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Disease on EC 2.4.1.155 - alpha-1,6-mannosyl-glycoprotein 6-beta-N-acetylglucosaminyltransferase

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DISEASE
TITLE OF PUBLICATION
LINK TO PUBMED
Adenocarcinoma
Clinical and prognostic implications of ?1, 6-N-acetylglucosaminyltransferase V in patients with gastric cancer.
Knockdown of Mgat5 Inhibits Breast Cancer Cell Growth with Activation of CD4+ T Cells and Macrophages.
Knockdown of Mgat5 inhibits CD133+ human pulmonary adenocarcinoma cell growth in vitro and in vivo.
Adenocarcinoma of Lung
Altered ?1,6-GlcNAc branched N-glycans impair TGF-?-mediated Epithelial-to-Mesenchymal Transition through Smad signalling pathway in human lung cancer.
miR-124-3p Regulates FGF2-EGFR Pathway to Overcome Pemetrexed Resistance in Lung Adenocarcinoma Cells by Targeting MGAT5.
Adenocarcinoma, Mucinous
High expression of N-acetylglucosaminyltransferase V in mucinous tumors of the ovary.
Adenoma
Altered mRNA expression of glycosyltransferases in human colorectal carcinomas and liver metastases.
Co-expression of matriptase and N-acetylglucosaminyltransferase V in thyroid cancer tissues--its possible role in prolonged stability in vivo by aberrant glycosylation.
Post-translational glycoprotein modifications regulate colon cancer stem cells and colon adenoma progression in Apc(min/+) mice through altered Wnt receptor signaling.
alpha-1,6-mannosyl-glycoprotein 6-beta-n-acetylglucosaminyltransferase deficiency
Loss of branched O-mannosyl glycans in astrocytes accelerates remyelination.
Mgat5 deficiency in T cells and experimental autoimmune encephalomyelitis.
N-acetylglucosaminyltransferase V (Mgat5)-mediated N-glycosylation negatively regulates Th1 cytokine production by T cells.
Reactivity of anti-HNK-1 antibodies to branched O-mannose glycans associated with demyelination.
Alzheimer Disease
A secreted type of beta1,6 N-acetylglucosaminyltransferase V (GnT-V), a novel angiogenesis inducer, is regulated by gamma-secretase.
Astrocytoma
Upregulated ?1-6 branch N-glycan marks early gliomagenesis but exhibited biphasic expression in the progression of astrocytic glioma.
Autoimmune Diseases
Genetic Variants of the MGAT5 Gene Are Functionally Implicated in the Modulation of T Cells Glycosylation and Plasma IgG Glycome Composition in Ulcerative Colitis.
Negative regulation of T-cell activation and autoimmunity by Mgat5 N-glycosylation.
Brain Injuries
Predominant expression of N-acetylglucosaminyltransferase V (GnT-V) in neural stem/progenitor cells.
Brain Neoplasms
Predictive value of N-acetylglucosaminyltransferase-V for superficial bladder cancer recurrence.
Radiosensitisation of human glioma cells by inhibition of ?1,6-GlcNAc branched N-glycans.
Breast Neoplasms
?1,6 GlcNAc branches-modified protein tyrosine phosphatase alpha enhances its stability and promotes focal adhesion formation in MCF-7 cells.
Beta1,6-branched oligosaccharides are increased in lymph node metastases and predict poor outcome in breast carcinoma.
Chitosan oligosaccharides inhibit epithelial cell migration through blockade of N-acetylglucosaminyltransferase V and branched GlcNAc structure.
Coexpression of beta1,6-N-acetylglucosaminyltransferase V glycoprotein substrates defines aggressive breast cancers with poor outcome.
Control of metastasis by Asn-linked, beta1-6 branched oligosaccharides in mouse mammary cancer cells.
Decreased miR-124-3p promoted breast cancer proliferation and metastasis by targeting MGAT5.
Inhibition of a specific N-glycosylation activity results in attenuation of breast carcinoma cell invasiveness-related phenotypes: inhibition of epidermal growth factor-induced dephosphorylation of focal adhesion kinase.
Knockdown of GnT-Va expression inhibits ligand-induced downregulation of the epidermal growth factor receptor and intracellular signaling by inhibiting receptor endocytosis.
Knockdown of Mgat5 Inhibits Breast Cancer Cell Growth with Activation of CD4+ T Cells and Macrophages.
Post-translational glycoprotein modifications regulate colon cancer stem cells and colon adenoma progression in Apc(min/+) mice through altered Wnt receptor signaling.
Specific posttranslational modification regulates early events in mammary carcinoma formation.
Targeted glycoproteomic identification of biomarkers for human breast carcinoma.
Carcinogenesis
Blocking of N-acetylglucosaminyltransferase V induces cellular endoplasmic reticulum stress in human hepatocarcinoma 7721 cells.
Decreased miR-124-3p promoted breast cancer proliferation and metastasis by targeting MGAT5.
Expression of integrins ?3?1 and ?5?1 and GlcNAc ?1,6 glycan branching influences metastatic melanoma cell migration on fibronectin.
Expression of N-acetylglucosaminyltransferase V in the development of human esophageal cancers: immunohistochemical data from carcinomas and nearby noncancerous lesions.
Hydrogen Sulfide Demonstrates Promising Antitumor Efficacy in Gastric Carcinoma by Targeting MGAT5.
N-Acetylglucosaminyltransferase V exacerbates murine colitis with macrophage dysfunction and enhances colitic tumorigenesis.
N-Acetylglucosaminyltransferase V regulates TGF-? response in hepatic stellate cells and the progression of steatohepatitis.
N-Glycans in cancer progression.
Positive expressions of N-acetylglucosaminyltransferase-V (GnT-V) and beta1-6 branching N-linked oligosaccharides in human testicular germ cells diminish during malignant transformation and progression.
Specific posttranslational modification regulates early events in mammary carcinoma formation.
Targeted glycoproteomic identification of biomarkers for human breast carcinoma.
Transcriptional regulation of the protocadherin ? cluster during Her-2 protein-induced mammary tumorigenesis results from altered N-glycan branching.
Carcinoma
?1,6-N-acetylglucosaminyltransferase V predicts recurrence and survival of patients with clear-cell renal cell carcinoma after surgical resection.
Altered mRNA expression of glycosyltransferases in human colorectal carcinomas and liver metastases.
Altered mRNA expression of glycosyltransferases in human gastric carcinomas.
