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Description
SATB1 + SATB2 Recombinant Mouse mAb (S-3382)Product Specification Host Mouse Antigen SATB1+SATB2 Synonyms DNA binding protein SATB1; Special AT rich sequence binding protein 1; DNA binding protein SATB2; Special AT rich sequence binding protein 2 Location Nucleus Accession Q01826 Q9UPW6 Clone Number S 3382 Antibody Type Mouse mAb Isotype IgG1,k Application WB, ICC Reactivity Hu, Ms, Rt Positive Sample HT 1080, Saso 2, NIH 3T3, normal mouse E18 foetal brain Purification Protein G Concentration 2
Product Specification
| Host | Mouse |
| Antigen | SATB1+SATB2 |
| Synonyms | DNA-binding protein SATB1; Special AT-rich sequence-binding protein 1; DNA-binding protein SATB2; Special AT-rich sequence-binding protein 2 |
| Location | Nucleus |
| Accession | Q01826、 Q9UPW6 |
| Clone Number | S-3382 |
| Antibody Type | Mouse mAb |
| Isotype | IgG1,k |
| Application | WB, ICC |
| Reactivity | Hu, Ms, Rt |
| Positive Sample | HT-1080, Saso-2, NIH/3T3, normal mouse E18 foetal brain |
| Purification | Protein G |
| Concentration | 2 mg/ml |
| Conjugation | Unconjugated |
| Physical Appearance | Liquid |
| Storage Buffer | PBS, 40% Glycerol, 0.05% BSA, 0.03% Proclin 300 |
| Stability & Storage | 12 months from date of receipt / reconstitution, -20 °C as supplied |
Dilution
| application | dilution | species |
| WB | 1:1000 | Hu, Ms, Rt |
| ICC | 1:500 | Hu |
Background
SATB1 and SATB2 are evolutionarily related, chromatin-remodeling transcription factors that share a common CUT-domain architecture for high-affinity binding to matrix-attachment regions, yet they orchestrate distinct developmental programs: SATB1 acts as a global organizer of T-cell chromatin during thymocyte maturation and promotes breast-cancer metastasis through epithelial-to-mesenchymal transition, whereas SATB2 is indispensable for craniofacial patterning, cortical neuron identity, and osteoblast differentiation by forming higher-order chromatin loops that juxtapose enhancers of lineage-specific genes; both proteins recruit histone-modifying enzymes and the NuRD complex, but their mutually exclusive expression patterns and differential interaction partners explain why SATB1 depletion enhances neural differentiation while SATB2 loss yields cleft palate and intellectual disability, making the SATB1/SATB2 balance a critical epigenetic switch in immunity, neurodevelopment, and tumorigenesis.
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