmits extracellular signals to the nucleus affecting gene expression.
Biological function summary
SMAD9 plays a role in the cellular processes of growth and differentiation particularly within the bone morphogenetic protein (BMP) signaling pathway. It operates as part of a complex with other SMAD proteins such as SMAD1 and SMAD5 forming heteromeric complexes that regulate the transcription of BMP-responsive genes. This gene transcription is vital for the development and repair of tissues as well as the maintenance of cellular homeostasis.
Pathways
SMAD9 participates significantly in the BMP and transforming growth factor-beta (TGF-β) signaling pathways. These pathways are important for a variety of cellular responses including proliferation apoptosis and differentiation. SMAD9 associates with BMP receptors to mediate the BMP signaling cascade acting synergistically with other SMAD family members like SMAD4 which is a common mediator in these pathways. This interrelation places SMAD9 at a pivotal point within the regulation of multiple cellular responses.
Research indicates that SMAD9 mutations or dysregulation can associate with pulmonary arterial hypertension (PAH) and certain forms of cancer. In PAH altered SMAD9 signaling disrupts normal vascular remodeling resulting in elevated pulmonary artery pressure. Additionally it can interact with other proteins like BMPR2 a receptor for BMP which also plays a significant role in the pathogenesis of PAH. Understanding the involvement of SMAD9 in these conditions can provide insights into potential therapeutic targets for treatment.