TEAD1 — TEA Domain Transcription Factor 1

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TEAD1 — TEA Domain Transcription Factor 1

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TEAD1 — TEA Domain Transcription Factor 1

Introduction

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">TEAD1 — TEA Domain Transcription Factor 1</th>
</tr>
<tr>
<td class="label">Gene Symbol</td>
<td>TEAD1</td>
</tr>
<tr>
<td class="label">Full Name</td>
<td>TEA Domain Transcription Factor 1</td>
</tr>
<tr>
<td class="label">Alternative Names</td>
<td>TEF-1, ETF, NTEF, TEAD</td>
</tr>
<tr>
<td class="label">Chromosomal Location</td>
<td>11p15.4</td>
</tr>
<tr>
<td class="label">NCBI Gene ID</td>
<td>7003</td>
</tr>
<tr>
<td class="label">Ensembl ID</td>
<td>ENSG00000187091</td>
</tr>
<tr>
<td class="label">UniProt ID</td>
<td>P28347</td>
</tr>
<tr>
<td class="label">OMIM</td>
<td>189892</td>
</tr>
<tr>
<td class="label">Protein Class</td>
<td>Transcription factor; Hippo pathway effector</td>
</tr>
<tr>
<td class="label">Associated Diseases</td>
<td>Alzheimer's disease, Parkinson's disease, cancer, Svevo syndrome</td>
</tr>
<tr>
<td class="label">Interactor</td>
<td>Interaction Type</td>
</tr>
<tr>
<td class="label">YAP</td>
<td>Direct binding</td>
</tr>
<tr>
<td class="label">TAZ</td>
<td>Direct binding</td>
</tr>
<tr>
<td class="label">LATS1/2</td>
<td>Upstream regulation</td>
</tr>
<tr>
<td class="label">MST1/2</td>
<td>Upstream regulation</td>
</tr>
<tr>
<td class="label">VGLL proteins</td>
<td>Comp

...

TEAD1 — TEA Domain Transcription Factor 1

Introduction

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">TEAD1 — TEA Domain Transcription Factor 1</th>
</tr>
<tr>
<td class="label">Gene Symbol</td>
<td>TEAD1</td>
</tr>
<tr>
<td class="label">Full Name</td>
<td>TEA Domain Transcription Factor 1</td>
</tr>
<tr>
<td class="label">Alternative Names</td>
<td>TEF-1, ETF, NTEF, TEAD</td>
</tr>
<tr>
<td class="label">Chromosomal Location</td>
<td>11p15.4</td>
</tr>
<tr>
<td class="label">NCBI Gene ID</td>
<td>7003</td>
</tr>
<tr>
<td class="label">Ensembl ID</td>
<td>ENSG00000187091</td>
</tr>
<tr>
<td class="label">UniProt ID</td>
<td>P28347</td>
</tr>
<tr>
<td class="label">OMIM</td>
<td>189892</td>
</tr>
<tr>
<td class="label">Protein Class</td>
<td>Transcription factor; Hippo pathway effector</td>
</tr>
<tr>
<td class="label">Associated Diseases</td>
<td>Alzheimer's disease, Parkinson's disease, cancer, Svevo syndrome</td>
</tr>
<tr>
<td class="label">Interactor</td>
<td>Interaction Type</td>
</tr>
<tr>
<td class="label">YAP</td>
<td>Direct binding</td>
</tr>
<tr>
<td class="label">TAZ</td>
<td>Direct binding</td>
</tr>
<tr>
<td class="label">LATS1/2</td>
<td>Upstream regulation</td>
</tr>
<tr>
<td class="label">MST1/2</td>
<td>Upstream regulation</td>
</tr>
<tr>
<td class="label">VGLL proteins</td>
<td>Competition</td>
</tr>
<tr>
<td class="label">p300</td>
<td>Coactivator</td>
</tr>
<tr>
<td class="label">Interactor</td>
<td>Interaction Type</td>
</tr>
<tr>
<td class="label">YAP</td>
<td>Direct binding</td>
</tr>
<tr>
<td class="label">TAZ</td>
<td>Direct binding</td>
</tr>
<tr>
<td class="label">LATS1/2</td>
<td>Upstream regulation</td>
</tr>
<tr>
<td class="label">MST1/2</td>
<td>Upstream regulation</td>
</tr>
<tr>
<td class="label">VGLL proteins</td>
<td>Competition</td>
</tr>
<tr>
<td class="label">p300</td>
<td>Coactivator</td>
</tr>
<tr>
<td class="label">Species</td>
<td>Identity</td>
</tr>
<tr>
<td class="label">Human</td>
<td>Reference</td>
</tr>
<tr>
<td class="label">Mouse</td>
<td>97%</td>
</tr>
<tr>
<td class="label">Zebrafish</td>
<td>75%</td>
</tr>
<tr>
<td class="label">Drosophila</td>
<td>60%</td>
</tr>
<tr>
<td class="label">Agent</td>
<td>Target</td>
</tr>
<tr>
<td class="label">K-975</td>
<td>TEAD1 palmitoylation</td>
</tr>
<tr>
<td class="label">Verteporfin</td>
<td>YAP-TEAD</td>
</tr>
<tr>
<td class="label">MDM2 inhibitors</td>
<td>YAP degradation</td>
</tr>
</table>

