research use only
Cat.No.: F4878
| Dilution |
|---|
|
| Application |
|---|
| WB, IP, IHC, ChIP |
| Reactivity |
|---|
| Mouse, Rat, Human |
| Source |
|---|
| Rabbit Monoclonal Antibody |
| Storage Buffer |
|---|
| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
|---|
| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW Observed MW |
|---|
| 48 kDa 50,70, 52 kDa |
| *Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. |
| Specificity |
|---|
| TEAD1 Antibody [H6K12] detects endogenous levels of total TEAD1 protein. |
| Clone |
|---|
| H6K12 |
| Synonym(s) |
|---|
| TCF13; TEF1; TEAD1; Transcriptional enhancer factor TEF-1; NTEF-1; Protein GT-IIC; TEA domain family member 1; Transcription factor 13; TEAD-1; TCF-13 |
| Background |
|---|
| TEAD1 is a member of the TEA domain (TEAD) family of transcription factors (TEAD1-4), which serve as key downstream effectors of the evolutionarily conserved Hippo signaling pathway that controls organ size, cell proliferation, and tumor suppression by regulating YAP/TAZ activity. Its N-terminal TEA DNA-binding domain (TEAD) adopts a three-helix bundle homeodomain fold, with key structural features including an L1 loop essential for cooperative binding to tandem M-CAT DNA sites, unstructured regions (e.g., residues 1–11, 24–31), and a hydrophobic core of 12 residues (e.g., Ile-13, Leu-21); chemical shift perturbations identify helix H3, L2 loop, and the back surface as the primary DNA-binding interface. TEAD1 primarily drives gene expression for cell proliferation and anti-apoptosis upon nuclear translocation of unphosphorylated YAP, forming YAP/TEAD1 complexes that bind TEA/ATTS consensus sequences to activate pro-growth genes, with critical roles in cardiac, skeletal, and smooth muscle development. In the Hippo-off state, YAP escapes LATS1/2 phosphorylation and 14-3-3 sequestration to enable this activity, while Hippo-on signaling inactivates it; TEAD1’s tissue-specific expression underscores its developmental importance. Dysregulated TEAD1 activity contributes to oncogenesis, as seen in YAP-driven hepatocellular carcinoma where dominant-negative TEAD1 suppresses tumorigenesis. |
| References |
|---|
|
Tel: +1-832-582-8158 Ext:3
If you have any other enquiries, please leave a message.