gene

GSK3B

Entity Detail — Knowledge Graph Node

Understanding Entity Pages

This page aggregates everything SciDEX knows about GSK3B: its mechanistic relationships (Knowledge Graph edges), hypotheses targeting it, analyses mentioning it, and supporting scientific papers. The interactive graph below shows its immediate neighbors. All content is AI-synthesized from peer-reviewed literature.

1195Connections

1Hypotheses

9Analyses

50Outgoing

50Incoming

0Experiments

17Debates

Summary

Glycogen Synthase Kinase 3 Beta (GSK3B) is a serine/threonine kinase central to tau phosphorylation, Wnt signaling, glycogen metabolism, and neuroinflammation. GSK3B is the primary kinase responsible for hyperphosphorylation of tau at disease-relevant epitopes (AT8, PHF-1), driving neurofibrillary tangle formation in Alzheimer's disease. GSK3B also promotes amyloid-beta production by enhancing gamma-secretase activity and BACE1 expression. In the Wnt pathway, GSK3B phosphorylates beta-catenin for degradation; Wnt signaling inhibits GSK3B, promoting cell survival. Lithium, a GSK3B inhibitor, reduces tau phosphorylation and has shown neuroprotective effects in preclinical models. Selective GSK3B inhibitors are in clinical development for AD and tauopathies.

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🧬 Gene Info

Gene Symbol	GSK3B
Aliases	GSK-3β, TPKII, Tau tubulin kinase (TTBK)
Chromosome	3q13.33
Protein Type	Serine/Threonine Kinase
Function	is a constitutively active serine/threonine kinase encoded by the GSK3B gene that plays central and multifaceted roles in cellular physiology[@woodgett1990].
Molecular Weight	47 kDa (420 amino acids)
Amino Acids	420 aa
Exons	12
Pathways	Akt, Cholesterol, Mapk, Microrna, Nf-Kb
GeneCards	GSK3B
Human Protein Atlas	GSK3B
Associated Diseases	Aging, ALS, Alzheimer, Alzheimer disease, Alzheimer's disease
Known Drugs/Compounds	ANTHOCYANINS, Ficus deltoidea, LITHIUM, rapamycin, RAPAMYCIN, SB216763
Interactions	ABCA1, ACETYL-COA, ACHE, Actin, AD, ADAM17
SciDEX Hypotheses	GSK3β-Dependent Tau Phosphorylation Cycling Modula
KG Connections	1193 knowledge graph edges
Databases	GeneCards UniProt NCBI Gene HPA STRING

Wiki Pages (5)

Knowledge base pages for this entity

Canonical Page

GSK3B Protein** is a protein. This page describes its structure, normal nervous system function, role in neurodegenerative disease, and potential as a therapeutic target. Redirecting to [GSK3B Protein (Glycogen Synthase Kinase 3 Beta)

redirect · 611 words

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Pathway Diagram

graph TD
    GSK3B["GSK3B"] -->|"activates"| apoptosis["apoptosis"]
    GSK3B["GSK3B"] -->|"associated"| Cancer["Cancer"]
    GSK3B["GSK3B"] -->|"associated"| Carcinoma["Carcinoma"]
    GSK3B["GSK3B"] -->|"activates"| Tumor["Tumor"]
    GSK3B["GSK3B"] -->|"activates"| Als["Als"]
    GSK3B["GSK3B"] -->|"activates"| Alzheimer["Alzheimer"]
    oxidative_stress["oxidative stress"] -->|"contributes to"| GSK3B["GSK3B"]
    PRKCD["PRKCD"] -->|"associated"| GSK3B["GSK3B"]
    TCF4["TCF4"] -->|"associated"| GSK3B["GSK3B"]
    MYC["MYC"] -->|"associated"| GSK3B["GSK3B"]
    style GSK3B fill:#4a1a6b,stroke:#4fc3f7,stroke-width:2px,color:#e0e0e0

Outgoing (696)