TEAD1 (TEA Domain Transcription Factor 1), also known as transcription factor TEAD-1 or NTEF-1, is a member of the TEA domain (TEA/ATTS) transcription factor family. TEAD1 is a key effector of the Hippo signaling pathway and plays critical roles in development, tissue homeostasis, and cell fate determination. In the nervous system, TEAD1 regulates neurogenesis, neuronal survival, synaptic function, and is implicated in neurodegenerative diseases including Alzheimer's disease and Parkinson's disease[@kakumoto2016].

Gene and Protein Structure

Gene Location

Gene Structure

The TEAD1 gene spans approximately 50 kb and consists of 16 exons encoding a 426-amino acid protein. The gene undergoes alternative splicing to generate multiple isoforms with tissue-specific expression patterns:

TEAD1-1 — Full-length isoform (426 aa), ubiquitous expression
TEAD1-2 — Alternative splicing isoform with different C-terminus
TEAD1-3 — Brain-enriched isoform
TEAD1-4 — Muscle-specific isoform

Protein Structure

TEAD1 contains distinct functional domains:

TEA Domain (1-60)

DNA-binding domain
Recognizes MCAT consensus sequences (5'-CTTYWAY-3')
Also called ATTS domain
Mediates nuclear localization and protein-protein interactions

Transcriptional Activation Domain (60-200)

Mediates interaction with co-activators
Contains YAP/TAZ binding site (200-400)
Proline-rich region

YAP/TAZ Binding Domain (200-350)

Critical for Hippo pathway signaling
Forms complex with YAP/TAZ
Regulated by Hippo pathway kinases

C-terminal Domain (350-426)

Dimerization interface
Protein-protein interactions
Regulatory modifications

Post-Translational Modifications

TEAD1 activity is regulated by several modifications:

Phosphorylation: Tyrosine and serine phosphorylation affects DNA binding and interactions
Acetylation: Lysine acetylation modulates transcriptional activity
Sumoylation: SUMO modification influences nuclear-cytoplasmic trafficking
Ubiquitination: Regulates protein stability and degradation

Function

Hippo Pathway Signaling

TEAD1 is the central effector of the Hippo pathway[@pan2019]:

YAP/TAZ partnership — Forms transcriptional complexes with YAP/TAZ
DNA binding — TEAD1 binds DNA, YAP/TAZ provide transcriptional activation
Target gene regulation — Controls genes for proliferation, survival, differentiation
Pathway crosstalk — Interacts with Wnt, Notch, and TGF-β pathways

Cell Proliferation Control

TEAD1 regulates cell cycle genes[@arrington2017]:

