Literature summary for 2.4.1.102 extracted from

Sumardika, I.W.; Youyi, C.; Kondo, E.; Inoue, Y.; Ruma, I.M.W.; Murata, H.; Kinoshita, R.; Yamamoto, K.I.; Tomida, S.; Shien, K.; Sato, H.; Yamauchi, A.; Futami, J.; Putranto, E.W.; Hibino, T.; Toyooka, S.; Nishibori, M.; Sakaguchi, M.
beta-1,3-Galactosyl-O-glycosyl-glycoprotein beta-1,6-N-acetylglucosaminyltransferase 3 increases MCAM stability, which enhances S100A8/A9-mediated cancer motility (2018), Oncol. Res., 26, 431-444 .

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Application

Application	Comment	Organism
medicine	GCNT3 is a potential molecular target in melanoma therapeutics through abrogation of the S100A8/A9-MCAM axis	Homo sapiens

Cloned(Commentary)

Cloned (Comment)	Organism
gene GCNT3, recombinant expression of C-terminally 3xMyc-6His-tagged wild-type enzyme and deletion mutant mutGCNT3	Homo sapiens

Protein Variants

Protein Variants	Comment	Organism
additional information	construction of a catalytic dead GCNT3 (mutGCNT3) cDNA designed for expression as C-terminally 3xMyc-6His-tagged deletion form (lacking the region from 323 aa through 438 aa). siRNA-mediated GCNT3 suppression in WM-266-4 cells. Forced expression of mutGCNT3 significantly downregulates migration activity of WM-266-4 cells under either the presence or absence of S100A8/A9 in culture	Homo sapiens

Inhibitors

Inhibitors	Comment	Organism	Structure
talniflumate	a specific inhibitor of GCNT3	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	O95395	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
breast cancer cell	-	Homo sapiens	-
carcinoma cell	GCNT3 is elevated in skin and mesothelioma cells and in some lung and breast cancer cells	Homo sapiens	-
lung cancer cell	-	Homo sapiens	-
melanoma cell	GCNT3 is overexpressed in highly metastatic melanomas	Homo sapiens	-
mesothelioma cell	-	Homo sapiens	-
additional information	quantitative RT-PCR expression analysis	Homo sapiens	-
skin	-	Homo sapiens	-
WM-115 cell	-	Homo sapiens	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
UDP-N-acetyl-alpha-D-glucosamine + O3-[beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl]-L-seryl/threonyl-[protein]	-	Homo sapiens	UDP + O3-(beta-D-galactosyl-(1->3)-[N-acetyl-beta-D-glucosaminyl-(1->6)]-N-acetyl-alpha-D-galactosaminyl)-L-seryl/threonyl-[protein]	-	?

Synonyms

Synonyms	Comment	Organism
beta-1,3-galactosyl-O-glycosyl-glycoprotein beta-1,6-N-acetylglucosaminyltransferase 3	-	Homo sapiens
gcnt3	-	Homo sapiens

General Information

General Information	Comment	Organism
malfunction	silencing and functional inhibition of GCNT3 greatly suppresses migration and invasion of melanoma cells, resulting in the loss of S100A8/A9 responsiveness. siRNA-mediated GCNT3 suppression and talniflumate-mediated GCNT3 suppression significantly attenuate the basal ability of in vitro migration of WM-266-4 cells	Homo sapiens
physiological function	beta-1,3-galactosyl-O-glycosyl-glycoprotein beta-1,6-N-acetylglucosaminyltransferase 3 (GCNT3) is a glycosyltransferase that transfers GlcNAc to N-acetylgalactosamine (GalNAc) of the core 1 acceptor structure to form the core 2 branch in the beta-1,6 linkage. In addition to the formation of the core 2 structure, GCNT3 also functions to form the core 4 structure. GCNT3 increases MCAM stability, which enhances S100A8/A9-mediated cancer motility. Among the novel S100A8/A9 receptors, GCNT3 favorably glycosylates the MCAM receptor, extending its half-life and leading to further elevation of S100A8/A9-mediated cellular motility in melanoma cells. GCNT3 plays a pivotal role in the maintenance of MCAM protein at a high level, resulting in the acquisition of strong responsiveness to S100A8/A9 that is linked to increased cellular migration and invasion. GCNT3 expression is positively correlated to MCAM expression in patients with high-grade melanomas. GCNT3 is an upstream regulator of MCAM protein. GCNT3 plays a key role in S100A8/A9-mediated cancer motility. GCNT3 controls MCAM stability by its catalytic activity-mediated glycosyl modification that correlates with a greater ability for cancer cell motility and invasion in response to extracellular S100A8/A9	Homo sapiens

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Release 2023.1 (January 2023)