Beta1,6-branched oligosaccharides and coarse vesicles: a common, pervasive phenotype in melanoma and other human cancers.
Chemical enhancers of cytokine signaling that suppress microfilament turnover and tumor cell growth.
Co-expression of matriptase and N-acetylglucosaminyltransferase V in thyroid cancer tissues--its possible role in prolonged stability in vivo by aberrant glycosylation.
Deletion of mouse embryo fibroblast N-acetylglucosaminyltransferase V stimulates alpha5beta1 integrin expression mediated by the protein kinase C signaling pathway.
Effect of GnT-V knockdown on the proliferation, migration and invasion of the SMMC7721/R human hepatocellular carcinoma drug-resistant cell line.
Expression of N-acetylglucosaminyltransferase V in gastric cancer correlates with metastasis and prognosis.
Expression of N-acetylglucosaminyltransferase V in the development of human esophageal cancers: immunohistochemical data from carcinomas and nearby noncancerous lesions.
Expression of N-acetylglucosaminyltransferase V in the subserosal layer correlates with postsurgical survival of pathological tumor stage 2 carcinoma of the gallbladder.
Expression of N-acetylglucosaminyltransferase v is associated with prognosis and histology in non-small cell lung cancers.
Hydrogen Sulfide Demonstrates Promising Antitumor Efficacy in Gastric Carcinoma by Targeting MGAT5.
Inhibition of a specific N-glycosylation activity results in attenuation of breast carcinoma cell invasiveness-related phenotypes: inhibition of epidermal growth factor-induced dephosphorylation of focal adhesion kinase.
Knockdown of GnT-Va expression inhibits ligand-induced downregulation of the epidermal growth factor receptor and intracellular signaling by inhibiting receptor endocytosis.
Mgat5 and Pten interact to regulate cell growth and polarity.
Negative expression of N-acetylglucosaminyltransferase V in oral squamous cell carcinoma correlates with poor prognosis.
Regulation of cytokine receptors by Golgi N-glycan processing and endocytosis.
Transcriptional regulation of the N-acetylglucosaminyltransferase V gene in human bile duct carcinoma cells (HuCC-T1) is mediated by Ets-1.
Carcinoma, Hepatocellular
Characterization of UDP-N-acetylglucosamine:alpha-6-d-mannoside beta-1,6-N-acetylglucosaminyltransferase V from a human hepatoma cell line Hep3B.
Determination of N-acetylglucosaminyltransferases III, IV and V in normal and hepatoma tissues of rats.
Effect of N-acetylglucosaminyltransferase V on the expressions of other glycosyltransferases.
Effects of epidermal growth factor and insulin on the activity of N-acetylglucosaminyltransferase V.
EGF-mediated migration signaling activated by N-acetylglucosaminyltransferase-V via receptor protein tyrosine phosphatase kappa.
Elevated activity of N-acetylglucosaminyltransferase V in human hepatocellular carcinoma.
Elevated expression of UDP-N-acetylglucosamine: alphamannoside beta1,6 N-acetylglucosaminyltransferase is an early event in hepatocarcinogenesis.
Hepatic aberrant glycosylation by N-acetylglucosaminyltransferase V accelerates HDL assembly.
Increase in beta1-6 GlcNAc branching caused by N-acetylglucosaminyltransferase V directs integrin beta1 stability in human hepatocellular carcinoma cell line SMMC-7721.
Increased expression of N-acetylglucosaminyltransferase-V in human hepatoma cells by retinoic acid and 1alpha,25-dihydroxyvitamin D3.
Loss of Barx1 promotes hepatocellular carcinoma metastasis through up-regulating MGAT5 and MMP9 expression and indicates poor prognosis.
N-acetylglucosaminyltransferase III and V messenger RNA levels in LEC rats during hepatocarcinogenesis.
N-acetylglucosaminyltransferase V activity in metastatic models of human hepatocellular carcinoma in nude mice.
N-Acetylglucosaminyltransferase V as a possible aid for the evaluation of tumor invasiveness in patients with hepatocellular carcinoma.
N-acetylglucosaminyltransferase V confers hepatoma cells with resistance to anoikis through EGFR/PAK1 activation.
Predictive value of N-acetylglucosaminyltransferase-V for superficial bladder cancer recurrence.
Prognostic significance of ?1,6-N-acetylglucosaminyltransferase V expression in patients with hepatocellular carcinoma.
The effect of receptor protein tyrosine phosphatase kappa on the change of cell adhesion and proliferation induced by N-acetylglucosaminyltransferase V.
The role of N-acetylglucosaminyltransferases V in the malignancy of human hepatocellular carcinoma.
Carcinoma, Ovarian Epithelial
High expression of N-acetylglucosaminyltransferase V in mucinous tumors of the ovary.
Carcinoma, Papillary
Co-expression of matriptase and N-acetylglucosaminyltransferase V in thyroid cancer tissues--its possible role in prolonged stability in vivo by aberrant glycosylation.
Carcinoma, Renal Cell
?1,6-N-acetylglucosaminyltransferase V predicts recurrence and survival of patients with clear-cell renal cell carcinoma after surgical resection.
Carcinoma, Squamous Cell
Expression of N-acetylglucosaminyltransferase V in the development of human esophageal cancers: immunohistochemical data from carcinomas and nearby noncancerous lesions.
Expression of N-acetylglucosaminyltransferase v is associated with prognosis and histology in non-small cell lung cancers.
Choriocarcinoma
N-acetylglucosaminyltransferase V regulates extravillous trophoblast invasion through glycosylation of alpha5beta1 integrin.
Colitis
Function of the glycosyltransferase GnT-V in colitis.
N-Acetylglucosaminyltransferase V exacerbates murine colitis with macrophage dysfunction and enhances colitic tumorigenesis.
Colitis, Ulcerative
Genetic Variants of the MGAT5 Gene Are Functionally Implicated in the Modulation of T Cells Glycosylation and Plasma IgG Glycome Composition in Ulcerative Colitis.
Colonic Neoplasms
Attachment of human colon cancer cells to vascular endothelium is enhanced by N-acetylglucosaminyltransferase V.
Comparative quantitation of aberrant glycoforms by lectin-based glycoprotein enrichment coupled with multiple-reaction monitoring mass spectrometry.
Functional proteomics study reveals that N-Acetylglucosaminyltransferase V reinforces the invasive/metastatic potential of colon cancer through aberrant glycosylation on tissue inhibitor of metalloproteinase-1.
