SMAD5 KO cell lysate available now. KO validated by Next Generation Sequencing. Free of charge wild type control included. Knockout achieved by CRISPR/Cas9; X = 1 bp insertion, 2 bp deletion, 4 bp deletion, 20 bp deletion, 11 bp deletion.
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SMAD5 KO cell lysate available now. KO validated by Next Generation Sequencing. Free of charge wild type control included. Knockout achieved by CRISPR/Cas9; X = 1 bp insertion, 2 bp deletion, 4 bp deletion, 20 bp deletion, 11 bp deletion.
Knockout cell lysate achieved by CRISPR/Cas9.
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Lysate preparation: Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10). This means that the protein of interest is denatured. If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions: Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
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 and patent pages.
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.
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.
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.
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