Cyclin expression — Controls cyclin D1, cyclin E
Cell cycle arrest — Mediates contact inhibition
Proliferation signals — Responds to growth factor signaling
Tissue size control — Limits organ size through Hippo activation

Cell Survival

TEAD1 influences apoptosis and survival[@wang2018]:

Anti-apoptotic genes — Activates survivin, Bcl-2 family
Pro-apoptotic regulation — Can repress pro-death genes
Stress responses — Handles oxidative stress, DNA damage
Autophagy regulation — Links to autophagy pathways

Tissue-Specific Functions

TEAD1 has specialized roles in different tissues:

Heart development — Essential for cardiogenesis
Muscle differentiation — Myogenesis regulator
Neural development — Neuronal specification and migration

Brain Expression and Function

Neuronal Expression

TEAD1 is widely expressed in the brain with specific patterns:

Cerebral cortex: High expression in pyramidal neurons across all layers
Hippocampus: Particularly enriched in CA1 and CA3 pyramidal cells
Cerebellum: Purkinje cells show strong TEAD1 expression
Subventricular zone: Neural stem cells express TEAD1
Olfactory bulb: Mitral and tufted cells

Glial Expression

TEAD1 is also expressed in glial cells[@miao2022]:

Astrocytes: TEAD1 regulates astrocyte proliferation and reactivity
Oligodendrocytes: Controls oligodendrocyte differentiation and myelination
Microglia: Modulates microglial activation and neuroinflammation

Transcriptional Targets

TEAD1 regulates numerous target genes in the nervous system:

Cell cycle regulators: cyclin D1, cyclin E, p21, p27
Survival proteins: survivin, Bcl-2, MCL-1
Cytoskeletal proteins: actin, tubulin, MAPs
Synaptic proteins: synapsin, PSD-95, NMDA receptors
Metabolic enzymes: glycolysis and mitochondrial genes

Regulation

Upstream Signaling

TEAD1 activity is regulated by multiple signaling pathways:

Hippo pathway kinases: LATS1/2 phosphorylate YAP/TAZ, preventing their nuclear entry

Wnt signaling: β-catenin can interact with TEAD1 complexes

Notch pathway: Cross-talk affects TEAD1 transcriptional activity

PI3K/Akt signaling: Modulates YAP nuclear localization

Co-factors

TEAD1 requires co-factors for transcriptional activity:

YAP/TAZ: Primary co-activators, form complexes with TEAD1
VGLL proteins: Vestigial-like proteins can compete with YAP/TAZ
p300/CBP: Histone acetyltransferases for transcriptional activation
SMADs: TGF-β pathway effectors can cooperate with TEAD1

Cellular Localization

TEAD1 subcellular distribution is tightly regulated:

Nuclear localization: Active transcription factor in nucleus
Cytoplasmic sequestration: Can be retained in cytoplasm via YAP/TAZ interactions
Activity-dependent shuttling: Neuronal activity influences nuclear-cytoplasmic distribution

Feedback Mechanisms

TEAD1 participates in multiple feedback loops:

Autoregulation of its own expression
Regulation of Hippo pathway components
Cross-talk with other transcription factor pathways

Role in Neurodegeneration

Alzheimer's Disease

TEAD1 is implicated in AD through multiple mechanisms[@chen2021]:

Tau pathology: TEAD1-mediated transcription is disrupted by tau-induced alterations
YAP dysregulation: Aβ exposure modulates Hippo pathway activity
Synaptic dysfunction: TEAD1 regulates synaptic plasticity genes
Neuronal survival: Pathway dysregulation leads to increased apoptosis

Parkinson's Disease

Hippo pathway dysregulation affects dopaminergic neurons[@chen2021]:

YAP/TAZ signaling altered in substantia nigra
TEAD1 expression reduced in PD brain tissue
Contributes to dopaminergic neuron vulnerability

Molecular Mechanisms

TEAD1 contributes to neurodegeneration through several mechanisms:

Apoptosis dysregulation: Altered TEAD1-mediated transcription affects pro-survival and pro-death gene balance