Lectin from Sambucus sieboldiana abrogates the anoikis resistance of colon cancer cells conferred by N-acetylglucosaminyltransferase V during hematogenous metastasis.
Post-translational glycoprotein modifications regulate colon cancer stem cells and colon adenoma progression in Apc(min/+) mice through altered Wnt receptor signaling.
Predictive value of N-acetylglucosaminyltransferase-V for superficial bladder cancer recurrence.
Colorectal Neoplasms
Altered mRNA expression of glycosyltransferases in human colorectal carcinomas and liver metastases.
Expression of N-acetylglucosaminyltransferase V in colorectal cancer correlates with metastasis and poor prognosis.
Quantitative analysis of an aberrant glycoform of TIMP1 from colon cancer serum by L-PHA-enrichment and SISCAPA with MRM mass spectrometry.
Silencing GnT-V reduces oxaliplatin chemosensitivity in human colorectal cancer cells through N-glycan alteration of organic cation transporter member 2.
Demyelinating Diseases
Genetics and the environment converge to dysregulate N-glycosylation in multiple sclerosis.
Mgat5 deficiency in T cells and experimental autoimmune encephalomyelitis.
Reactivity of anti-HNK-1 antibodies to branched O-mannose glycans associated with demyelination.
Diabetes Mellitus, Type 1
Incorporating parental information into family-based association tests.
Encephalomyelitis
Mgat5 deficiency in T cells and experimental autoimmune encephalomyelitis.
Encephalomyelitis, Autoimmune, Experimental
Mgat5 deficiency in T cells and experimental autoimmune encephalomyelitis.
Endometrial Neoplasms
Expression of N-acetylglucosaminyltransferase V in endometrial cancer correlates with poor prognosis.
Esophageal Neoplasms
Expression of N-acetylglucosaminyltransferase V in the development of human esophageal cancers: immunohistochemical data from carcinomas and nearby noncancerous lesions.
Fatty Liver
N-Acetylglucosaminyltransferase V regulates TGF-? response in hepatic stellate cells and the progression of steatohepatitis.
Fibrosarcoma
Aberrant N-glycosylation of beta1 integrin causes reduced alpha5beta1 integrin clustering and stimulates cell migration.
Knockdown of GnT-Va expression inhibits ligand-induced downregulation of the epidermal growth factor receptor and intracellular signaling by inhibiting receptor endocytosis.
N-acetylglucosaminyltransferase V expression levels regulate cadherin-associated homotypic cell-cell adhesion and intracellular signaling pathways.
Regulation of homotypic cell-cell adhesion by branched N-glycosylation of N-cadherin extracellular EC2-3 domains.
Glioblastoma
Phostine PST3.1a Targets MGAT5 and Inhibits Glioblastoma-Initiating Cell Invasiveness and Proliferation.
Upregulated ?1-6 branch N-glycan marks early gliomagenesis but exhibited biphasic expression in the progression of astrocytic glioma.
Glioma
?1,6 GlcNAc branches-modified protein tyrosine phosphatase Mu attenuates its tyrosine phosphatase activity and promotes glioma cell migration through PLC?-PKC pathways.
Antigenic profiling of glioma cells to generate allogeneic vaccines or dendritic cell-based therapeutics.
Beta1,6-N-acetylglucosamine-bearing N-glycans in human gliomas: implications for a role in regulating invasivity.
Glioma stem cells invasive phenotype at optimal stiffness is driven by MGAT5 dependent mechanosensing.
Radiosensitisation of human glioma cells by inhibition of ?1,6-GlcNAc branched N-glycans.
Terminally sialylated and fucosylated complex N-glycans are involved in the malignant behavior of high-grade glioma.
Upregulated ?1-6 branch N-glycan marks early gliomagenesis but exhibited biphasic expression in the progression of astrocytic glioma.
Hepatitis
N-acetylglucosaminyltransferase III and V messenger RNA levels in LEC rats during hepatocarcinogenesis.
Hepatitis, Chronic
Elevated expression of UDP-N-acetylglucosamine: alphamannoside beta1,6 N-acetylglucosaminyltransferase is an early event in hepatocarcinogenesis.
N-Acetylglucosaminyltransferase V regulates TGF-? response in hepatic stellate cells and the progression of steatohepatitis.
Infections
?1,6 GlcNAc branches-modified protein tyrosine phosphatase Mu attenuates its tyrosine phosphatase activity and promotes glioma cell migration through PLC?-PKC pathways.
Galectin-3 plays a role in minute virus of mice infection.
N-acetylglucosaminyltransferase V-deficiency increases susceptibility to murine malaria.
Liver Cirrhosis
Elevated expression of UDP-N-acetylglucosamine: alphamannoside beta1,6 N-acetylglucosaminyltransferase is an early event in hepatocarcinogenesis.
Knockdown of N-acetylglucosaminyl transferase v ameliorates hepatotoxin-induced liver fibrosis in mice.
Oligosaccharide modification by N-acetylglucosaminyltransferase-V in macrophages are involved in pathogenesis of bleomycin-induced scleroderma.
The role of N-acetylglucosaminyltransferases V in the malignancy of human hepatocellular carcinoma.
Liver Diseases
N-Acetylglucosaminyltransferase V regulates TGF-? response in hepatic stellate cells and the progression of steatohepatitis.
Liver Neoplasms
IGF2BP1 promotes the liver cancer stem cell phenotype by regulating MGAT5 mRNA stability via m6A RNA methylation.
Prognostic significance of ?1,6-N-acetylglucosaminyltransferase V expression in patients with hepatocellular carcinoma.
Lung Neoplasms
Altered ?1,6-GlcNAc branched N-glycans impair TGF-?-mediated Epithelial-to-Mesenchymal Transition through Smad signalling pathway in human lung cancer.
Down-regulation of N-acetylglucosaminyltransferase V by tumorigenesis- or metastasis-suppressor gene and its relation to metastatic potential of human hepatocarcinoma cells.
Expression of N-acetylglucosaminyltransferase v is associated with prognosis and histology in non-small cell lung cancers.
High Throughput Multiplex SNP-analysis in Chronic Obstructive Pulmonary Disease and Lung Cancer.
N-acetylglucosaminyltransferase V modulates radiosensitivity and migration of small cell lung cancer through epithelial-mesenchymal transition.
Purification and characterization of UDP-N-acetylglucosamine: alpha-6-D-mannoside beta 1-6N-acetylglucosaminyltransferase (N-acetylglucosaminyltransferase V) from a human lung cancer cell line.
