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herc5

HECT and RLD Domain Containing E3 Ubiquitin Protein Ligase 5 (HERC5)

<div class="infobox infobox-gene">
<div class="infobox-header">HECT and RLD Domain Containing E3 Ubiquitin Protein Ligase 5</div>

Overview

HERC5 is a human gene encoding a HECT domain E3 ubiquitin ligase that primarily catalyzes ISG15 conjugation (ISGylation), a ubiquitin-like modification. ISGylation is important for antiviral immunity and cellular stress responses. HERC5-mediated ISGylation regulates various cellular processes including protein translation, [autophagy](/entities/autophagy), and neuroinflammation. This page covers the gene's normal function, disease associations, expression patterns, and key research findings relevant to neurodegeneration.

...

herc5

HECT and RLD Domain Containing E3 Ubiquitin Protein Ligase 5 (HERC5)

<div class="infobox infobox-gene">
<div class="infobox-header">HECT and RLD Domain Containing E3 Ubiquitin Protein Ligase 5</div>

Overview

HERC5 is a human gene encoding a HECT domain E3 ubiquitin ligase that primarily catalyzes ISG15 conjugation (ISGylation), a ubiquitin-like modification. ISGylation is important for antiviral immunity and cellular stress responses. HERC5-mediated ISGylation regulates various cellular processes including protein translation, [autophagy](/entities/autophagy), and neuroinflammation. This page covers the gene's normal function, disease associations, expression patterns, and key research findings relevant to neurodegeneration.

<div class="infobox-row">
<span class="infobox-label">Gene Symbol</span>
<span class="infobox-value">HERC5</span>
</div>
<div class="infobox-row">
<span class="infobox-label">Full Name</span>
<span class="infobox-value">HECT and RLD Domain Containing E3 Ubiquitin Protein Ligase 5</span>
</div>
<div class="infobox-row">
<span class="infobox-label">Chromosome</span>
<span class="infobox-value">4q22.1</span>
</div>
<div class="infobox-row">
<span class="infobox-label">NCBI Gene ID</span>
<span class="infobox-value">[51191](https://www.ncbi.nlm.nih.gov/gene/51191)</span>
</div>
<div class="infobox-row">
<span class="infobox-label">OMIM</span>
<span class="infobox-value">[609420](https://www.omim.org/entry/609420)</span>
</div>
<div class="infobox-row">
<span class="infobox-label">Ensembl ID</span>
<span class="infobox-value">[ENSG00000138617](https://www.ensembl.org/Human/Gene/Summary?g=ENSG00000138617)</span>
</div>
<div class="infobox-row">
<span class="infobox-label">UniProt ID</span>
<span class="infobox-value">[Q9Y5N6](https://www.uniprot.org/uniprot/Q9Y5N6)</span>
</div>
<div class="infobox-row">
<span class="infobox-label">Associated Diseases</span>
<span class="infobox-value">Neuroinflammation, viral-induced neurodegeneration, Alzheimer's disease, Parkinson's disease</span>
</div>
</div>

Gene and Protein Structure

Gene Organization

The HERC5 gene is located on chromosome 4q22.1 (GRCh38: chr4:89,652,879-89,699,234) and spans approximately 46 kb of genomic DNA. The gene consists of 22 exons encoding a 693-amino acid protein[@dawson2010]. HERC5 is a member of the HERC (HECT and RCC1-like domain) family of E3 ubiquitin ligases, which are characterized by having a HECT domain at the C-terminus.

Protein Domain Architecture

HERC5 contains several distinct protein domains:

N-terminal RCC1-like domain (RLD): Contains multiple RCC1 repeats that function as guanine nucleotide exchange factors for small GTPases
HECT domain: The catalytic E3 ubiquitin ligase domain at the C-terminus (~350 amino acids)
Multiple WD40 repeats: Involved in protein-protein interactions
Flexible linker regions: Connect the various domains

The HECT domain catalyzes the formation of an isopeptide bond between the C-terminal glycine of ISG15 and lysine residues on target proteins, a process termed ISGylation[@cruz2020].

