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Search results for: Nacetylgalactosaminyltransferase

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#39493373   2024/10/26 To Up

Exercise Attenuates Doxorubicin-Induced Myocardial Injury by Inhibiting TSHR and Regulating Macrophage Polarization Through miR-30d-5p/GALNT7.

Doxorubicin (DOX) is an extensively used chemotherapeutic agent that induces cardiotoxicity. Studies have reported that exercise (EXE) can alleviate DOX-induced cardiotoxicity. Therefore, this study aimed to explore the mechanism by which EXE attenuates DOX-induced myocardial injury. In this study, cell and animal models of DOX-induced myocardial injury were constructed. The animal model was subjected to EXE intervention. In this study, in vitro experiments revealed that miR-30d-5p negatively regulated polypeptide N-acetylgalactosaminyltransferase 7 (GALNT7) and that GALNT7 negatively regulated the expression of thyroid stimulating hormone receptor (TSHR). miR-30d-5p downregulated the expression of GALNT7, promoted the expression of TSHR, and promoted macrophage M1 polarization, thus aggravating cardiomyocyte injury. In vivo experiments revealed that EXE intervention significantly downregulated miR-30d-5p and TSHR expression, upregulated GALNT7, reduced inflammation, and promoted M2 macrophage polarization, thereby alleviating DOX-induced myocardial injury. In addition, overexpression of miR-30d-5p or knockdown of GALNT7 weakened the intervention effect of EXE, whereas overexpression of GALNT7 or knockdown of TSHR promoted the effect of EXE. EXE can modulate the miR-30d-5p/GALNT7 axis to inhibit the expression of TSHR, thereby regulating the polarization of macrophages to the M2 phenotype and ultimately alleviating DOX-induced myocardial injury, which provides new targets and strategies for the clinical treatment of myocardial injury.
Haiyan Wu, Ruoyu Zhou, Hanxin Kong, Jieqiong Yang, Suijuan Liu, Xiaolin Wei, Kunzhi Li, Yunmei Zhang

1888 related Products with: Exercise Attenuates Doxorubicin-Induced Myocardial Injury by Inhibiting TSHR and Regulating Macrophage Polarization Through miR-30d-5p/GALNT7.

96 wells (1 kit)100ul100ug50 ul100ug100ug Lyophilized2ug1 g0.5 ml5ug5ug100 mg

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#39471744   2024/09/24 To Up

Resolving and functional analysis of RNA editing sites in sheep ovaries and associations with litter size.

Sheep litter size is a critical trait in mutton production. While litter size regulation in relation to DNA transcription have been rigorously investigated, the function of RNA editing remains less explored. To elucidate the mechanisms controlling sheep fecundity at the RNA editing level and identify pivotal RNA editing sites, this study scrutinised RNA editing sites (RESs) in follicular and luteal phases of ovaries from sheep with high and low fecundity, and the functions of population-specific RESs were subsequently analysed. A total of 2 182 475 RESs, 74.61% of which were A-to-I and C-to-U sites, were identified. These RESs were fairly evenly dispersed over the chromosomes, with 46.8% showing close clustering (inter-site distance < 300 bp). Notably, 93% were primarily situated in intronic and intergenic regions. In the follicular phase, pivotal RESs were found in the introns of genes including LPS responsive beige-like anchor, MCC regulator of Wnt signalling, and RWD domain containing 3, among others, and in the exon region of EvC ciliary complex subunit 2. In the luteal phase, RESs were observed in the introns of genes such as H/ACA ribonucleoprotein assembly factor and SDA1 domain-containing 1, and the exon and 3'UTR regions of polypeptide N-acetylgalactosaminyltransferase 15 and ilvB acetolactate synthase-like, respectively. High-fecundity sheep showed RESs in the follicular phase in genes such as fibrillin 1, cyclin-dependent kinase 6, and roundabout 1, and in genes such as autophagy-related 2B and versican in the luteal phase. Thirteen RESs specific to the follicular phase and eight specific to the luteal phase were identified in high-fecundity sheep ovaries. These RESs offer promising molecular targets and enhance understanding of multiple births in sheep from the perspective of posttranscriptional alterations.
X F Ma, A J Liu, Z Zheng, B X Hu, Y X Zhi, C Liu, S J Tian

2157 related Products with: Resolving and functional analysis of RNA editing sites in sheep ovaries and associations with litter size.

200ug10 mg1000 200ul200ul25 mg1000 tests100ug10 mg100 mg10 mg

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#39433745   2024/10/21 To Up

Oncogenic GALNT5 confers FOLFIRINOX resistance via activating the MYH9/ NOTCH/ DDR axis in pancreatic ductal adenocarcinoma.

