Abcam, ab269470, Human SMAD5 knockout HEK-293 cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
SMAD5 KO cell line available to order. KO validated by Next Generation Sequencing. Free of charge wild type control available. Knockout achieved by CRISPR/Cas9; X = 1 bp insertion, 2 bp deletion, 4 bp deletion, 20 bp deletion, 11 bp deletion. 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-293,
Species or organism:Human,
Tissue:Kidney,
Form:LiquidSee storage information,
Knockout validation:Next Generation Sequencing,
Mutation description:Knockout achieved by CRISPR/Cas9; X = 1 bp insertion, 2 bp deletion, 4 bp deletion, 20 bp deletion, 11 bp deletion

Product details:
We will provide viable cells that proliferate on revival.
Western blot data indicates that the CRISPR gene edit may have resulted in a truncation of the protein of interest. Please see data images.
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-SMAD5, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Next Generation 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.
SMAD5 also known as Mothers Against Decapentaplegic Homolog 5 is a protein involved in the signal transduction regulated by the transforming growth factor-beta (TGF-beta) superfamily of cytokines. This protein has a molecular mass of approximately 52 kDa and is ubiquitously expressed across various tissues. Mechanically SMAD5 functions as an intracellular mediator that translocates from the cytoplasm to the nucleus upon activation to regulate transcription. It participates actively in transmitting signals from surface receptors into the nucleus influencing gene expression.
Biological function summary
SMAD5 plays a central role in the bone morphogenetic protein (BMP) signaling pathway which is critical for embryonic development and tissue homeostasis. It forms a complex with receptor-regulated SMADs (R-SMADs) and co-SMAD (SMAD4) upon phosphorylation by BMP type I receptors. This complex then moves to the nucleus where it regulates expression of target genes. Through this mechanism SMAD5 impacts processes such as bone formation differentiation and cellular differentiation.
Pathways
Several key cellular signaling processes involve SMAD5. Primarily it contributes to the BMP pathway which is integral to skeletal development and repair. SMAD5 interacts with other SMAD proteins like SMAD1 and SMAD8 which all act downstream of the BMP receptors. Additionally SMAD5 participates in crosstalk with the TGF-beta signaling pathway enabling the fine-tuning of cellular responses to a variety of external cues. This connection places SMAD5 within a network of signaling events important for regulating different cell functions and maintaining cellular homeostasis.
SMAD5's function has links to abnormal bone and cartilage development such as in fibrodysplasia ossificans progressiva (FOP) and pulmonary hypertension (PH). These conditions occur due to dysregulation within the BMP signaling pathway. For example mutations in SMAD5 or its regulatory proteins can cause inappropriate signal propagation leading to ossification in FOP or altered vascular remodeling in PH. The interplay between SMAD5 and SMAD4 another key player in these pathways highlights the complex nature of SMAD-related pathologies.