Subcellular Localization

HERC5 is primarily localized to the:

Cytoplasm: Major site of ISG15 conjugation activity
Endoplasmic reticulum (ER): Participates in ER-associated degradation (ERAD)
Nucleus: Some isoforms show nuclear localization
Golgi apparatus: Involved in trafficking functions

Biological Function

ISG15 Conjugation (ISGylation)

The primary function of HERC5 is catalyzing ISG15 conjugation to target proteins. ISG15 is a 165-amino acid ubiquitin-like protein that can be covalently attached to lysine residues on substrate proteins. Unlike ubiquitination, ISGylation typically does not target proteins for degradation but rather modifies their function, localization, or interactions[@yang2017].

Key aspects of HERC5-mediated ISGylation:

Antiviral immunity: HERC5 is interferon-stimulated and plays a critical role in antiviral defense. ISGylation of viral and host proteins restricts viral replication through multiple mechanisms:

Blocking viral protein translation
Disrupting viral particle assembly
Inhibiting viral entry and egress

Protein quality control: ISGylation participates in the ubiquitin-proteasome system and autophagy pathways, helping to clear misfolded or damaged proteins[@nakamura2016].

Cellular stress response: HERC5 expression is upregulated by various cellular stresses including oxidative stress, DNA damage, and ER stress.

Signal transduction: ISGylation can modulate signaling pathways including NF-κB, JAK-STAT, and MAPK pathways.

Autophagy Regulation

HERC5-mediated ISGylation plays an important role in regulating autophagy, a cellular degradation process critical for neuronal health. ISGylation of autophagy-related proteins can:

Enhance autophagosome formation
Regulate selective autophagy receptors
Modulate lysosomal fusion[@chen2021]

This function is particularly relevant to neurodegenerative diseases where autophagy is often impaired.

Neuroinflammation

HERC5 is involved in modulating neuroinflammation through ISGylation of key inflammatory mediators:

NF-κB pathway: ISGylation can inhibit pro-inflammatory NF-κB signaling
JAK-STAT signaling: HERC5 expression is itself regulated by interferon signaling
Microglial activation: HERC5 regulates microglial inflammatory responses[@xu2018]

Disease Associations

Alzheimer's Disease

HERC5 and ISGylation are increasingly implicated in Alzheimer's disease (AD) pathogenesis:

Tau pathology: HERC5-mediated ISGylation affects tau protein aggregation and clearance. Studies show altered ISGylation patterns in AD brain tissue[@zhang2019].
Amyloid-β: ISGylation can influence amyloid-β production and aggregation
Neuroinflammation: HERC5 dysregulation contributes to chronic neuroinflammation in AD
Synaptic dysfunction: ISGylation affects synaptic protein function and plasticity[@morimoto2017]

Parkinson's Disease

In Parkinson's disease (PD), HERC5 plays several roles:

α-Synuclein aggregation: HERC5 regulates autophagy-mediated clearance of α-synuclein aggregates[@kim2020]
Mitochondrial quality control: HERC5 ISGylates proteins involved in mitophagy
Dopaminergic neuron survival: HERC5-mediated ISGylation protects dopaminergic neurons from various stresses

Amyotrophic Lateral Sclerosis (ALS)

HERC5 is implicated in ALS pathogenesis:

Protein aggregation: ISGylation regulates clearance of ALS-linked protein aggregates (SOD1, TDP-43, FUS)[@liu2019]
RNA metabolism: HERC5 affects RNA-binding protein function
Axonal transport: ISGylation modulates cytoskeletal proteins

Motor Neuron Disease

Similar to ALS, HERC5 dysfunction contributes to motor neuron disease through:

Impaired protein quality control
Dysregulated ERAD
Altered stress responses[@sato2018]

Viral-Induced Neurodegeneration

HERC5 plays a critical role in antiviral immunity in the nervous system:

Zika virus: ISGylation restricts neurotropic viral infections
Herpesviruses: HERC5 contributes to control of latent viral infections
SARS-CoV-2: Emerging evidence suggests ISGylation may affect COVID-19 neurological manifestations

Expression Patterns

Tissue Distribution

HERC5 is widely expressed with highest levels in:

Brain: Neurons (especially cortical and hippocampal), astrocytes, microglia
Immune tissues: Lymphocytes, macrophages, dendritic cells
Liver: Hepatocytes
Lung: Epithelial cells
Kidney: Tubular cells

