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Description
SMAD2-Knockout HeLa Cell LysateProduct Specification Host Human Mutations 165bp deletion in exon1 and exon2 Application WB Concentration 2 mg ml Physical Appearance Liquid Storage Buffer Supplied in SDS Sample Buffer: 50 mM Tris HCl (pH 6. 8 at 25C), 2% w v SDS, 10% glycerol, 1% v v Mercaptoethanol, 0. 01% w v bromophenol blue or phenol red. Stability & Storage 20 C for 1 months under sterile conditions; 80 C for 24 months under sterile conditions. Please avoid repeated freeze thaw
Product Specification
| Host | Human |
| Mutations | 165bp deletion in exon1 and exon2 |
| Application | WB |
| Concentration | 2 mg/ml |
| Physical Appearance | Liquid |
| Storage Buffer | Supplied in SDS Sample Buffer: 50 mM Tris-HCl (pH 6.8 at 25°C), 2% w/v SDS, 10% glycerol, 1% v/v β-Mercaptoethanol, 0.01% w/v bromophenol blue or phenol red. |
| Stability & Storage | -20 °C for 1 months under sterile conditions; |
Background
SMAD2, also known as MADR2 or JV18-1, is a 58 kDa signaling protein widely expressed in various tissues, including epithelial and mesenchymal cells. It functions as a central intracellular mediator of the transforming growth factor-beta (TGF-β) receptor signaling pathway. Upon TGF-β stimulation, SMAD2 undergoes phosphorylation at serine residues, converting it into its active phosphorylated form. This activated SMAD2 then forms a heteromeric complex with SMAD4, which translocates into the nucleus. Within the nucleus, the complex binds to specific DNA sequences and regulates the transcription of target genes involved in critical biological processes such as cell proliferation, differentiation, apoptosis, and extracellular matrix production. Furthermore, SMAD2 is a key component of the activin receptor signaling pathway and cooperates with other proteins like SMAD3 to precisely modulate cellular responses to external stimuli, thereby maintaining cellular homeostasis. Dysregulation of SMAD2 signaling is closely associated with various pathological conditions, including fibrosis and cancer, where its excessive activation promotes fibrotic tissue deposition and tumor progression. Therefore, a deeper understanding of the regulatory mechanisms of SMAD2 is essential for developing therapeutic strategies targeting these diseases.
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