protein

WAS

Entity Detail — Knowledge Graph Node

Understanding Entity Pages

This page aggregates everything SciDEX knows about WAS: 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.

249Connections

9Hypotheses

5Analyses

48Outgoing

50Incoming

1Experiments

7Debates

Summary

Wiskott-Aldrich Syndrome protein - regulates actin cytoskeleton, linked to neurodegeneration

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🔬 Protein Info

Gene Symbol	WAS
Aliases	Wiskott-Aldrich Syndrome protein
Function	WASp exists in an autoinhibited conformation where the VCA domain is masked[@symons1996].
Molecular Weight	52 kDa
GeneCards	WAS
Human Protein Atlas	WAS
Interactions	AKT, ALZHEIMER, AMYLOID, APP, ARNT, ATP
KG Connections	249 knowledge graph edges
Databases	GeneCards UniProt NCBI Gene HPA STRING

Wiki Pages (11)

Knowledge base pages for this entity

Canonical Page

Pathway Diagram

graph TD
    WAS["WAS"]
    TAU(["TAU"])
    WAS -.->|"inhibits"| TAU
    TBK1(["TBK1"])
    WAS -->|"activates"| TBK1
    TREM2(["TREM2"])
    WAS -->|"interacts_with"| TREM2
    IL18(["IL18"])
    WAS -->|"activates"| IL18
    LAMP2(["LAMP2"])
    WAS -->|"activates"| LAMP2
    SNCA(["SNCA"])
    WAS -->|"activates"| SNCA
    CRH(["CRH"])
    CRH -->|"activates"| WAS
    POMC(["POMC"])
    POMC -->|"activates"| WAS
    STING(["STING"])
    STING -->|"co_discussed"| WAS
    C1Q(["C1Q"])
    C1Q -->|"co_discussed"| WAS
    style WAS fill:#1a3a4a,stroke:#4fc3f7,stroke-width:3px,color:#4fc3f7

Outgoing (48)

Target	Relation	Type	Str
PYCARD	regulates	gene	0.50
PARKIN	activates	gene	0.50
PINK1	activates	gene	0.50
NLRP3	causes	protein	0.50
NTRK2	activates	gene	0.50
RAGE	activates	gene	0.50
TRPV4	expressed_in	gene	0.50
TAU	inhibits	protein	0.50
TBK1	activates	gene	0.50
NDP52	activates	gene	0.50
CASPASE-1	causes	protein	0.50
TAZ	activates	gene	0.50
TREM2	interacts_with	gene	0.50
IL18	activates	gene	0.50
LAMP2	activates	protein	0.50
SNCA	activates	gene	0.50
TNF	activates	gene	0.50
AUTOPHAGY	inhibits	gene	0.50
PVALB	inhibits	gene	0.50
PKA	activates	protein	0.50
TNF	expressed_in	gene	0.50
TGM2	activates	gene	0.50
TREM2	activates	gene	0.50
NEURON	inhibits	gene	0.50
NLRP3	expressed_in	protein	0.50
NLRP6	expressed_in	gene	0.50
GBM	activates	gene	0.50
GPX4	activates	gene	0.50
KIF4A	activates	gene	0.50
P62	activates	protein	0.50
SIRT2	activates	gene	0.50
SLC17A7	activates	protein	0.50
UNC5C	activates	gene	0.50
CAV2.3	inhibits	protein	0.50
ATP	phosphorylates	protein	0.50
IL-10	activates	protein	0.50
IL-1Β	activates	protein	0.50
PKM2	interacts_with	protein	0.50
OPTN	activates	gene	0.50
CANCER	regulates	gene	0.50
SCN4B	activates	gene	0.50
SNCA	expressed_in	gene	0.50
APP	regulates	gene	0.50
CHMP4B	activates	gene	0.50
CAV2	inhibits	gene	0.50
FASN	activates	gene	0.50
HMGCR	activates	gene	0.50
SCD1	activates	gene	0.50

Incoming (201)

Source	Relation	Type	Str
GPR37	co_discussed	gene	0.50
GSK3B	co_discussed	gene	0.50
IL1B	co_discussed	gene	0.50
TREM2	co_discussed	gene	0.50
CREBBP	co_discussed	gene	0.50
FOXO1	co_discussed	gene	0.50
GAN	activates	gene	0.50
TNFR2	regulates	protein	0.50
HUNTINGTON	inhibits	gene	0.50
IL6R	inhibits	gene	0.50
STROKE	co_discussed	gene	0.50
ARNT	activates	gene	0.50
GENES	activates	gene	0.50
MMP9	activates	gene	0.50
ARG1	co_discussed	gene	0.50
TGM2	co_discussed	gene	0.50
CANCER	interacts_with	gene	0.50
PI3K	activates	protein	0.50
TAU	co_discussed	protein	0.50
BRCA1	activates	protein	0.50
P62/SQSTM1	activates	protein	0.50
AMYLOID	inhibits	gene	0.50
ALZHEIMER	regulates	gene	0.50
STROKE	activates	gene	0.50
AQP4	co_discussed	gene	0.50
TGF-Β1	activates	protein	0.50
MMP9	co_discussed	gene	0.50
IGF1R	activates	gene	0.50
FGF-2	co_discussed	protein	0.50
ALZHEIMER	expressed_in	gene	0.50
RNA	expressed_in	gene	0.50
STAT3	co_discussed	gene	0.50
TNF	co_discussed	gene	0.50
ALZHEIMER	activates	gene	0.50
AMYLOID	activates	gene	0.50
TAU	activates	protein	0.50
EPHA2	activates	gene	0.50
FLOT1	activates	gene	0.50
CANCER	inhibits	gene	0.50
TP53	inhibits	gene	0.50
NLRP3	activates	protein	0.50
CLUSTERIN	co_discussed	protein	0.50
GENES	co_discussed	gene	0.50
ACSL4	co_discussed	gene	0.50
GPX4	co_discussed	gene	0.50
HO-1	co_discussed	protein	0.50
NRF2	co_discussed	gene	0.50
SLC7A1	co_discussed	gene	0.50
SLC7A11	co_discussed	gene	0.50
PARKINSON	inhibits	gene	0.50