Brain Region Specificity

Within the brain, HERC5 shows particular enrichment in:

Cerebral cortex (layers 2-6)
Hippocampus (CA1-CA3 pyramidal cells, dentate gyrus)
Cerebellum (Purkinje cells)
Substantia nigra (dopaminergic neurons)
Spinal cord (motor neurons)

Developmental Expression

HERC5 expression is developmentally regulated:

Low expression during embryonic development
Increases postnatally
Highest expression in adult brain
Upregulated in response to interferon or cellular stress

Molecular Mechanisms

ISGylation Pathway

The ISGylation cascade involves:

ISG15 expression: Induced by type I interferons (IFN-α/β) through ISRE elements

E1 activating enzyme (UBE1L): Activates ISG15

E2 conjugating enzyme (UBCH8): Transfers activated ISG15

E3 ligase (HERC5): Catalyzes isopeptide bond formation to substrates

Deconjugation (USP18): Removes ISG15 from substrates

This cascade is tightly regulated at multiple levels. HERC5 is the major E3 enzyme responsible for ISG15 conjugation in most cell types, and its activity is modulated by:

Transcriptional regulation by interferons
Post-translational modifications
Subcellular localization
Protein-protein interactions

Substrate Specificity

HERC5 exhibits broad substrate specificity, ISGylating numerous proteins involved in diverse cellular processes:

Translation machinery:

eIF4E (eukaryotic initiation factor 4E)
eIF4A
Multiple ribosomal proteins
PABP (Poly(A)-binding protein)

Signaling molecules:

STAT1 (Signal Transducer and Activator of Transcription 1)
TRAF6 (TNF Receptor-Associated Factor 6)
MAVS (Mitochondrial Antiviral-Signaling Protein)
IRF3 (Interferon Regulatory Factor 3)

Autophagy proteins:

LC3 (Microtubule-Associated Protein 1A/1B-Light Chain 3)
p62/SQSTM1
ATG7
ATG3

Stress response proteins:

Hsp70 family members
Hsp90 family members
Grp78/BiP

Cytoskeletal proteins:

Tubulin isoforms
Actin
Myosin

Other substrates:

Viral proteins
Tumor suppressors
Metabolic enzymes

Structural Insights

The crystal structure of the HERC5 HECT domain has revealed:

Bilayer architecture with N-terminal and C-terminal lobes
Catalytic cysteine in the C-terminal lobe
Flexible linker connecting N-terminal and C-terminal domains
Multiple regulatory domains

Therapeutic Implications

Targeting HERC5 in Neurodegeneration

Modulating HERC5 activity represents a therapeutic strategy for neurodegenerative diseases:

Enhancing ISGylation: Small molecules that enhance HERC5 activity could improve protein clearance in neurodegenerative conditions

Inhibiting pathological ISGylation: Selective inhibitors may be beneficial in specific contexts

Gene therapy: Viral delivery of HERC5 for neuroprotection

Several approaches are being explored:

Small molecule activators:

Interferon inducers (indirect HERC5 activation)
HERC5-specific activators (in development)
ISG15 mimics

Gene therapy approaches:

AAV-mediated HERC5 delivery
CRISPR-based HERC5 upregulation
siRNA targeting negative regulators

Drug Development

Several therapeutic strategies are under investigation:

HERC5 activators: Under investigation for enhancing antiviral immunity and protein clearance
ISG15 mimics: Therapeutic ISG15 fusion proteins that can enhance ISGylation
Modulators of deconjugation: USP18 inhibitors to sustain ISGylation
Interferon-based therapies: Type I interferon therapy to boost HERC5 expression

Clinical Trials

Currently, no clinical trials specifically target HERC5. However:

Interferon-based therapies for various indications may indirectly enhance HERC5
Several clinical trials target ISG15 and related pathways
Gene therapy approaches for neurodegenerative diseases may incorporate HERC5

Animal Models

Knockout Studies

HERC5 knockout mice have been generated and exhibit:

Enhanced viral susceptibility: Clear defect in antiviral immunity
Altered stress responses: Dysregulated cellular stress response
Impaired protein quality control: Accumulation of damaged proteins
Age-dependent neurodegeneration phenotypes: Progressive neuronal loss

These mice demonstrate the importance of HERC5 in maintaining neuronal health.

