Product Info

IHC 1:50-1:200, WB 1:500-1:2000, ELISA(peptide) 1:20000-1:40000
*The optimal dilutions should be determined by the end user.
Monoclonal [AFB20117]
Nrf2 Antibody detects endogenous levels of total Nrf2.
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


erythroid derived 2; HEBP1; like 2; NF E2 related factor 2; NF-E2-related factor 2; NF2L2_HUMAN; NFE2 related factor 2; NFE2-related factor 2; Nfe2l2; Nrf 2; NRF2; Nuclear factor (erythroid derived 2) like 2; Nuclear factor; nuclear factor erythroid 2 like 2; Nuclear factor erythroid 2 related factor 2; Nuclear factor erythroid 2-related factor 2; Nuclear factor erythroid derived 2 like 2;



A synthesized peptide derived from human nrf2, corresponding to a region within the internal amino acids.

Q16236 NF2L2_HUMAN:

Widely expressed. Highest expression in adult muscle, kidney, lung, liver and in fetal muscle.


PTMs - Q16236 As Substrate

Site PTM Type Enzyme
S40 Phosphorylation P05771 (PRKCB) , P17252 (PRKCA)
K44 Ubiquitination
K64 Ubiquitination
T80 Phosphorylation
S215 Phosphorylation
S301 Phosphorylation
S344 Phosphorylation P49841 (GSK3B)
S347 Phosphorylation P49841 (GSK3B)
S351 Phosphorylation
S356 Phosphorylation
T395 Phosphorylation Q00535 (CDK5)
S408 Phosphorylation
S433 Phosphorylation Q00535 (CDK5)
R437 Methylation
K438 Acetylation
T439 Phosphorylation Q00535 (CDK5)
K443 Acetylation
K445 Acetylation
S447 Phosphorylation
K462 Acetylation
K462 Ubiquitination
K472 Acetylation
K487 Acetylation
K506 Acetylation
K508 Acetylation
K516 Acetylation
K516 Ubiquitination
K518 Acetylation
K518 Sumoylation
K518 Ubiquitination
K533 Acetylation
K536 Acetylation
K538 Acetylation
K541 Acetylation
K543 Acetylation
K548 Acetylation
K548 Ubiquitination
K554 Acetylation
K554 Ubiquitination
K555 Acetylation
S558 Phosphorylation
T559 Phosphorylation
Y561 Phosphorylation
K574 Ubiquitination
Y576 Phosphorylation P06241 (FYN)
S577 Phosphorylation
K596 Acetylation
K599 Acetylation

Research Backgrounds


Transcription factor that plays a key role in the response to oxidative stress: binds to antioxidant response (ARE) elements present in the promoter region of many cytoprotective genes, such as phase 2 detoxifying enzymes, and promotes their expression, thereby neutralizing reactive electrophiles. In normal conditions, ubiquitinated and degraded in the cytoplasm by the BCR(KEAP1) complex. In response to oxidative stress, electrophile metabolites inhibit activity of the BCR(KEAP1) complex, promoting nuclear accumulation of NFE2L2/NRF2, heterodimerization with one of the small Maf proteins and binding to ARE elements of cytoprotective target genes. The NFE2L2/NRF2 pathway is also activated in response to selective autophagy: autophagy promotes interaction between KEAP1 and SQSTM1/p62 and subsequent inactivation of the BCR(KEAP1) complex, leading to NFE2L2/NRF2 nuclear accumulation and expression of cytoprotective genes. May also be involved in the transcriptional activation of genes of the beta-globin cluster by mediating enhancer activity of hypersensitive site 2 of the beta-globin locus control region.


Ubiquitinated in the cytoplasm by the BCR(KEAP1) E3 ubiquitin ligase complex leading to its degradation. In response to oxidative stress, electrophile metabolites, such as sulforaphane, modify KEAP1, leading to inhibit activity of the BCR(KEAP1) complex, promoting NFE2L2/NRF2 nuclear accumulation and activity. In response to autophagy, the BCR(KEAP1) complex is inactivated (By similarity).

Phosphorylation of Ser-40 by PKC in response to oxidative stress dissociates NFE2L2 from its cytoplasmic inhibitor KEAP1, promoting its translocation into the nucleus.

Acetylation at Lys-596 and Lys-599 increases nuclear localization whereas deacetylation by SIRT1 enhances cytoplasmic presence.

Glycation impairs transcription factor activity by preventing heterodimerization with small Maf proteins. Deglycation by FN3K restores activity.

Subcellular Location:

Cytoplasm>Cytosol. Nucleus.
Note: Cytosolic under unstressed conditions: ubiquitinated and degraded by the BCR(KEAP1) E3 ubiquitin ligase complex (PubMed:15601839, PubMed:21196497). Translocates into the nucleus upon induction by electrophilic agents that inactivate the BCR(KEAP1) E3 ubiquitin ligase complex (PubMed:21196497).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Widely expressed. Highest expression in adult muscle, kidney, lung, liver and in fetal muscle.

Subunit Structure:

Heterodimer; heterodimerizes with small Maf proteins (By similarity). Interacts (via the bZIP domain) with MAFG and MAFK; required for binding to antioxidant response elements (AREs) on DNA (By similarity). Interacts with KEAP1; the interaction is direct and promotes ubiquitination by the BCR(KEAP1) E3 ubiquitin ligase complex. Forms a ternary complex with PGAM5 and KEAP1. Interacts with EEF1D at heat shock promoter elements (HSE). Interacts via its leucine-zipper domain with the coiled-coil domain of PMF1. Interacts with CHD6; involved in activation of the transcription (By similarity). Interacts with ESRRB; represses NFE2L2 transcriptional activity (By similarity).

(Microbial infection) Interacts with herpes virus 8 protein LANA1.


The ETGE motif, and to a lower extent the DLG motif, mediate interaction with KEAP1.

Belongs to the bZIP family. CNC subfamily.

Research Fields

· Genetic Information Processing > Folding, sorting and degradation > Protein processing in endoplasmic reticulum.   (View pathway)

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma.   (View pathway)


1). Dai Y et al. Maf1 mitigates sevoflurane-induced microglial inflammatory damage and attenuates microglia-mediated neurotoxicity in HT-22 cells by activating the AMPK/Nrf2 signaling. Neurotoxicology 2022 May;90:237-245. (PubMed: 35430185) [IF=4.398]

Restrictive clause


Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.

For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.