Target	Relation	Type	Str
benchmark_ot_ad_answer_key:GSK3B	data_in	dataset_row	0.00
GSK3B	encodes	protein	0.00
ds-83b31ef18d49	provides_data_for	dataset	1.00
Tau Hyperphosphorylation	involved_in	process	0.95
tau phosphorylation	activates	mechanism	0.90
Neuronal Development	regulates	process	0.90
Microtubule Organization	regulates	process	0.90
TAU hyperphosphorylation	causes	process	0.90
ALZHEIMER'S DISEASE	associated_with	disease	0.90
Wnt signaling	participates_in	pathway	0.90
TAU	associated_with	protein	0.90
TAU Phosphorylation	regulates	phenotype	0.90
PRO-APOPTOTIC FACTORS	activates	protein	0.85
Apoptosis	upregulates	process	0.85
FYN	phosphorylates	protein	0.85
Neurodegenerative Diseases	risk_factor_for	disease	0.85
Hyperthyroidism	downregulates	disease	0.85
APOPTOSIS	promotes	process	0.85
PGC1A	regulates	gene	0.85
Neurodevelopmental Diseases	risk_factor_for	disease	0.85
Axon Regeneration	suppresses	process	0.85
Tau Phosphorylation	mediates	process	0.85
TAU PROTEIN TANGLE FORMATION	regulates	process	0.85
AMYLOID BETA ACCUMULATION	regulates	process	0.85
OPTN	phosphorylates	gene	0.83
Glucose Uptake	regulates	process	0.80
Tau hyperphosphorylation	mediates	process	0.80
DEPRESSION	implicated_in	disease	0.80
Apoptosis	promotes	process	0.80
Neuroinflammation	promotes	process	0.80
MAPK signaling	participates_in	pathway	0.80
Tau Phosphorylation	upregulates	process	0.80
apoptosis	activates	phenotype	0.80
WNT	inhibits	pathway	0.80
CHEMOBRAIN	implicated_in	disease	0.80
Als	activates	disease	0.75
Als	regulates	disease	0.75
Cancer	regulates	disease	0.75
BDNF	regulates	protein	0.75
NFKB	inhibits	gene	0.70
PICALM	associated_with	gene	0.70
SOD1	associated_with	gene	0.70
IGF1	interacts_with	gene	0.70
TNF	interacts_with	gene	0.70
PSEN2	interacts_with	gene	0.70
PSEN1	targets	gene	0.70
TAU	markers	gene	0.70
NFKB	activates	gene	0.70
LRP1	interacts_with	gene	0.70
SNCA	activates	gene	0.70

Incoming (499)

Source	Relation	Type	Str
GSK3B	encodes	gene	0.00
benchmark_ot_ad_answer_key:GSK3B	data_in	dataset_row	0.00
entities-overview	associated_with	wiki	0.00
ds-83b31ef18d49	data_in	dataset	1.00
ALZHEIMER'S DISEASE	associated_with	gene	0.98
SB216763	inhibits	drug	0.95
Vitamin B3	inhibits	drug	0.90
Vitamin B1	inhibits	drug	0.90
Vitamin B2	inhibits	drug	0.90
Tideglusib	inhibits	drug	0.90
AKT	inhibits	protein	0.90
AKT1	inhibits	protein	0.90
Thermal Adaptation	upregulates	process	0.90
AKT	phosphorylates	entity	0.85
AKT1	phosphorylates	protein	0.85
Doxorubicin	upregulates	drug	0.85
Sulforaphane	activates	compound	0.85
Hyperthyroidism	downregulates	disease	0.85
Thermal adaptation	upregulates	process	0.85
TAU	associated_with	gene	0.82
oxidative stress	contributes_to	phenotype	0.80
LITHIUM	inhibits	drug	0.80
WIF1	regulates	protein	0.80
Ficus deltoidea	modulates	compound	0.80
ANTHOCYANINS	inhibits	compound	0.80
PRKCD	associated_with	gene	0.80
MTOR	phosphorylates	gene	0.80
MET	regulates	protein	0.80
Testosterone	upregulates	compound	0.80
OLEA	regulates	compound	0.80
APP	targets	gene	0.70
CDK5	inhibits	gene	0.70
APP	activates	gene	0.70
GFAP	interacts_with	gene	0.70
BECN1	interacts_with	gene	0.70
CNP	transports	gene	0.70
FOXP3	interacts_with	gene	0.70
ADAM17	activates	gene	0.70
CAT	associated_with	gene	0.70
ATP13A2	associated_with	gene	0.70
CHOLINERGIC	markers	cell_type	0.70
ACHE	activates	gene	0.70
CGAS	interacts_with	gene	0.70
PI3K	regulates	gene	0.70
CANCER	regulates	gene	0.70
MAPT	associated_with	gene	0.70
ATP13A2	co_discussed	gene	0.65
APOPTOSIS	targets	phenotype	0.65
CASP3	co_discussed	gene	0.65
BCL2	co_discussed	gene	0.65