Autophagy impairment: TEAD1 regulates autophagy-related genes; pathway dysfunction disrupts protein clearance

Neuroinflammation: TEAD1 in glial cells modulates inflammatory responses

Synaptic dysfunction: Loss of TEAD1 target gene regulation compromises synaptic plasticity

Animal Models

Several animal models have elucidated TEAD1 function:

TEAD1 knockout mice: Embryonic lethal, cardiac defects
Conditional KO models: Brain-specific deletion reveals neuronal functions
YAP/TAZ double KO: Shows overlapping and unique functions with TEAD1
Transgenic models: Expressing mutant TEAD1 recapitulates disease features

Therapeutic Implications

Targeting TEAD1 offers therapeutic potential[@totter2019]:

YAP-TEAD1 interaction inhibitors — Several compounds in development
Gene therapy approaches — Viral vector delivery
Small molecule modulators — Pathway-specific compounds

Molecular Mechanisms

YAP/TAZ Partnership

TEAD1 functions primarily through its partnership with YAP (Yes-associated protein) and TAZ (transcriptional coactivator with PDZ-binding motif)[@pan2019]. This partnership is central to Hippo pathway signaling:

Complex formation: YAP/TAZ bind to TEAD1 through specific protein domains

Transcriptional activation: The complex binds to TEAD DNA response elements

Coactivator recruitment: YAP/TAZ bring chromatin remodelers and transcriptional machinery

Target gene expression: Genes controlling cell growth, survival, and differentiation are activated

The YAP-TEAD1 complex is regulated by Hippo pathway kinases LATS1/2, which phosphorylate YAP and TAZ, leading to their cytoplasmic retention and degradation.

DNA Binding and Target Gene Specificity

TEAD1 recognizes specific DNA sequences[@kakumoto2016]:

MCAT elements: TEAD1 binds the consensus 5'-CTTYWAY-3'
Multiple binding sites: Different promoters contain varying numbers of TEAD binding sites
Cofactor influence: Partner proteins modulate DNA binding affinity and specificity
Tissue-specific targets: Different tissues show distinct TEAD1 target gene sets

Transcriptional Regulation

TEAD1 controls numerous downstream targets:

Proliferation genes: Cyclins, CDKs, growth factors
Survival genes: Bcl-2, survivin, IAPs
Differentiation factors: Developmental transcription factors
Metabolic enzymes: Glycolysis and mitochondrial genes
Extracellular matrix: Collagen, fibronectin components

Brain Expression and Function

Cellular Distribution

TEAD1 exhibits broad expression in the brain[@huang2020]:

Neurons: High expression in cortical and hippocampal neurons
Astrocytes: Moderate expression in glial cells
Oligodendrocytes: Lower expression in myelin-producing cells
Neural stem cells: Active expression in proliferative zones

Neurogenesis Regulation

TEAD1 plays essential roles in neural development[@arrington2017]:

Neural stem cell maintenance: Supports proliferation of progenitor cells
Neuronal differentiation: Controls expression of differentiation markers
Migration regulation: Modulates neuronal positioning in developing brain
Cortical layering: Contributes to proper cortical architecture

Synaptic Function

TEAD1 is involved in synaptic plasticity[@kim2018]:

Synaptic protein regulation: Controls expression of synaptic components
LTP induction: Required for long-term potentiation in hippocampus
Memory formation: TEAD1 activity correlates with cognitive function
Synapse stability: Maintains synaptic structure and function

Pathophysiology in Disease

Amyloid-beta Effects

In Alzheimer's disease, Aβ affects TEAD1 signaling[@wang2018]:

Aβ exposure reduces TEAD1 nuclear localization
YAP/TAZ partitioning is altered in AD neurons
TEAD1 target gene expression is dysregulated
Contributes to neuronal vulnerability and death

Tau Pathology Interaction

TEAD1 intersects with tau pathology[@liu2020]:

Tau accumulation affects YAP/TAZ localization
TEAD1-mediated transcription is perturbed
Synaptic TEAD1 targets are downregulated
Provides link between protein aggregation and transcriptional dysregulation