Chemotherapy resistance has been a great challenge in pancreatic ductal adenocarcinoma(PDAC) treatments. Current first-line chemotherapy regimens for PDAC include gemcitabine-based regimens such as AG regimen (albumin paclitaxel and gemcitabine), fluorouracil-based regiments such as FOLFIRINOX regimen ((5-fluorouracil5-FU), oxaliplatin, Irinotecan) and platinum-based regimens for patients with BRCA mutations. large amounts of work have been done on exploring the mechanism underlying resistance of gemcitabine-based and platinum-based regimens, while little research has been achieved on the mechanism of FOLFIRINOX regimens resistance. Hence, we identified Polypeptide N-Acetylgalactosaminyltransferase 5, (GALNT5) as a vital regulator and a potential therapeutic target in FOLFIRINOX regimens resistance. Colony formation assays and flow cytometry assays were performed to explore the roles of GALNT5 in cell proliferation and apoptosis in PDAC treated with FOLFIRINOX. IC50 alterations were calculated in GALNT5 knockdown and overexpressed cell lines. RNA-seq followed by GSEA (gene set enrichment analysis) was displayed to explore the potential mechanism. WB (western blotting), real-time PCR, and IF (immunofluorescence) were performed to validate relative pathways. The mouse orthotopic xenograft PDAC model was established to examine GALNT5 functions in vivo. GALNT5 was highly expressed in PDAC tissues and predicted poor prognosis in PDAC. Upregulation of GALNT5 in PDAC cells conferred FOLFIRINOX resistance on PDAC by inhibiting DNA damage. Moreover, GALNT5 interacted with MYH9, thus participating in the activation of the NOTCH pathways, resulting in hampering FOI-induced DNA damage. Functions of GALNT5 promoting FOLFIRINOX resistance were validated in vivo. In this study, we found that aberrantly overexpressed GALNT5 in PDAC took part in the activation of the NOTCH pathway by interacting with MYH9, thus inhibiting the DDR to achieve FOLFIRINOX resistance and causing poor prognosis. We identified GALNT5 as a potential therapeutic target for PDAC patients resistant to FOLFIRINOX chemotherapy.
Qinyuan Jia, Yuheng Zhu, Hongfei Yao, Yifan Yin, Zonghao Duan, Jiahao Zheng, Ding Ma, Minwei Yang, Jianyu Yang, Junfeng Zhang, Dejun Liu, Rong Hua, Yanmiao Huo, Xueliang Fu, Yongwei Sun, Wei Liu

1261 related Products with: Oncogenic GALNT5 confers FOLFIRINOX resistance via activating the MYH9/ NOTCH/ DDR axis in pancreatic ductal adenocarcinoma.

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#39105355   2024/08/06 To Up

N-acetylgalactosaminyltransferase GALNT6 is a potential therapeutic target of clear cell renal cell carcinoma progression.

High expression of truncated O-glycans Tn antigen predicts adverse clinical outcome in patients with clear cell renal cell carcinoma (ccRCC). To understand the biosynthetic underpinnings of Tn antigen changes in ccRCC, we focused on N-acetylgalactosaminyltransferases (GALNTs, also known as GalNAcTs) known to be involved in Tn antigen synthesis. Data from GSE15641 profile and local cohort showed that GALNT6 was significantly upregulated in ccRCC tissues. The current study aimed to determine the role of GALNT6 in ccRCC, and whether GALNT6-mediated O-glycosylation aggravates malignant behaviors. Gain- and loss-of-function experiments showed that overexpression of GALNT6 accelerated ccRCC cell proliferation, migration, and invasion, as well as promoted ccRCC-derived xenograft tumor growth and lung metastasis. In line with this, silencing of GALNT6 yielded the opposite results. Mechanically, high expression of GALNT6 led to the accumulation of Tn antigen in ccRCC cells. By undertaking immunoprecipitation coupled with liquid chromatography/mass spectrometry, vicia villosa agglutinin blot, and site-directed mutagenesis assays, we found that O-glycosylation of prohibitin 2 (PHB2) at Ser161 was required for the GALNT6-induced ccRCC cell proliferation, migration, and invasion. Additionally, we identified lens epithelium-derived growth factor (LEDGF) as a key regulator of GALNT6 transcriptional induction in ccRCC growth and an upstream contributor to ccRCC aggressive behavior. Collectively, our findings indicate that GALNT6-mediated abnormal O-glycosylation promotes ccRCC progression, which provides a potential therapeutic target in ccRCC development.
Luhaoran Sun, Zeyu Li, Peng Shu, Min Lu

1568 related Products with: N-acetylgalactosaminyltransferase GALNT6 is a potential therapeutic target of clear cell renal cell carcinoma progression.

0.1ml (1mg/ml)0.1ml (1mg/ml) 100ul0.1ml (1mg/ml)

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#39098533   2024/08/02 To Up

In vivo mapping of the mouse Galnt3-specific O-glycoproteome.