Lymphatic Metastasis
Expression of N-acetylglucosaminyltransferase V in the development of human esophageal cancers: immunohistochemical data from carcinomas and nearby noncancerous lesions.
N-acetylglucosaminyltransferase III and V messenger RNA levels in LEC rats during hepatocarcinogenesis.
The implication of N-acetylglucosaminyltransferase V expression in gastric cancer.
Lymphoma
Alpha-2,6-sialylation of L-PHA reactive oligosaccharides and expression of N-acetylglucosaminyltransferase V in human diffuse large B cell lymphoma.
Lymphoma, B-Cell
Alpha-2,6-sialylation of L-PHA reactive oligosaccharides and expression of N-acetylglucosaminyltransferase V in human diffuse large B cell lymphoma.
Lymphoma, Large B-Cell, Diffuse
Alpha-2,6-sialylation of L-PHA reactive oligosaccharides and expression of N-acetylglucosaminyltransferase V in human diffuse large B cell lymphoma.
Malaria
N-acetylglucosaminyltransferase V-deficiency increases susceptibility to murine malaria.
Melanoma
A peptide recognized by human cytolytic T lymphocytes on HLA-A2 melanomas is encoded by an intron sequence of the N-acetylglucosaminyltransferase V gene.
Beta1,6-branched oligosaccharides regulate melanin content and motility in macrophage-melanoma fusion hybrids.
Characterization of glycosylation and adherent properties of melanoma cell lines.
Co-localization of beta1,6-branched oligosaccharides and coarse melanin in macrophage-melanoma fusion hybrids and human melanoma cells in vitro.
Diverse expression of N-acetylglucosaminyltransferase V and complex-type ?1,6-branched N-glycans in uveal and cutaneous melanoma cells.
Expression of c-Met proto-oncogene in metastatic macrophage x melanoma fusion hybrids: implication of its possible role in MSH-induced motility.
Fusion hybrids with macrophage and melanoma cells up-regulate N-acetylglucosaminyltransferase V, beta1-6 branching, and metastasis.
GnT-V expression and metastatic phenotypes in macrophage-melanoma fusion hybrids is down-regulated by 5-Aza-dC: evidence for methylation sensitive, extragenic regulation of GnT-V transcription.
GnT-V, macrophage and cancer metastasis: a common link.
Implication of N-acetylglucosaminyltransferases III and V in cancer: gene regulation and signaling mechanism.
Membrane protein regulators of melanoma pulmonary colonisation identified using a CRISPRa screen and spontaneous metastasis assay in mice.
Overexpression of N-acetylglucosaminyltransferases III and V in human melanoma cells. Implications for MCAM N-glycosylation.
Transforming growth factor beta up-regulates expression of the N-acetylglucosaminyltransferase V gene in mouse melanoma cells.
Upregulation of alpha and beta integrin subunits in metastatic macrophage-melanoma fusion hybrids.
Melanoma, Experimental
Co-localization of beta1,6-branched oligosaccharides and coarse melanin in macrophage-melanoma fusion hybrids and human melanoma cells in vitro.
Expression of c-Met proto-oncogene in metastatic macrophage x melanoma fusion hybrids: implication of its possible role in MSH-induced motility.
UDP-GlcNAc concentration is an important factor in the biosynthesis of beta1,6-branched oligosaccharides: regulation based on the kinetic properties of N-acetylglucosaminyltransferase V.
Mouth Neoplasms
Negative expression of N-acetylglucosaminyltransferase V in oral squamous cell carcinoma correlates with poor prognosis.
Multiple Sclerosis
Hypomorphic MGAT5 polymorphisms promote multiple sclerosis cooperatively with MGAT1 and interleukin-2 and 7 receptor variants.
MGAT5 alters the severity of multiple sclerosis.
MGAT5 and disease severity in progressive multiple sclerosis.
Negative regulation of T-cell activation and autoimmunity by Mgat5 N-glycosylation.
Oligosaccharide modification by N-acetylglucosaminyltransferase-V in macrophages are involved in pathogenesis of bleomycin-induced scleroderma.
Nasopharyngeal Carcinoma
Down-regulation of GnT-V enhances nasopharyngeal carcinoma cell CNE-2 radiosensitivity in vitro and in vivo.
Down-regulation of GnT-V inhibits nasopharyngeal carcinoma cell CNE-2 malignancy in vitro and in vivo.
Inhibition of N-acetylglucosaminyltransferase V enhances the cetuximab-induced radiosensitivity of nasopharyngeal carcinoma cells likely through EGFR N-glycan alterations.
Reversal effect of GnT-V on the radioresistance of human nasopharyngeal carcinoma cells by alteration ?1, 6-GlcNAc branched N-glycans.
Neoplasm Metastasis
A secreted type of beta 1,6-N-acetylglucosaminyltransferase V (GnT-V) induces tumor angiogenesis without mediation of glycosylation: a novel function of GnT-V distinct from the original glycosyltransferase activity.
A secreted type of beta1,6 N-acetylglucosaminyltransferase V (GnT-V), a novel angiogenesis inducer, is regulated by gamma-secretase.
Addition of beta1-6 GlcNAc branching to the oligosaccharide attached to Asn 772 in the serine protease domain of matriptase plays a pivotal role in its stability and resistance against trypsin.
Altered ?1,6-GlcNAc and bisecting GlcNAc-branched N-glycan on integrin ?1 are associated with early spontaneous miscarriage in humans.
Altered mRNA expression of glycosyltransferases in human colorectal carcinomas and liver metastases.
Attachment of human colon cancer cells to vascular endothelium is enhanced by N-acetylglucosaminyltransferase V.
Beta1,6-branched oligosaccharides and coarse vesicles: a common, pervasive phenotype in melanoma and other human cancers.
Beta1,6-branched oligosaccharides are increased in lymph node metastases and predict poor outcome in breast carcinoma.
Coexpression of beta1,6-N-acetylglucosaminyltransferase V glycoprotein substrates defines aggressive breast cancers with poor outcome.
Correlation of glycosyltransferases mRNA expression in extrahepatic bile duct carcinoma with clinical pathological characteristics.
Decreased miR-124-3p promoted breast cancer proliferation and metastasis by targeting MGAT5.
Down-regulation of N-acetylglucosaminyltransferase V by tumorigenesis- or metastasis-suppressor gene and its relation to metastatic potential of human hepatocarcinoma cells.
Downregulation of the GnT-V gene inhibits metastasis and invasion of BGC823 gastric cancer cells.