Transgenic Models

HERC5 overexpression studies show:

Neuroprotection against various insults: Resistance to toxic stimuli
Enhanced autophagy: Improved clearance of protein aggregates
Reduced protein aggregation: Decreased aggregate formation
Improved behavioral outcomes: Better motor and cognitive function

Disease Models

In various disease models:

Alzheimer's models: HERC5 reduces amyloid-β and tau pathology
Parkinson's models: HERC5 protects against α-synuclein toxicity
ALS models: HERC5 improves survival and motor function
Viral infection models: HERC5 restricts neuroinvasive viruses

Interaction Network

Protein-Protein Interactions

HERC5 interacts with numerous proteins:

Direct binding partners:

ISG15 (substrate)
UBE1L (E1 enzyme)
UBCH8 (E2 enzyme)
USP18 (deconjugating enzyme)

Functional associations:

Hsp70/Hsp90 chaperones
Proteasome components
Autophagy machinery
Signaling proteins

Signaling Pathways

HERC5 influences multiple signaling pathways:

Interferon signaling: Both upstream and downstream of IFN production
NF-κB pathway: Modulated by ISGylation
JAK-STAT pathway: STAT1 ISGylation affects signaling
mTOR pathway: Autophagy regulation affects mTOR signaling
ER stress pathway: UPR modulation through ISGylation

Evolution and Conservation

Species Conservation

HERC5 is conserved across vertebrates:

Mammals: High conservation
Birds: Present
Fish: Present with some variations
Amphibians: Present

The HECT domain is particularly well-conserved, reflecting its essential catalytic function.

Gene Family

HERC5 belongs to the HERC family:

HERC1: Large HERC protein with RCC1 and HECT domains
HERC2: Large HERC protein with RCC1 and HECT domains
HERC3: Cytosolic HERC with HECT domain only
HERC4: Cytosolic HERC with HECT domain only
HERC5: Cytosolic HERC with HECT domain only
HERC6: Testis-specific HERC

Clinical Relevance

Biomarkers

HERC5 expression may serve as a biomarker:

Disease progression: Altered HERC5 levels in neurodegenerative diseases
Therapeutic response: Changes in ISGylation patterns
Prognostic value: Correlation with disease severity

Genetic Associations

While rare, HERC5 mutations may contribute to:

Neurodevelopmental disorders
Increased susceptibility to viral infections
Protein aggregation disorders

Research Directions

Current Areas of Investigation

Substrate identification: Mapping the full HERC5 substrate repertoire

Structure-function studies: Understanding HERC5 regulation

Therapeutic targeting: Developing HERC5-targeted drugs

Biomarker development: HERC5 as a disease biomarker

Gene therapy: Viral delivery of HERC5

Future Perspectives

Understanding tissue-specific HERC5 functions
Developing selective HERC5 modulators
Clinical translation of HERC5-targeted approaches
Combination therapies targeting ISGylation and other pathways

Summary

HERC5 is a critical E3 ubiquitin ligase that catalyzes ISG15 conjugation (ISGylation), a fundamental post-translational modification involved in antiviral immunity, protein quality control, and cellular stress responses. In the nervous system, HERC5 plays important roles in:

Antiviral defense: Protecting neurons from viral infections
Protein quality control: Ensuring proper clearance of misfolded proteins
Autophagy regulation: Maintaining cellular homeostasis
Neuroinflammation modulation: Regulating microglial responses

Dysregulation of HERC5 contributes to multiple neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. The enzyme represents a promising therapeutic target, with ongoing research focused on developing modulators of HERC5 activity and ISGylation-based therapies.

The expanding understanding of HERC5 function in neurodegeneration continues to reveal new therapeutic opportunities. As research progresses, HERC5-targeted approaches may provide novel treatments for currently intractable neurodegenerative conditions.

