Datasheet

生物学的記述

Specificity	TEAD1 Antibody [H6K12] detects endogenous levels of total TEAD1 protein.
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.

Specificity

TEAD1 Antibody [H6K12] detects endogenous levels of total TEAD1 protein.

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.

使用情報

Application

WB, IP, IHC, ChIP

Dilution

WB	IP	IHC	CHIP
1:1000 - 1:10000	1:10 - 1:100	1:1000	1:2000

Reactivity

Mouse, Rat, Human

Source

Rabbit Monoclonal Antibody

MW

48 kDa

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

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/28964625/
https://pubmed.ncbi.nlm.nih.gov/36484096/

TEAD1 Antibody [H6K12]

生物学的記述

使用情報

References

Application Data