Elevated expression of N-acetylglucosaminyltransferase V in first trimester human placenta.
Evaluating the function of matriptase and N-acetylglucosaminyltransferase V in prostate cancer metastasis.
Expression of N-acetylglucosaminyltransferase V in colorectal cancer correlates with metastasis and poor prognosis.
Expression of N-acetylglucosaminyltransferase V in gastric cancer correlates with metastasis and prognosis.
Expression of N-acetylglucosaminyltransferase V in the development of human esophageal cancers: immunohistochemical data from carcinomas and nearby noncancerous lesions.
Expression of N-acetylglucosaminyltransferase V in the subserosal layer correlates with postsurgical survival of pathological tumor stage 2 carcinoma of the gallbladder.
Expression of N-acetylglucosaminyltransferase v is associated with prognosis and histology in non-small cell lung cancers.
Fusion hybrids with macrophage and melanoma cells up-regulate N-acetylglucosaminyltransferase V, beta1-6 branching, and metastasis.
Galectin-3 plays a role in minute virus of mice infection.
Glycans and cancer: role of N-glycans in cancer biomarker, progression and metastasis, and therapeutics.
GnT-V expression and metastatic phenotypes in macrophage-melanoma fusion hybrids is down-regulated by 5-Aza-dC: evidence for methylation sensitive, extragenic regulation of GnT-V transcription.
GnT-V, macrophage and cancer metastasis: a common link.
Hydrogen Sulfide Demonstrates Promising Antitumor Efficacy in Gastric Carcinoma by Targeting MGAT5.
Identification of liver metastasis-related genes in a novel human pancreatic carcinoma cell model by microarray analysis.
Implication of GnT-V in cancer metastasis: a glycomic approach for identification of a target protein and its unique function as an angiogenic cofactor.
Implication of N-acetylglucosaminyltransferases III and V in cancer: gene regulation and signaling mechanism.
Knockdown of Mgat5 Inhibits Breast Cancer Cell Growth with Activation of CD4+ T Cells and Macrophages.
Lectin from Sambucus sieboldiana abrogates the anoikis resistance of colon cancer cells conferred by N-acetylglucosaminyltransferase V during hematogenous metastasis.
Loss of Barx1 promotes hepatocellular carcinoma metastasis through up-regulating MGAT5 and MMP9 expression and indicates poor prognosis.
Membrane protein regulators of melanoma pulmonary colonisation identified using a CRISPRa screen and spontaneous metastasis assay in mice.
Metabolic homeostasis and tissue renewal are dependent on beta1,6GlcNAc-branched N-glycans.
Modulation of CD147-induced matrix metalloproteinase activity: role of CD147 N-glycosylation.
N-acetylglucosaminyltransferase III and V messenger RNA levels in LEC rats during hepatocarcinogenesis.
N-acetylglucosaminyltransferase III antagonizes the effect of N-acetylglucosaminyltransferase V on alpha3beta1 integrin-mediated cell migration.
N-acetylglucosaminyltransferase V inhibits the invasion of trophoblast cells by attenuating MMP2/9 activity in early human pregnancy.
N-Acetylglucosaminyltransferase V regulates TGF-? response in hepatic stellate cells and the progression of steatohepatitis.
N-glycosylation by N-acetylglucosaminyltransferase V enhances the interaction of CD147/basigin with integrin ?1 and promotes HCC metastasis.
Negative expression of N-acetylglucosaminyltransferase V in oral squamous cell carcinoma correlates with poor prognosis.
NMR structural characterization of substrates bound to N-acetylglucosaminyltransferase V.
Oligosaccharide modification by N-acetylglucosaminyltransferase-V in macrophages are involved in pathogenesis of bleomycin-induced scleroderma.
Physiological roles of N-acetylglucosaminyltransferase V(GnT-V) in mice.
Prometastatic effect of N-acetylglucosaminyltransferase V is due to modification and stabilization of active matriptase by adding beta 1-6 GlcNAc branching.
Regulation of cytokine receptors by Golgi N-glycan processing and endocytosis.
Regulation of the GnT-V promoter by transcription factor Ets-1 in various cancer cell lines.
Relationship between metastasis-associated phenotypes and N-glycan structure of surface glycoproteins in human hepatocarcinoma cells.
Sequences of the mouse N-acetylglucosaminyltransferase V (Mgat5) mRNA and an mRNA expressed by an Mgat5-deficient cell line.
Structure and mechanism of cancer-associated N-acetylglucosaminyltransferase-V.
Suppression of tumor growth and metastasis in Mgat5-deficient mice.
Suppression of tumor-related glycosylation of cell surface receptors by the 16-kDa membrane subunit of vacuolar H+-ATPase.
Synthesis and evaluation of a radioiodinated trisaccharide derivative as a synthetic substrate for a sensitive N-acetylglucosaminyltransferase V radioassay.
TGF-?1 Causes EMT by regulating N-Acetyl Glucosaminyl Transferases via Downregulation of Non Muscle Myosin II-A through JNK/P38/PI3K pathway in lung cancer.
The Caenorhabditis elegans gene, gly-2, can rescue the N-acetylglucosaminyltransferase V mutation of Lec4 cells.
The cancer cell--leukocyte fusion theory of metastasis.
The implication of N-acetylglucosaminyltransferase V expression in gastric cancer.
The Role of N-acetylglucosaminyltransferase III and V in the Post-Transcriptional Modifications of E-cadherin.
Three-dimensional homology model of GlcNAc-TV glycosyltransferase.
Transforming growth factor beta up-regulates expression of the N-acetylglucosaminyltransferase V gene in mouse melanoma cells.
True significance of N-acetylglucosaminyltransferases GnT-III, V and ?1,6 fucosyltransferase in epithelial-mesenchymal transition and cancer.
Upregulation of N-acetylglucosaminyltransferase-V by heparin-binding EGF-like growth factor induces keratinocyte proliferation and epidermal hyperplasia.
[GnT-V overexpression in human hepatocarcinoma cells affects its migration and expression of cell adhesion molecules]
Neoplasms
A genetic strategy involving a glycosyltransferase promoter and a lipid translocating enzyme to eliminate cancer cells.
A secreted type of beta 1,6-N-acetylglucosaminyltransferase V (GnT-V) induces tumor angiogenesis without mediation of glycosylation: a novel function of GnT-V distinct from the original glycosyltransferase activity.
A secreted type of beta1,6 N-acetylglucosaminyltransferase V (GnT-V), a novel angiogenesis inducer, is regulated by gamma-secretase.