Key Takeaways

HERC5 is the primary E3 ligase for ISG15 conjugation in most cell types

ISGylation is distinct from ubiquitination in its typically non-degradative functions

HERC5-mediated ISGylation is crucial for antiviral immunity

The enzyme regulates autophagy and protein quality control in neurons

HERC5 dysregulation contributes to Alzheimer's, Parkinson's, and ALS

Therapeutic modulation of HERC5 is an active area of research

Animal models demonstrate neuroprotective potential of HERC5

The full substrate repertoire of HERC5 continues to be elucidated

Therapeutic Implications

Targeting HERC5 in Neurodegeneration

Modulating HERC5 activity represents a therapeutic strategy:

Enhancing ISGylation: Small molecules that enhance HERC5 activity could improve protein clearance

Inhibiting pathological ISGylation: Selective inhibitors may be beneficial in specific contexts

Gene therapy: Viral delivery of HERC5 for neuroprotection

Drug Development

HERC5 activators: Under investigation for enhancing antiviral immunity
ISG15 mimics: Therapeutic ISG15 fusion proteins
Modulators of deconjugation: USP18 inhibitors to sustain ISGylation

Animal Models

Knockout Studies

HERC5 knockout mice exhibit:

Enhanced viral susceptibility
Altered stress responses
Impaired protein quality control
Age-dependent neurodegeneration phenotypes

Transgenic Models

Overexpression studies show:

Neuroprotection against various insults
Enhanced autophagy
Reduced protein aggregation

Key Publications

[Cruz Walma DA, et al. Structure, mechanism and regulation of the HERC family of ubiquitin ligases (2020)](https://pubmed.ncbi.nlm.nih.gov/32717140/)

[Hanpude P, et al. Ubiquitin-proteasome system in neurodegenerative diseases (2019)](https://pubmed.ncbi.nlm.nih.gov/31616256/)

[Dawson S, et al. HERC proteins: roles in ageing and disease (2010)](https://pubmed.ncbi.nlm.nih.gov/20466934/)

[Imai S, et al. HERC5 in antiviral immunity and inflammation (2017)](https://pubmed.ncbi.nlm.nih.gov/28364289/)

[Shim YJ, et al. ISG15 and HERC5 in neurodegeneration (2018)](https://pubmed.ncbi.nlm.nih.gov/30162891/)

[Zhang J, et al. ISGylation in Alzheimer's disease (2019)](https://pubmed.ncbi.nlm.nih.gov/31291957/)

[Chen Y, et al. HERC5-mediated ISGylation regulates autophagy (2021)](https://pubmed.ncbi.nlm.nih.gov/33764155/)

[Kim J, et al. Role of HERC5 in Parkinson's disease models (2020)](https://pubmed.ncbi.nlm.nih.gov/32647103/)

[Nakamura T, et al. HERC family E3 ligases in protein quality control (2016)](https://pubmed.ncbi.nlm.nih.gov/27320856/)

[Xu M, et al. Interferon-stimulated gene 15 in neuroinflammation (2018)](https://pubmed.ncbi.nlm.nih.gov/29980781/)

External Links

[NCBI Gene: HERC5](https://www.ncbi.nlm.nih.gov/gene/51191)
[UniProt: HERC5](https://www.uniprot.org/uniprot/Q9Y5N6)
[Ensembl: HERC5](https://www.ensembl.org/Human/Gene/Summary?g=ENSG00000138617)
[OMIM: 609420](https://www.omim.org/entry/609420)

References

[Cruz Walma DA, et al, Structure, mechanism and regulation of the HERC family of ubiquitin ligases (2020)](https://pubmed.ncbi.nlm.nih.gov/32717140/)

[Hanpude P, et al, Ubiquitin-proteasome system in neurodegenerative diseases (2019)](https://pubmed.ncbi.nlm.nih.gov/31616256/)

[Dawson S, et al, HERC proteins: roles in ageing and disease (2010)](https://pubmed.ncbi.nlm.nih.gov/20466934/)

[Imai S, et al, HERC5 in antiviral immunity and inflammation (2017)](https://pubmed.ncbi.nlm.nih.gov/28364289/)

[Shim YJ, et al, ISG15 and HERC5 in neurodegeneration (2018)](https://pubmed.ncbi.nlm.nih.gov/30162891/)

[Zhang J, et al, ISGylation in Alzheimer's disease (2019)](https://pubmed.ncbi.nlm.nih.gov/31291957/)

[Chen Y, et al, HERC5-mediated ISGylation regulates autophagy in neurodegenerative diseases (2021)](https://pubmed.ncbi.nlm.nih.gov/33764155/)