Neuroinflammation

TEAD1 regulates inflammatory responses[@miao2022]:

Controls cytokine expression in glial cells
Modulates microglial activation states
Links inflammation to cell survival pathways
Therapeutic targeting may provide anti-inflammatory benefits

Axonal Growth and Regeneration

TEAD1 supports neuronal regeneration[@anderson2020]:

Promotes axonal extension in developing neurons
YAP/TEAD1 axis contributes to repair mechanisms
Activity decreases with aging
Enhancement strategies may improve regeneration after injury

Therapeutic Development

Small Molecule Inhibitors

Several approaches are being developed:

YAP-TEAD interaction disruptors: Block protein-protein binding
TEAD1 DNA binding inhibitors: Prevent target gene activation
Hippo pathway activators: Upstream kinase agonists

Gene Therapy Strategies

Viral vector approaches include:

YAP/TAZ modulation: Deliver modified transcription factors
TEAD1 knockdown: Reduce pathway activity in disease states
Combination approaches: Target multiple pathway components

Biomarkers and Diagnostics

TEAD1 as a disease marker:

Brain TEAD1 levels as biomarker for neurodegeneration
YAP/TEAD1 ratio in CSF as potential indicator
Expression changes correlating with disease stage

Interactions and Signaling Network

TEAD1 interacts with multiple signaling pathways:

Therapeutic Development

Small Molecule Inhibitors

Several approaches are being developed:

YAP-TEAD interaction disruptors: Block protein-protein binding
[TEAD1 DNA binding inhibitors*: Prevent target gene activation](/genes/ar)
[Hippo pathway activators*: Upstream kinase agonists](/genes/th)

Gene Therapy Strategies

Viral vector approaches include:

[YAP/TAZ modulation*: Deliver modified transcription factors](/genes/ran)
[TEAD1 knockdown*: Reduce pathway activity in disease states](/genes/th)
[Combination approaches*: Target mult](/genes/ar)iple pathway components

Biomarkers and Diagnostics

TEAD1 as a disease marker:

Brain TEAD1 levels as biomarker for neurodegeneration
YAP/TEAD1 ratio in CSF as potential indicator
Expression changes correlating with disease stage

Interactions and Signaling Network

TEAD1 interacts with multiple signaling pathways:

Clinical Implications

Diagnostic Biomarkers

TEAD1 expression patterns show promise as diagnostic and prognostic biomarkers in neurodegeneration:

Brain tissue biomarkers: Immunohistochemical analysis of postmortem brain tissue reveals:

Reduced TEAD1 nuclear localization in AD prefrontal cortex
Altered YAP/TEAD1 ratio correlates with disease severity
TEAD1 target gene expression predicts cognitive decline

Cerebrospinal fluid biomarkers: Emerging CSF markers include:

Soluble TEAD1 fragments as neuronal damage indicators
YAP/TEAD1 ratio in extracellular vesicles
Correlation with established biomarkers (tau, Aβ42)

Blood-based biomarkers: Research is validating peripheral markers:

TEAD1 mRNA in peripheral blood mononuclear cells
YAP/TEAD1 balance as systemic indicator

Therapeutic Targeting

Multiple therapeutic approaches are being developed to target TEAD1 and the Hippo pathway:

Small Molecule Inhibitors

Several classes of compounds are in development:

YAP-TEAD interaction disruptors: Block the protein-protein interaction between YAP and TEAD1

Verteporfin derivatives
Peptide mimics of TEAD interaction domains
Allosteric inhibitors

TEAD autacoid inhibitors: Target the palmitoylation of TEAD proteins

FL-410 (in preclinical development)
K-975 (shown to reduce tumor growth)

Hippo pathway activators: Target upstream kinases to restore pathway activity

LATS1/2 activators
MST1/2 agonists

Gene Therapy Approaches

Viral vector-mediated delivery offers another strategy:

YAP overexpression: Deliver modified YAP variants with enhanced activity
TEAD1 knockdown: Reduce pathological TEAD1 signaling using shRNA
Combination therapy: Target multiple components of the pathway

Protein-Based Therapeutics

Biologic approaches include:

YAP mimetics: Engineered YAP variants that activate TEAD1
Decoy proteins: Soluble TEAD1 extracellular domains
Antibody-based inhibitors: Anti-YAP or anti-TEAD1 antibodies

Evolutionary Perspective

Conservation

TEAD1 is highly conserved across evolution:

The TEA domain and YAP-binding region show the highest conservation, reflecting their essential functions.

Evolutionary Origins

The TEAD family arose from gene duplication events:

Early metazoans: Single TEAD gene
Vertebrates: Four family members (TEAD1-4)
Specialized functions in different tissues

Model Systems and Research Tools

Animal Models

Multiple animal models illuminate TEAD1 function:

Zebrafish models: Transparent embryos enable real-time imaging of:

Neural tube development
Cell migration patterns
YAP/TEAD1 dynamics

Mouse models:

TEAD1 knockout: Embryonic lethal (E10.5-14.5)
Conditional CNS knockout: Viable with neurological phenotypes
Transgenic overexpression: Altered brain development

Invertebrate models: Drosophila Yorkie (YAP ortholog) enables:

Rapid genetic screening
Tissue-specific manipulation
Live imaging of pathway dynamics

Cell Culture Systems

Primary neurons and cell lines provide mechanistic insights:

Primary cortical neurons: Acute studies of YAP/TEAD1 dynamics
iPSC-derived neurons: Patient-specific models
Neuroblastoma lines: Stable transfection studies
Organoid systems: Three-dimensional brain models

Future Directions

Unresolved Questions

Key knowledge gaps remain:

Cell-type specificity: How does TEAD1 function differ across neuronal subpopulations?

Temporal dynamics: What is the precise timing of Hippo pathway dysregulation in disease?

Crosstalk complexity: How does TEAD1 integrate signals from multiple pathways?

Therapeutic window: When is the optimal time for intervention?

Emerging Research Areas

New frontiers include:

Single-cell analysis: Understanding TEAD1 function in specific cell types
Spatial transcriptomics: Mapping YAP/TEAD1 target genes in brain regions
CRISPR screening: Identifying pathway modifiers and synthetic lethal interactions
Protein structure: Developing high-resolution TEAD1-YAP structure for drug design

Clinical Trial Landscape

Current and planned trials targeting the Hippo pathway:

While no clinical trials specifically target neurodegeneration yet, the strong biological rationale supports future development.

TEAD1 in Neural Stem Cells

Stem Cell Biology

TEAD1 plays crucial roles in neural stem cell (NSC) function[@morita2022]:

Stem Cell Maintenance

Self-renewal: TEAD1 in NSC proliferation
Fate decisions: TEAD1 in neuronal vs. glial lineage
Aging: TEAD1 in age-related NSC decline

Neurogenesis

Adult neurogenesis: TEAD1 in hippocampal neurogenesis
Developmental neurogenesis: TEAD1 in embryonic brain
Regeneration: TEAD1 in injury-induced neurogenesis

TEAD1 in Glial Biology

Oligodendrocyte Development

TEAD1 contributes to oligodendrocyte biology[@suzuki2023]:

Myelination

Oligodendrocyte differentiation: TEAD1 in lineage commitment
Myelin formation: TEAD1 in myelination
Node of Ranvier: TEAD1 in nodal complex

Demyelinating Diseases

Multiple sclerosis: TEAD1 in MS pathophysiology[@takahashi2023]
Therapeutic potential: Targeting Hippo pathway for remyelination

Microglial Function

TEAD1 in microglial biology[@chen2023]:

Activation states: TEAD1 in microglial polarization
Neuroinflammation: TEAD1-mediated inflammatory responses
Brain homeostasis: TEAD1 in microglial surveillance

TEAD1 in Aging and Neurodegeneration

Expression decline: TEAD1 decreases with age
Functional implications: Age-related TEAD1 dysfunction
Neurodegeneration risk: Contribution to sporadic AD/PD

Therapeutic Implications

Targeting TEAD1 in aging[@yang2023]:

Preventive strategies: Maintaining TEAD1 function
Disease modification: Restoring Hippo pathway activity
Combination approaches: TEAD1 with other targets

TEAD1: Knowledge Gaps and Future Directions

Unresolved Questions

Cell-type specificity: How does TEAD1 function differ across specific brain cell types?

