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FLASH GENE

Symbol

NFE2L2

contributors: mct/npt/pgu/shn - updated : 02-07-2019

HGNC name	nuclear factor (erythroid-derived 2)-like 2
HGNC id	7782

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral       gain of function in lung cancers tumoral       gain of function constitutive NFE2L2 activation might cause drug resistance in tumours constitutional     --low   resulted in decreased HDAC2 in lung, and increased inflammatory lung response which was not reversed by steroid

Susceptibility

to acute lung injury

Variant & Polymorphism SNP	increasing the risk of acute lung injury

Candidate gene
Marker
Therapy target
	System Type Disorder Pubmed cancer     inhibition of NFE2L2 could be used to enhance chemotherapeutic sensitivity respiratory lung   NFE22 targeting might provide clinical benefit by reducing both oxidative stress and inflammation in COPD (chronic obstructive pulmonary disease) digestive     Nrf2 activation by synthetic triterpenoids is a promising candidate target to protect the gastrointestinal tract against acute ionizing radiation osteoarticular bone others KEAP1-NFE2L2 axis may be a therapeutic target for the treatment of bone destructive disease reproduction fertility   therapeutic intervention targeting PARK7 for the treatment of asthenozoospermia

ANIMAL & CELL MODELS

	Nrf2(-/-) mice were highly susceptible to N-acetyl-p-aminophenol treatment and died of liver failure
	mice targeted disruption of Nrf2 causes regenerative immune-mediated hemolytic anemia due to increased sequestration of damaged erythrocytes .
	Nrf2-deficient mice show decolourization of the incisors
	Disruption of the Nrf2 gene in mice led to earlier-onset and more extensive cigarette smoke-induced emphysema
	Disruption of Nrf2 dramatically increased the mortality of mice in response to endotoxin- and cecal ligation and puncture-induced septic shock
	Nrf2-deficient mice developed tumors more readily in response to carcinogen exposure and caloric exposure was ineffective in suppressing tumors in the KO mice
	expression levels of NRF1 is significantly decreased in both Alzheimer's disease hippocampal tissues and AD-causing amyloid precursor protein mutant cells
	Nrf2-null mice develop diffuse white matter injury without overt loss of neurons
	Nrf2 KO mice during acidosis showed increased expression of renal markers of oxidative stress and injury and Nrf2 activity was increased during metabolic acidosis in WT kidney