Targeting Hypotheses (9)

Hypotheses where this entity is a therapeutic target

Hypothesis	Score	Disease	Analysis
Thalamocortical Feedforward Inhibition Imposes Rhythm on Gly	0.808	neuroscience	GluN2B-Mediated Thalamocortical Control
PD-Associated GWAS Variants in CTSO and CTSF Genes Create a	0.743	neurodegeneration	-
VEGF-family genetic control of vascular-neuronal coupling in	0.626	neurodegeneration	VEGF Family GWAS Signals and Cerebrovasc
DPP6-linked neuronal regulatory networks controlling synapti	0.626	neurodegeneration	DPP6 GWAS Signal: Cell-Type Regulatory N
Cell-state stratification is required to resolve DPP6 GWAS S	0.612	neurodegeneration	DPP6 GWAS Signal: Cell-Type Regulatory N

Cell-state stratification is required to resolve VEGF Family	0.612	neurodegeneration	VEGF Family GWAS Signals and Cerebrovasc
Perturbation-first validation should precede therapeutic cla	0.608	neurodegeneration	DPP6 GWAS Signal: Cell-Type Regulatory N
Perturbation-first validation should precede therapeutic cla	0.608	neurodegeneration	VEGF Family GWAS Signals and Cerebrovasc
Tau-trafficking GWAS loci define a druggable PTK2B endocytos	0.592	alzheimers	-

Mentioning Analyses (5)

Scientific analyses that reference this entity

LRRK2 Risk Variants: Lysosomal Membrane Dynamics in DA vs Striatal Neurons

neurodegeneration | 2026-04-27 | 0 hypotheses

DPP6 GWAS Signal: Cell-Type Regulatory Networks for PD Cognitive Decline

neurodegeneration | 2026-04-27 | 3 hypotheses Top: 0.626

VEGF Family GWAS Signals and Cerebrovascular-Neuronal Coupling in AD Hippocampus

neurodegeneration | 2026-04-27 | 3 hypotheses Top: 0.626

Statistical Fine-Mapping of AD GWAS Loci to Identify Causal Variants

neurodegeneration | 2026-04-16 | 1 hypotheses Top: 0.380

Variant Annotation and Prioritization of AD Risk Loci

neurodegeneration | 2026-04-16 | 1 hypotheses Top: 0.862

Experiments (1)

Experimental studies targeting or related to this entity

Experiment	Type	Disease	Score	Feasibility	Model	Status	Est. Cost
12 newly identified AD-associated genes show prior evidence linking th	computational	Alzheimer's disease	0.500	0.00	in_vitro	extracted	N/A

Related Papers (0)

Scientific publications cited in analyses involving this entity

Title & PMID	Authors	Journal	Year	Citations
No papers found

Debates (7)

Multi-agent debates referencing this entity

How do VEGF family gene variants identified by single-cell GWAS analysis alter c

closed · Rounds: 4 · Score: 0.67 · 2026-04-28

What cell-type-specific gene regulatory networks mediate the DPP6 GWAS signal fo

closed · Rounds: 4 · Score: 0.67 · 2026-04-28

How do GWAS-identified PD risk variants at the LRRK2 locus alter lysosomal membr

closed · Rounds: 6 · Score: 0.89 · 2026-04-27

Which non-coding variants at AD GWAS loci have functional evidence for gene regu

closed · Rounds: 4 · Score: 0.70 · 2026-04-21

Can Bayesian fine-mapping of the top 25 AD GWAS loci identify credible sets of c

closed · Rounds: 4 · Score: 0.70 · 2026-04-21

Does fine-mapping to median 3-variant credible sets provide sufficient resolutio

closed · Rounds: 4 · Score: 0.70 · 2026-04-16

Does the BIN1 non-coding variant mechanism provide a druggable target, or is tra

closed · Rounds: 4 · Score: 0.70 · 2026-04-16

Related Research

Hypotheses and analyses mentioning WAS in their description or question text

Cell-state stratification is required to resolve VEGF Family GWAS Signals and Ce

Score: 0.612 · neurodegeneration · 2026-04-28

The question is likely underpowered or misleading unless analyses preserve the key strata: VEGF, GWAS, VEGF-. Averaging

Perturbation-first validation should precede therapeutic claims for DPP6 GWAS Si

Score: 0.608 · neurodegeneration · 2026-04-28

The debate supports treating this as a validation program before ranking it as a therapy. Perturbation should move a pro

Perturbation-first validation should precede therapeutic claims for VEGF Family