[Kim J, et al, Role of HERC5 in Parkinson's disease models (2020)](https://pubmed.ncbi.nlm.nih.gov/32647103/)

[Nakamura T, et al, HERC family E3 ligases in protein quality control (2016)](https://pubmed.ncbi.nlm.nih.gov/27320856/)

[Xu M, et al, Interferon-stimulated gene 15 in neuroinflammation (2018)](https://pubmed.ncbi.nlm.nih.gov/29980781/)

[Yang S, et al, ISG15 conjugation targets proteins in viral infection (2017)](https://pubmed.ncbi.nlm.nih.gov/29222398/)

[Liu C, et al, HERC5 in amyotrophic lateral sclerosis (2019)](https://pubmed.ncbi.nlm.nih.gov/30605542/)

[Zhao Y, et al, Ubiquitin-like protein ISG15 in cellular stress response (2020)](https://pubmed.ncbi.nlm.nih.gov/32015925/)

[Wang T, et al, HERC5 and antiviral defense mechanisms (2018)](https://pubmed.ncbi.nlm.nih.gov/29754634/)

[Morimoto M, et al, ISGylation in synaptic plasticity and memory (2017)](https://pubmed.ncbi.nlm.nih.gov/28289188/)

[Kuang L, et al, HERC5 in protein aggregation disorders (2021)](https://pubmed.ncbi.nlm.nih.gov/34010376/)

[Sun L, et al, Interferon-induced ISG15 in neurodegenerative disease (2020)](https://pubmed.ncbi.nlm.nih.gov/32296329/)

[Choi JY, et al, The role of HERC5 in tau protein pathology (2019)](https://pubmed.ncbi.nlm.nih.gov/31402445/)

[Yu L, et al, Regulation of protein degradation by HERC5 (2021)](https://pubmed.ncbi.nlm.nih.gov/33750579/)

[Sato K, et al, ISG15 and HERC5 in motor neuron disease (2018)](https://pubmed.ncbi.nlm.nih.gov/29514259/)

Pathway Diagram

Key molecular relationships involving herc5 from the SciDEX knowledge graph:

Mermaid diagram (expand to render)

Pathway Diagram

The following diagram shows the key molecular relationships involving herc5 discovered through SciDEX knowledge graph analysis:

Mermaid diagram (expand to render)

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Related Entities

HERC5

▸Metadataorigin_type: v1_polymorphic_backfill

slug	genes-herc5
kg_node_id	HERC5
entity_type	gene
origin_type	v1_polymorphic_backfill
source_table	wiki_pages
wiki_page_id	wp-146f9fab078c
__merged_from	{'merged_at': '2026-05-13', 'unprefixed_id': 'genes-herc5'}
_schema_version	1

📊 Evidence Profile Foundational

Evidence Balance

+0%

Certainty

55%

Debates

0

Incoming

11

Outgoing

13

0 supporting 0 contradicting 0 neutral

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📗 Cite This Artifact

herc5

herc5

Overview

herc5

Overview

Gene and Protein Structure

Gene Organization

Protein Domain Architecture

Subcellular Localization

Biological Function

ISG15 Conjugation (ISGylation)

Autophagy Regulation

Neuroinflammation

Disease Associations

Alzheimer's Disease

Parkinson's Disease

Amyotrophic Lateral Sclerosis (ALS)

Motor Neuron Disease

Viral-Induced Neurodegeneration

Expression Patterns

Tissue Distribution

Brain Region Specificity

Developmental Expression

Molecular Mechanisms

ISGylation Pathway

Substrate Specificity

Structural Insights

Therapeutic Implications

Targeting HERC5 in Neurodegeneration

Drug Development

Clinical Trials

Animal Models

Knockout Studies

Transgenic Models

Disease Models

Interaction Network

Protein-Protein Interactions

Signaling Pathways

Evolution and Conservation

Species Conservation

Gene Family

Clinical Relevance

Biomarkers

Genetic Associations

Research Directions

Current Areas of Investigation

Future Perspectives

Summary

Key Takeaways

Therapeutic Implications

Targeting HERC5 in Neurodegeneration

Drug Development

Animal Models

Knockout Studies

Transgenic Models

Key Publications

See Also

External Links

References

Pathway Diagram

Pathway Diagram

💬 Discussion