The UDP-N-acetylgalactosamine polypeptide:N-acetylgalactosaminyltransferase (GalNAc-T) family of enzymes initiates O-linked glycosylation by catalyzing the addition of the first GalNAc sugar to serine or threonine on proteins destined to be membrane-bound or secreted. Defects in individual isoforms of the GalNAc-T family can lead to certain congenital disorders of glycosylation (CDG). The polypeptide N-acetylgalactosaminyltransferase 3 (GALNT)3-CDG, is caused by mutations in GALNT3, resulting in hyperphosphatemic familial tumoral calcinosis due to impaired glycosylation of the phosphate-regulating hormone fibroblast growth factor 23 (FGF23) within osteocytes of the bone. Patients with hyperphosphatemia present altered bone density, abnormal tooth structure, and calcified masses throughout the body. It is therefore important to identify all potential substrates of GalNAc-T3 throughout the body to understand the complex disease phenotypes. Here, we compared the Galnt3 mouse model, which partially phenocopies GALNT3-CDG, with WT mice and used a multicomponent approach using chemoenzymatic conditions, a product-dependent method constructed using EThcD triggered scans in a mass spectrometry workflow, quantitative O-glycoproteomics, and global proteomics to identify 663 Galnt3-specific O-glycosites from 269 glycoproteins across multiple tissues. Consistent with the mouse and human phenotypes, functional networks of glycoproteins that contain GalNAc-T3-specific O-glycosites involved in skeletal morphology, mineral level maintenance, and hemostasis were identified. This library of in vivo GalNAc-T3-specific substrate proteins and O-glycosites will serve as a valuable resource to understand the functional implications of O-glycosylation and to unravel the underlying causes of complex human GALNT3-CDG phenotypes.
Kruti Dalal, Weiming Yang, E Tian, Aliona Chernish, Peggy McCluggage, Alexander J Lara, Kelly G Ten Hagen, Lawrence A Tabak

2639 related Products with: In vivo mapping of the mouse Galnt3-specific O-glycoproteome.

4 Membranes/Box0.2 mg100.00 ug4 Arrays/Slide25 µg0.25 mg1 mg4 Membranes/Box4 Membranes/Box1 mg

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#38971758   2024/07/06 To Up

CCDC88C, an O-GalNAc glycosylation substrate of GALNT6, drives breast cancer metastasis by promoting c-JUN-mediated CEMIP transcription.

Coiled-coil domain containing 88C (CCDC88C) is a component of non-canonical Wnt signaling, and its dysregulation causes colorectal cancer metastasis. Dysregulated expression of CCDC88C was observed in lymph node metastatic tumor tissues of breast cancer. However, the role of CCDC88C in breast cancer metastasis remains unclear. To address this, the stable BT549 and SKBR3 cell lines with CCDC88C overexpression or knockdown were developed. Loss/gain-of-function experiments suggested that CCDC88C drove breast cancer cell motility in vitro and lung and liver metastasis in vivo. We found that CCDC88C led to c-JUN-induced transcription activation. Overlapping genes were identified from the genes modulated by CCDC88C and c-JUN. CEMIP, one of these overlapping genes, has been confirmed to confer breast cancer metastasis. We found that CCDC88C regulated CEMIP mRNA levels via c-JUN and it exerted pro-metastatic capabilities in a CEMIP-dependent manner. Moreover, we identified the CCDC88C as a substrate of polypeptide N-acetylgalactosaminyltransferase 6 (GALNT6). GALNT6 was positively correlated with CCDC88C protein abundance in the normal breast and breast cancer tissues, indicating that GALNT6 might be associated with expression patterns of CCDC88C in breast cancer. Our data demonstrated that GALNT6 maintained CCDC88C stability by promoting its O-linked glycosylation, and the modification was critical for the pro-metastatic potential of CCDC88C. CCDC88C also could mediate the pro-metastatic potential of GALNT6 in breast cancer. Collectively, our findings uncover that CCDC88C may increase the risk of breast cancer metastasis and elucidate the underlying molecular mechanisms.
Boya Deng, Siyang Zhang, Yingying Zhou, Ting Sun, Ying Zhu, Jing Fei, Ailin Li, Yuan Miao

1525 related Products with: CCDC88C, an O-GalNAc glycosylation substrate of GALNT6, drives breast cancer metastasis by promoting c-JUN-mediated CEMIP transcription.

100ul100ul96T1 kit(96 Wells)

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#38916164   2024/06/24 To Up

Novel genetic mutation associated with hyperphosphatemic familial tumoral calcinosis/hyperostosis-hyperphosphatemia syndrome treated with denosumab: a case report.

