Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 2.7.1.171 extracted from

  • Sanghvi, V.R.; Leibold, J.; Mina, M.; Mohan, P.; Berishaj, M.; Li, Z.; Miele, M.M.; Lailler, N.; Zhao, C.; de Stanchina, E.; Viale, A.; Akkari, L.; Lowe, S.W.; Ciriello, G.; Hendrickson, R.C.; Wendel, H.G.
    The oncogenic action of NRF2 depends on de-glycation by fructosamine-3-kinase (2019), Cell, 178, 807-819.e21 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.7.1.171

Protein Variants

Protein Variants Comment Organism
additional information knockdown of FN3K with two different shRNAs in HepG2 cells and in H3255 cells. The mutant cells have higher levels of NRF2, and both FACS assay and immunoblot show reduction of NRF2 protein upon knockdown of either FN3K or NRF2. FN3K deficiency leads to increased proteasomal and MG132-sensitive degradation of the glycated NRF2 protein Homo sapiens

Metals/Ions

Metals/Ions Comment Organism Structure
Mg2+ required Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
ATP + [protein]-N6-D-fructosyl-L-lysine Homo sapiens
-
 ADP + [protein]-N6-(3-O-phospho-D-fructosyl)-L-lysine
-
 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens Q9H479
-
-

Source Tissue

Source Tissue Comment Organism Textmining
HEK-293T cell
-
 Homo sapiens
-
Hep-G2 cell
-
 Homo sapiens
-
hepatoma cell
-
 Homo sapiens
-
HuH-1 cell
-
 Homo sapiens
-
lung cancer cell
-
 Homo sapiens
-
NCI-H3255 cell
-
 Homo sapiens
-
NCI-H460 cell
-
 Homo sapiens
-
non-small cell lung cancer cell
-
 Homo sapiens
-
PC-9 cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
ATP + [protein]-N6-D-fructosyl-L-lysine
-
 Homo sapiens ADP + [protein]-N6-(3-O-phospho-D-fructosyl)-L-lysine
-
 ?

Synonyms

Synonyms Comment Organism
FN3K
-
 Homo sapiens
fructosamine-3-kinase
-
 Homo sapiens

Cofactor

Cofactor Comment Organism Structure
ATP
-
 Homo sapiens

General Information

General Information Comment Organism
malfunction N-acetyl cysteine treatment partially rescues the effects of FN3K loss on NRF2 driven tumor phenotypes. FN3K deficiency increases NRF2 glycation and impairs its ability to counter ROS stress in liver and lung cancer cells. Pre-treatment with the ROS scavenger and GSH precursor N-acetyl cysteine (NAC) reverses H2O2 and DLS toxicity and restores glutathione balance in FN3K-deficient HepG2 and H3255 cells, respectively. FN3K deficiency leads to increased proteasomal and MG132-sensitive degradation of the glycated NRF2 protein. Glycation also affects NRF2 function in KEAP1 mutant cells, for example gene and protein expression analyses of FN3K deficient and control Huh-1 liver cancer cells (KEAP1N414Y) show loss of NRF2 targets and resultant redox imbalance as indicated by increased glutathione oxidation Homo sapiens
physiological function fructosamine-3-kinase (FN3K) is a kinase that triggers protein deglycation. Transcription factor NRF2 activity depends on FN3K activity, NRF2 transcription factor controls a cell stress program that is implicated in cancer. Role for the glycation of cellular proteins and implicates FN3K as targetable modulator of NRF2 activity in cancer. The development of hepatocellular carcinoma triggered by MYC and Keap1 inactivation depends on FN3K in vivo, role of FN3K-sensitive NRF2 glycation in liver cancer in vivo, overview Homo sapiens