Aberrant N-glycosylation of beta1 integrin causes reduced alpha5beta1 integrin clustering and stimulates cell migration.
Addition of beta1-6 GlcNAc branching to the oligosaccharide attached to Asn 772 in the serine protease domain of matriptase plays a pivotal role in its stability and resistance against trypsin.
Alteration in N -acetylglucosaminyltransferase activities and glycan structure in tissue and bile glycoproteins from extrahepatic bile duct carcinoma.
Altered ?1,6-GlcNAc branched N-glycans impair TGF-?-mediated Epithelial-to-Mesenchymal Transition through Smad signalling pathway in human lung cancer.
Attachment of human colon cancer cells to vascular endothelium is enhanced by N-acetylglucosaminyltransferase V.
Beta1,6-branched oligosaccharides and coarse vesicles: a common, pervasive phenotype in melanoma and other human cancers.
Beta1,6-branched oligosaccharides are increased in lymph node metastases and predict poor outcome in breast carcinoma.
Caveolin-1 regulation of dynamin-dependent, raft-mediated endocytosis of cholera toxin b-subunit occurs independently of caveolae.
Co-expression of matriptase and N-acetylglucosaminyltransferase V in thyroid cancer tissues--its possible role in prolonged stability in vivo by aberrant glycosylation.
Coexpression of beta1,6-N-acetylglucosaminyltransferase V glycoprotein substrates defines aggressive breast cancers with poor outcome.
Complex N-glycan and metabolic control in tumor cells.
Correlated gene expression between beta-1,4-galactosyltransferase V and N-acetylglucosaminyltransferase V in human cancer cell lines.
Correlation of glycosyltransferases mRNA expression in extrahepatic bile duct carcinoma with clinical pathological characteristics.
Deletion of mouse embryo fibroblast N-acetylglucosaminyltransferase V stimulates alpha5beta1 integrin expression mediated by the protein kinase C signaling pathway.
Down-regulation of GnT-V inhibits nasopharyngeal carcinoma cell CNE-2 malignancy in vitro and in vivo.
Down-regulation of N-acetylglucosaminyltransferase V by tumorigenesis- or metastasis-suppressor gene and its relation to metastatic potential of human hepatocarcinoma cells.
Down-regulation of N-acetylglucosaminyltransferase-V induces ER stress by changing glycosylation and function of GLUT1.
E-cadherin and adherens-junctions stability in gastric carcinoma: Functional implications of glycosyltransferases involving N-glycan branching biosynthesis, N-acetylglucosaminyltransferases III and V.
Ectopic expression of N-acetylglucosaminyltransferase V accelerates hepatic triglyceride synthesis.
EGF-mediated migration signaling activated by N-acetylglucosaminyltransferase-V via receptor protein tyrosine phosphatase kappa.
Elevated expression of N-acetylglucosaminyltransferase V in first trimester human placenta.
Enhanced Epithelial-Mesenchymal Transition-like Phenotype in N-Acetylglucosaminyltransferase V Transgenic Mouse Skin Promotes Wound Healing.
Expression of integrins ?3?1 and ?5?1 and GlcNAc ?1,6 glycan branching influences metastatic melanoma cell migration on fibronectin.
Expression of N-acetylglucosaminyltransferase V in colorectal cancer correlates with metastasis and poor prognosis.
Expression of N-acetylglucosaminyltransferase V in endometrial cancer correlates with poor prognosis.
Expression of N-acetylglucosaminyltransferase V in gastric cancer correlates with metastasis and prognosis.
Expression of N-acetylglucosaminyltransferase V in the development of human esophageal cancers: immunohistochemical data from carcinomas and nearby noncancerous lesions.
Expression of N-acetylglucosaminyltransferase V in the subserosal layer correlates with postsurgical survival of pathological tumor stage 2 carcinoma of the gallbladder.
Expression of N-acetylglucosaminyltransferase v is associated with prognosis and histology in non-small cell lung cancers.
Functional proteomics study reveals that N-Acetylglucosaminyltransferase V reinforces the invasive/metastatic potential of colon cancer through aberrant glycosylation on tissue inhibitor of metalloproteinase-1.
Fusion hybrids with macrophage and melanoma cells up-regulate N-acetylglucosaminyltransferase V, beta1-6 branching, and metastasis.
Galectin-3 plays a role in minute virus of mice infection.
Generation of antibodies recognizing an aberrant glycoform of human tissue inhibitor of metalloproteinase-1 (TIMP-1) using decoy immunization and phage display.
Glioma stem cells invasive phenotype at optimal stiffness is driven by MGAT5 dependent mechanosensing.
Glycans and cancer: role of N-glycans in cancer biomarker, progression and metastasis, and therapeutics.
Glycoprotein glycosylation and cancer progression.
Glycosylation regulates NK cell-mediated effector function through PI3K pathway.
GnT-V expression and metastatic phenotypes in macrophage-melanoma fusion hybrids is down-regulated by 5-Aza-dC: evidence for methylation sensitive, extragenic regulation of GnT-V transcription.
GnT-V promotes chemosensitivity to gemcitabine in bladder cancer cells through ?1,6 GlcNAc branch modification of human equilibrative nucleoside transporter 1.
GnT-V, macrophage and cancer metastasis: a common link.
Hepatic aberrant glycosylation by N-acetylglucosaminyltransferase V accelerates HDL assembly.
High expression of N-acetylglucosaminyltransferase V in mucinous tumors of the ovary.
Identification of liver metastasis-related genes in a novel human pancreatic carcinoma cell model by microarray analysis.
Implication of GnT-V in cancer metastasis: a glycomic approach for identification of a target protein and its unique function as an angiogenic cofactor.
Implication of N-acetylglucosaminyltransferases III and V in cancer: gene regulation and signaling mechanism.
In vivo delivery of bio-nanocapsules displaying L4-PHA isolectin to malignant tumors overexpressing N-acetylglucosaminyltransferase V.
In vivo delivery of bionanocapsules displaying Phaseolus vulgaris agglutinin-L4 isolectin to malignant tumors overexpressing N-acetylglucosaminyltransferase V.
Inhibition of a specific N-glycosylation activity results in attenuation of breast carcinoma cell invasiveness-related phenotypes: inhibition of epidermal growth factor-induced dephosphorylation of focal adhesion kinase.
Inhibition of N-acetylglucosaminyltransferase V enhances sensitivity of radiotherapy in human prostate cancer.