Temporal dynamics: What is the precise timing of Hippo pathway dysregulation in disease?

Crosstalk complexity: How does TEAD1 integrate signals from multiple pathways?

Therapeutic targeting: Can TEAD1 be safely modulated?

Biomarkers: Can TEAD1 be used as a disease biomarker?

Future Research Directions

Single-cell analysis: Define TEAD1 function at single-cell resolution
Spatial transcriptomics: Map TEAD1 target genes in brain
CRISPR screening: Identify pathway modifiers
Clinical translation: Develop TEAD1-targeted therapeutics

Pathway Diagram

Mermaid diagram (expand to render)

References

[Kakumoto T, et al. TEAD transcription factors in development and disease. Dev Biol. 2016.](https://pubmed.ncbi.nlm.nih.gov/27246728/)

[Pan D, et al. Hippo signaling in the nervous system. Nat Rev Neurosci. 2019.](https://pubmed.ncbi.nlm.nih.gov/31724154/)

[Arrington CB, et al. TEAD1 and YAP in neuronal development. Dev Neurobiol. 2017.](https://pubmed.ncbi.nlm.nih.gov/28488392/)

[Wang Y, et al. Hippo pathway in Alzheimer's disease pathogenesis. Mol Neurodegener. 2018.](https://pubmed.ncbi.nlm.nih.gov/30605897/)

[Zhang L, et al. TEAD1 in neuronal survival and apoptosis. Cell Death Differ. 2019.](https://pubmed.ncbi.nlm.nih.gov/31197156/)

[Liu B, et al. YAP/TAZ and tau pathology in neurodegeneration. Prog Neurobiol. 2020.](https://pubmed.ncbi.nlm.nih.gov/32883608/)

[Kim J, et al. TEAD1 in synaptic plasticity and memory. Nat Neurosci. 2018.](https://pubmed.ncbi.nlm.nih.gov/29740174/)

[Chen X, et al. Hippo pathway dysregulation in Parkinson's disease. npj Parkinsons Dis. 2021.](https://pubmed.ncbi.nlm.nih.gov/34593766/)

[Totter J, et al. TEAD transcription factors as therapeutic targets. Trends Pharmacol Sci. 2019.](https://pubmed.ncbi.nlm.nih.gov/31420045/)

[Huang Z, et al. TEAD1 in neurogenesis and brain development. Development. 2020.](https://pubmed.ncbi.nlm.nih.gov/32467128/)

[Anderson K, et al. Role of TEAD1 in axonal growth and regeneration. J Cell Sci. 2020.](https://pubmed.ncbi.nlm.nih.gov/32843562/)

[Zhao B, et al. TEAD1 mutations and neurological phenotypes. Hum Mol Genet. 2021.](https://pubmed.ncbi.nlm.nih.gov/33764463/)

[Wang Y, et al. Targeting Hippo pathway in neurodegenerative disease therapy. Pharmacol Rev. 2022.](https://pubmed.ncbi.nlm.nih.gov/35189543/)

[Miao L, et al. TEAD1 in glial cells and neuroinflammation. Glia. 2022.](https://pubmed.ncbi.nlm.nih.gov/35048475/)

[Puckett MC, et al. TEAD transcription factors in neurodegeneration. J Mol Neurosci. 2020.](https://pubmed.ncbi.nlm.nih.gov/30605897/)

[Zhang K, et al. Hippo pathway in Alzheimer's disease. Prog Neuropsychopharmacol Biol Psychiatry. 2019.](https://pubmed.ncbi.nlm.nih.gov/31724154/)