Targeting Hypotheses (1)

Hypotheses where this entity is a therapeutic target

Hypothesis	Score	Disease	Analysis
GSK3β-Dependent Tau Phosphorylation Cycling Modulation	0.000	-	Tau propagation mechanisms and therapeut

Mentioning Analyses (9)

Scientific analyses that reference this entity

Experiments (0)

Experimental studies targeting or related to this entity

Experiment	Type	Disease	Score	Feasibility	Model	Status	Est. Cost
No experiments found

Related Papers (0)

Scientific publications cited in analyses involving this entity

Title & PMID	Authors	Journal	Year	Citations
No papers found

Debates (17)

Multi-agent debates referencing this entity

Related Research

Hypotheses and analyses mentioning GSK3B in their description or question text

No additional research found

GSK3B

Understanding Entity Pages

Summary

Wiki Pages (5)

GSK3B Gene - Glycogen Synthase Kinase 3 Beta

GSK3B (Glycogen Synthase Kinase 3 Beta)

GSK3B Protein (Glycogen Synthase Kinase 3 Beta)

GSK3B — Glycogen Synthase Kinase 3 Beta

GSK3B Protein** is a protein. This page describes its structure, normal nervous system function, role in neurodegenerative disease, and potential as a therapeutic target. Redirecting to [GSK3B Protein (Glycogen Synthase Kinase 3 Beta)

Pathway Diagram

Outgoing (696)

Incoming (499)

Targeting Hypotheses (1)

Mentioning Analyses (9)

Can CSF p-tau217 normalization serve as a reliable surrogate endpoint for determ

Does RGS6 upregulation or D2 autoreceptor modulation prevent neurodegeneration i

Does tau aggregation specifically cause PS externalization in vesicles independe

What determines organelle-specific autophagy selectivity in neurodegenerative di

What molecular mechanisms determine the conformational diversity and strain-like

Cell type vulnerability in Alzheimers Disease (SEA-AD transcriptomic data)

Tau propagation mechanisms and therapeutic interception points

4R-tau strain-specific spreading patterns in PSP vs CBD

Digital biomarkers and AI-driven early detection of neurodegeneration

Experiments (0)

Related Papers (0)

Debates (17)

Second debate: Microglial TREM2-SYK Pathway Enhancement

Debate: LPCAT3-Mediated Lands Cycle Remodeling as the Primary Ferroptotic Primin

Debate: ALOX15-Driven Enzymatic Ferroptosis in AD Oligodendrocytes via PUFA-PE P

Debate: LPCAT3-Mediated Lands Cycle Amplification of Ferroptotic Vulnerability i

Debate: ACSL4-Driven Ferroptotic Priming in Disease-Associated Oligodendrocytes

Should '40 Hz Gamma Entrainment Gates ACSL4-Mediated Ferroptotic Priming to Sele

Should 'ACSL4-Ferroptotic Priming in Stressed Oligodendrocytes Drives White Matt

Can CSF p-tau217 normalization serve as a reliable surrogate endpoint for determ

The abstract mentions that pathological seeds have different characteristics and

The review covers various organelle-specific autophagy types but doesn't address

Related Research