Inhibition of N-acetylglucosaminyltransferase V enhances the cetuximab-induced radiosensitivity of nasopharyngeal carcinoma cells likely through EGFR N-glycan alterations.
Knockdown of Mgat5 Inhibits Breast Cancer Cell Growth with Activation of CD4+ T Cells and Macrophages.
Knockdown of Mgat5 inhibits CD133+ human pulmonary adenocarcinoma cell growth in vitro and in vivo.
Lectin from Sambucus sieboldiana abrogates the anoikis resistance of colon cancer cells conferred by N-acetylglucosaminyltransferase V during hematogenous metastasis.
Lectin precipitation using phytohemagglutinin-L(4) coupled to avidin-agarose for serological biomarker discovery in colorectal cancer.
Loss of expression of N-acetylglucosaminyltransferase Va results in altered gene expression of glycosyltransferases and galectins.
Membrane protein regulators of melanoma pulmonary colonisation identified using a CRISPRa screen and spontaneous metastasis assay in mice.
Metabolic homeostasis and tissue renewal are dependent on beta1,6GlcNAc-branched N-glycans.
Metastases: the glycan connection.
Mevalonate Pathway Inhibition Slows Breast Cancer Metastasis via Reduced N-glycosylation Abundance and Branching.
Mgat5 and Pten interact to regulate cell growth and polarity.
Mgat5 modulates the effect of early life stress on adult behavior and physical health in mice.
miR-124-3p Regulates FGF2-EGFR Pathway to Overcome Pemetrexed Resistance in Lung Adenocarcinoma Cells by Targeting MGAT5.
Modulation of CD147-induced matrix metalloproteinase activity: role of CD147 N-glycosylation.
N-acetylglucosaminyltransferase III and V messenger RNA levels in LEC rats during hepatocarcinogenesis.
N-acetylglucosaminyltransferase V and beta1-6 branching N-linked oligosaccharides are associated with good prognosis of patients with bladder cancer.
N-Acetylglucosaminyltransferase V as a possible aid for the evaluation of tumor invasiveness in patients with hepatocellular carcinoma.
N-acetylglucosaminyltransferase V confers hepatoma cells with resistance to anoikis through EGFR/PAK1 activation.
N-acetylglucosaminyltransferase V expression levels regulate cadherin-associated homotypic cell-cell adhesion and intracellular signaling pathways.
N-acetylglucosaminyltransferase V inhibits the invasion of trophoblast cells by attenuating MMP2/9 activity in early human pregnancy.
N-acetylglucosaminyltransferase V mediates cell migration and invasion of mouse mammary tumor cells 4TO7 via RhoA and Rac1 signaling pathway.
N-acetylglucosaminyltransferase V modulates radiosensitivity and migration of small cell lung cancer through epithelial-mesenchymal transition.
N-acetylglucosaminyltransferase V regulates extravillous trophoblast invasion through glycosylation of alpha5beta1 integrin.
N-Acetylglucosaminyltransferase V regulates TGF-? response in hepatic stellate cells and the progression of steatohepatitis.
N-Acetylglucosaminyltransferase V triggers overexpression of MT1-MMP and reinforces the invasive/metastatic potential of cancer cells.
N-glycosylation by N-acetylglucosaminyltransferase V enhances the interaction of CD147/basigin with integrin ?1 and promotes HCC metastasis.
N-Glycosylation of laminin-332 regulates its biological functions. A novel function of the bisecting GlcNAc.
Negative expression of N-acetylglucosaminyltransferase V in oral squamous cell carcinoma correlates with poor prognosis.
NMR structural characterization of substrates bound to N-acetylglucosaminyltransferase V.
Oligosaccharide modification by N-acetylglucosaminyltransferase-V in macrophages are involved in pathogenesis of bleomycin-induced scleroderma.
Overexpression and ?-1,6-N-acetylglucosaminylation-initiated aberrant glycosylation of TIMP-1; A "double whammy" strategy in colon cancer progression.
Physiological roles of N-acetylglucosaminyltransferase V(GnT-V) in mice.
Plasma membrane domain organization regulates EGFR signaling in tumor cells.
Positive expressions of N-acetylglucosaminyltransferase-V (GnT-V) and beta1-6 branching N-linked oligosaccharides in human testicular germ cells diminish during malignant transformation and progression.
Post-translational glycoprotein modifications regulate colon cancer stem cells and colon adenoma progression in Apc(min/+) mice through altered Wnt receptor signaling.
Potential of N-glycan in cell adhesion and migration as either a positive or negative regulator.
Predictive value of N-acetylglucosaminyltransferase-V for superficial bladder cancer recurrence.
Preventing E-cadherin aberrant N-glycosylation at Asn-554 improves its critical function in gastric cancer.
Prognostic significance of ?1,6-N-acetylglucosaminyltransferase V expression in patients with hepatocellular carcinoma.
Quantitative analysis of an aberrant glycoform of TIMP1 from colon cancer serum by L-PHA-enrichment and SISCAPA with MRM mass spectrometry.
Recognition of glycan and protein substrates by N-acetylglucosaminyltransferase-V.
Regulation of cytokine receptors by Golgi N-glycan processing and endocytosis.
Regulation of homotypic cell-cell adhesion by branched N-glycosylation of N-cadherin extracellular EC2-3 domains.
Regulation of the GnT-V promoter by transcription factor Ets-1 in various cancer cell lines.
Relationship between metastasis-associated phenotypes and N-glycan structure of surface glycoproteins in human hepatocarcinoma cells.
Sequences of the mouse N-acetylglucosaminyltransferase V (Mgat5) mRNA and an mRNA expressed by an Mgat5-deficient cell line.
Specific posttranslational modification regulates early events in mammary carcinoma formation.
Structure and mechanism of cancer-associated N-acetylglucosaminyltransferase-V.
Suppression of tumor growth and metastasis in Mgat5-deficient mice.
Synthesis and evaluation of a radioiodinated trisaccharide derivative as a synthetic substrate for a sensitive N-acetylglucosaminyltransferase V radioassay.
The Caenorhabditis elegans gene, gly-2, can rescue the N-acetylglucosaminyltransferase V mutation of Lec4 cells.
The effect of receptor protein tyrosine phosphatase kappa on the change of cell adhesion and proliferation induced by N-acetylglucosaminyltransferase V.
THE IMPACT OF ALCOHOL ON PRO-METASTATIC N-GLYCOSYLATION IN PROSTATE CANCER.
