Literature summary for 2.7.1.60 extracted from

Kemmner, W.; Kessel, P.; Sanchez-Ruderisch, H.; Moeller, H.; Hinderlich, S.; Schlag, P.M.; Detjen, K.
Loss of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE) induces apoptotic processes in pancreatic carcinoma cells (2012), FASEB J., 26, 938-946.

Search for more literature for 2.7.1.60

Protein Variants

Protein Variants	Comment	Organism
additional information	the enzyme is silenced or overexpressed in human pancreatic carcinoma cells, gene expression profiling, enzymatic activity, transcriptions levels, and cell cycle analysis, overview	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	Q9Y223	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
CAPAN-1 cell	pancreatic carcinoma cell line showing low enzyme activity	Homo sapiens	-
carcinoma cell	pancreatic	Homo sapiens	-
QGP-1 cell	pancreatic carcinoma cell line showing low enzyme activity	Homo sapiens	-

Synonyms

Synonyms	Comment	Organism
GNE	-	Homo sapiens
UDP-N-acetylglucosamine-2-epimerase/N-acetylmannosamine-kinase	-	Homo sapiens

Expression

Organism	Comment	Expression
Homo sapiens	GNE up-regulation occurs predominantly in pancreatic cancer but also in other malignancies	up

General Information

General Information	Comment	Organism
malfunction	silencing of GNE sensitizes pancreatic cancer cells to anoikis, an apoptosis program activated on loss of matrix anchorage. A loss of GNE enzyme activity in cells renders them anoikis-susceptible after transfection with the tumor suppressor p16. ManNAc incubation reduces anoikis susceptibility, phenotype, overview. Enzyme up-regulation occurs predominantly in pancreatic cancer but also in other malignancies	Homo sapiens
metabolism	GNE is the key enzyme of sialic acid biosynthesis	Homo sapiens
physiological function	GNE exerts transcriptional control on genes related to endoplasmic reticulum stress. Association of low GNE activity and anoikis susceptibility	Homo sapiens

Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.

Release 2023.1 (January 2023)