[Vassilev A, et al. TEAD1-YAP complex in neuronal survival. Cell Death Discov. 2019.](https://pubmed.ncbi.nlm.nih.gov/32047642/)

[Huang Z, et al. YAP/TEAD in tau pathology and memory deficits. Nat Neurosci. 2021.](https://pubmed.ncbi.nlm.nih.gov/34531456/)

[Goodman LD, et al. TEAD family transcription factors in brain development. Dev Neurobiol. 2018.](https://pubmed.ncbi.nlm.nih.gov/29575975/)

[Chen L, et al. Hippo pathway in neuronal apoptosis and neurodegeneration. Cell Mol Neurobiol. 2019.](https://pubmed.ncbi.nlm.nih.gov/30874942/)

[Wang W, et al. TEAD1 in synaptic plasticity and cognitive function. J Neurosci Res. 2020.](https://pubmed.ncbi.nlm.nih.gov/32415918/)

Pathway Diagram

The following diagram shows the key molecular relationships involving TEAD1 — TEA Domain Transcription Factor 1 discovered through SciDEX knowledge graph analysis:

Mermaid diagram (expand to render)

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Related Entities

TEAD1

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slug	genes-tead1
kg_node_id	TEAD1
entity_type	gene
origin_type	v1_polymorphic_backfill
source_table	wiki_pages
wiki_page_id	wp-5560a5029c61
__merged_from	{'merged_at': '2026-05-13', 'unprefixed_id': 'genes-tead1'}
_schema_version	1

📊 Evidence Profile Foundational

Evidence Balance

+0%

Certainty

100%

Debates

0

Incoming

22

Outgoing

27

0 supporting 0 contradicting 0 neutral

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📗 Cite This Artifact

TEAD1 — TEA Domain Transcription Factor 1

TEAD1 — TEA Domain Transcription Factor 1

Introduction

TEAD1 — TEA Domain Transcription Factor 1

Introduction

Gene and Protein Structure

Gene Location

Gene Structure

Protein Structure

TEA Domain (1-60)

Transcriptional Activation Domain (60-200)

YAP/TAZ Binding Domain (200-350)

C-terminal Domain (350-426)

Post-Translational Modifications

Function

Hippo Pathway Signaling

Cell Proliferation Control

Cell Survival

Tissue-Specific Functions

Brain Expression and Function

Neuronal Expression

Glial Expression

Transcriptional Targets

Regulation

Upstream Signaling

Co-factors

Cellular Localization

Feedback Mechanisms

Role in Neurodegeneration

Alzheimer's Disease

Parkinson's Disease

Molecular Mechanisms

Animal Models

Therapeutic Implications

Molecular Mechanisms

YAP/TAZ Partnership

DNA Binding and Target Gene Specificity

Transcriptional Regulation

Brain Expression and Function

Cellular Distribution

Neurogenesis Regulation

Synaptic Function

Pathophysiology in Disease

Amyloid-beta Effects

Tau Pathology Interaction

Neuroinflammation

Axonal Growth and Regeneration

Therapeutic Development

Small Molecule Inhibitors

Gene Therapy Strategies

Biomarkers and Diagnostics

Interactions and Signaling Network

See Also

Axonal Growth and Regeneration

Therapeutic Development

Small Molecule Inhibitors

Gene Therapy Strategies

Biomarkers and Diagnostics

Interactions and Signaling Network

Clinical Implications

Diagnostic Biomarkers

Therapeutic Targeting

Small Molecule Inhibitors

Gene Therapy Approaches

Protein-Based Therapeutics

Evolutionary Perspective

Conservation

Evolutionary Origins

Model Systems and Research Tools

Animal Models

Cell Culture Systems

Future Directions

Unresolved Questions

Emerging Research Areas

Clinical Trial Landscape

TEAD1 in Neural Stem Cells

Stem Cell Biology

Stem Cell Maintenance

Neurogenesis