gene

EDEM2

Entity Detail — Knowledge Graph Node

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This page aggregates everything SciDEX knows about EDEM2: 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.

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Summary

Page for EDEM2 — ER Degradation Enhancer

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🧬 Gene Info

Gene Symbol	EDEM2
Full Name	ER Degradation Enhancer
Chromosome	7p22.1
Protein Type	Gene
Function	is a key regulator of endoplasmic reticulum-associated degradation (ERAD).
Primary Expression	all tissues with high expression in: - Brain: Neurons, astrocytes, microglia -
Subcellular Localization	Endoplasmic reticulum membrane
Amino Acids	639 aa
GeneCards	EDEM2
Human Protein Atlas	EDEM2
ER stress	Dopaminergic neurons are particularly sensitive to ER stress
[Tau](/proteins/tau) pathology	EDEM2 dysfunction may contribute to tau aggregation
Adaptive response	EDEM2 is upregulated in AD brain as a protective response
Protein aggregation	EDEM2 dysfunction may contribute to Lewy body formation
ER stress response	Motor neurons experience chronic ER stress
Associated Diseases	neurodegeneration
Databases	GeneCards UniProt NCBI Gene HPA STRING

Wiki Pages (1)

Knowledge base pages for this entity

Canonical Page

EDEM2 — ER Degradation Enhancer

gene · 635 words

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Pathway Diagram

graph TD
    EDEM2["EDEM2"]
    neurodegeneration["neurodegeneration"]
    EDEM2 -->|"implicated_in"| neurodegeneration
    style EDEM2 fill:#4a1a6b,stroke:#4fc3f7,stroke-width:2px,color:#e0e0e0

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Targeting Hypotheses (0)

Hypotheses where this entity is a therapeutic target

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Mentioning Analyses (0)

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Experiments (0)

Experimental studies targeting or related to this entity

Experiment	Type	Disease	Score	Feasibility	Model	Status	Est. Cost
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Related Papers (0)

Scientific publications cited in analyses involving this entity

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Debates (0)

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Related Research

Hypotheses and analyses mentioning EDEM2 in their description or question text

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