The role of N-acetylglucosaminyltransferases V in the malignancy of human hepatocellular carcinoma.
Three-dimensional homology model of GlcNAc-TV glycosyltransferase.
Transcriptional regulation of the protocadherin ? cluster during Her-2 protein-induced mammary tumorigenesis results from altered N-glycan branching.
Transforming growth factor beta up-regulates expression of the N-acetylglucosaminyltransferase V gene in mouse melanoma cells.
True significance of N-acetylglucosaminyltransferases GnT-III, V and ?1,6 fucosyltransferase in epithelial-mesenchymal transition and cancer.
Upregulated ?1-6 branch N-glycan marks early gliomagenesis but exhibited biphasic expression in the progression of astrocytic glioma.
Upregulation of alpha and beta integrin subunits in metastatic macrophage-melanoma fusion hybrids.
Upregulation of N-acetylglucosaminyltransferase-V by heparin-binding EGF-like growth factor induces keratinocyte proliferation and epidermal hyperplasia.
[GnT-V overexpression in human hepatocarcinoma cells affects its migration and expression of cell adhesion molecules]
Neoplasms, Germ Cell and Embryonal
Positive expressions of N-acetylglucosaminyltransferase-V (GnT-V) and beta1-6 branching N-linked oligosaccharides in human testicular germ cells diminish during malignant transformation and progression.
Neuroblastoma
High expression of N-acetylglucosaminyltransferase V in favorable neuroblastomas: Involvement of its effect on apoptosis.
Integrin-dependent neuroblastoma cell adhesion and migration on laminin is regulated by expression levels of two enzymes in the O-mannosyl-linked glycosylation pathway, PomGnT1 and GnT-Vb.
Receptor tyrosine phosphatase beta (RPTPbeta) activity and signaling are attenuated by glycosylation and subsequent cell surface galectin-1 binding.
Ovarian Neoplasms
5-AZA-dC induces epigenetic changes associated with modified glycosylation of secreted glycoproteins and increased EMT and migration in chemo-sensitive cancer cells.
High expression of N-acetylglucosaminyltransferase V in mucinous tumors of the ovary.
In this issue: Proteomics 16/2008.
Parasitic Diseases
N-acetylglucosaminyltransferase V-deficiency increases susceptibility to murine malaria.
Periodontitis
The role of extracellular matrix metalloproteinase inducer glycosylation in regulating matrix metalloproteinases in periodontitis.
Pheochromocytoma
Comparison of the expression of cell surface poly-N-acetyllactosamine-type oligosaccharides in PC12 cells with those in its variant PC12D.
N-acetylglucosaminyltranferase VB expression enhances beta1 integrin- dependent PC12 neurite outgrowth on laminin and collagen.
N-acetylglucosaminyltransferase V modifies TrKA protein, regulates the receptor function.
Pre-Eclampsia
The Role of MGAT5 in Human Umbilical Vein Endothelial Cells: Possible Relevance to the Pathological Mechanism of Preeclampsia.
Prostatic Neoplasms
Evaluating the function of matriptase and N-acetylglucosaminyltransferase V in prostate cancer metastasis.
Inhibition of N-acetylglucosaminyltransferase V enhances sensitivity of radiotherapy in human prostate cancer.
[Short hairpin RNA targeting N-acetylglucosaminyltransferase V inhibits the proliferation of prostate cancer PC-3 cell line]
Psoriasis
Genome-Wide Pathway Analysis Identifies Genetic Pathways Associated with Psoriasis.
Pulmonary Disease, Chronic Obstructive
The polymorphisms of FGFR2 and MGAT5 affect the susceptibility to COPD in the Chinese people.
Sarcoma
Regulation of N-acetylglucosaminyltransferase V activity. Kinetic comparisons of parental, Rous sarcoma virus-transformed BHK, and L-phytohemagglutinin-resistant BHK cells using synthetic substrates and an inhibitory substrate analog.
Sarcoma, Avian
An enzyme-linked immunosorbent assay for N-acetylglucosaminyltransferase-V.
Regulation of N-acetylglucosaminyltransferase V activity. Kinetic comparisons of parental, Rous sarcoma virus-transformed BHK, and L-phytohemagglutinin-resistant BHK cells using synthetic substrates and an inhibitory substrate analog.
Transcriptional regulation of N-acetylglucosaminyltransferase V by the src oncogene.
Seminoma
Positive expressions of N-acetylglucosaminyltransferase-V (GnT-V) and beta1-6 branching N-linked oligosaccharides in human testicular germ cells diminish during malignant transformation and progression.
Small Cell Lung Carcinoma
N-acetylglucosaminyltransferase V modulates radiosensitivity and migration of small cell lung cancer through epithelial-mesenchymal transition.
Squamous Cell Carcinoma of Head and Neck
Negative expression of N-acetylglucosaminyltransferase V in oral squamous cell carcinoma correlates with poor prognosis.
Stomach Neoplasms
Clinical and prognostic implications of ?1, 6-N-acetylglucosaminyltransferase V in patients with gastric cancer.
Diagnostic utility of glycosyltransferase mRNA expression in gastric cancer.
Downregulation of the GnT-V gene inhibits metastasis and invasion of BGC823 gastric cancer cells.
E-cadherin and adherens-junctions stability in gastric carcinoma: Functional implications of glycosyltransferases involving N-glycan branching biosynthesis, N-acetylglucosaminyltransferases III and V.
Expression of N-acetylglucosaminyltransferase V in gastric cancer correlates with metastasis and prognosis.
Prometastatic effect of N-acetylglucosaminyltransferase V is due to modification and stabilization of active matriptase by adding beta 1-6 GlcNAc branching.
The implication of N-acetylglucosaminyltransferase V expression in gastric cancer.
Thyroid Neoplasms
Co-expression of matriptase and N-acetylglucosaminyltransferase V in thyroid cancer tissues--its possible role in prolonged stability in vivo by aberrant glycosylation.
Tics
Specific posttranslational modification regulates early events in mammary carcinoma formation.
Urinary Bladder Neoplasms
Glycosylation in bladder cancer.
GnT-V promotes chemosensitivity to gemcitabine in bladder cancer cells through ?1,6 GlcNAc branch modification of human equilibrative nucleoside transporter 1.
N-acetylglucosaminyltransferase V and beta1-6 branching N-linked oligosaccharides are associated with good prognosis of patients with bladder cancer.
Predictive value of N-acetylglucosaminyltransferase-V for superficial bladder cancer recurrence.