In this case report, a novel N-acetylgalactosaminyltransferase 3 homozygous mutation (c.782 G>A; p.R261Q) associated with hyperphosphatemic familial tumoral calcinosis/hyperostosis-hyperphosphatemia syndrome is described. The patient had elbow, pelvis, and lower limb pain and a hard mass in the hip and olecranon regions. Increased levels of inorganic phosphorus (Pi) and C-reactive protein were observed. After treating the patient with conventional drugs, we tested denosumab, which reduced but did not normalize the Pi.
G Fabbriciani, A Colombini, C Messina, G Adami

1553 related Products with: Novel genetic mutation associated with hyperphosphatemic familial tumoral calcinosis/hyperostosis-hyperphosphatemia syndrome treated with denosumab: a case report.



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#38915682   2024/06/11 To Up

Gangliosides in neural stem cell fate determination and nerve cell specification--preparation and administration.

Gangliosides are sialylated glycosphingolipids with essential but enigmatic functions in healthy and disease brains. GD3 is the predominant species in neural stem cells (NSCs) and GD3-synthase (sialyltransferase II; ) knockout (GD3S-KO) revealed reduction of postnatal NSC pools with severe behavioral deficits including cognitive impairment, depression-like phenotypes, and olfactory dysfunction. Exogenous administration of GD3 significantly restored the NSC pools and enhanced the stemness of NSCs with multipotency and self-renewal, followed by restored neuronal functions. Our group discovered that GD3 is involved in the maintenance of NSC fate determination by interacting with epidermal growth factor receptors (EGFRs), by modulating expression of cyclin-dependent kinase (CDK) inhibitors p27 and p21, and by regulating mitochondrial dynamics via associating a mitochondrial fission protein, the dynamin-related protein-1 (Drp1). Furthermore, we discovered that nuclear GM1 promotes neuronal differentiation by an epigenetic regulatory mechanism. GM1 binds with acetylated histones on the promoter of as well as on the in differentiated neurons. In addition, epigenetic activation of the GM2S gene was detected as accompanied by an apparent induction of neuronal differentiation in NSCs responding to an exogenous supplement of GM1. Interestingly, GM1 induced epigenetic activation of the gene, with recruitment of Nurr1 and PITX3, dopaminergic neuron-associated transcription factors, to the promoter region. In this way, GM1 epigenetically regulates dopaminergic neuron specific gene expression, and it would modify Parkinson's disease. Multifunctional gangliosides significantly modulate lipid microdomains to regulate functions of important molecules on multiple sites: the plasma membrane, mitochondrial membrane, and nuclear membrane. Versatile gangliosides regulate functional neurons as well as sustain NSC functions via modulating protein and gene activities on ganglioside microdomains. Maintaining proper ganglioside microdomains benefits healthy neuronal development and millions of senior citizens with neurodegenerative diseases. Here, we introduce how to isolate GD3 and GM1 and how to administer them into the mouse brain to investigate their functions on NSC fate determination and nerve cell specification.
Yutaka Itokazu, Toshio Ariga, Takahiro Fuchigami, Dongpei Li

1956 related Products with: Gangliosides in neural stem cell fate determination and nerve cell specification--preparation and administration.

3 inhibitors5 Modulators3 Modulators1 mg3 Modulators10 ug8 Modulators10 Modulators5 Modulators25 ml.100ug Lyophilized100 µg

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#38845941   2024/05/21 To Up

Comprehensive pan-cancer analysis reveals the versatile role of GALNT7 in epigenetic alterations and immune modulation in cancer.

Cancer is a leading cause of mortality globally, characterized by intricate molecular alterations, including epigenetic changes such as glycosylation. This study presents a comprehensive pan-cancer analysis of Polypeptide N-Acetylgalactosaminyltransferase 7 (GALNT7), an enzyme involved in mucin-type O-linked protein glycosylation. GALNT7 has previously been linked to various cancers, but a unified analysis across cancer types is lacking. Leveraging data from TCGA, GTEx, and other sources, we scrutinized GALNT7's expression, prognostic relevance, links to immune-related genes, immune cell infiltration, and its involvement in tumor genetic heterogeneity across 33 cancer types. GALNT7 exhibited diverse expression patterns across cancer types, showcasing its potential as an oncogenic factor, with its expression levels linked to both positive and negative prognoses, highlighting the context-specific nature of its role in cancer progression. We delved into the intricate interplay between GALNT7 and immune genes, unveiling positive and negative correlations, underscoring complex interactions in the tumor microenvironment. GALNT7 was found to impact immune cell infiltration, which could have implications for treatment strategies. Additionally, GALNT7 displayed associations with genetic tumor aspects, encompassing genomic instability, DNA repair issues, and genetic mutations, hinting at its pivotal role in shaping the genetic landscape of diverse cancers. Enrichment analysis uncovered potential functions of GALNT7 beyond glycosylation, such as its participation in signaling pathways and its association with various diseases, notably cancer. This comprehensive analysis elucidates the multifaceted role of GALNT7 in cancer biology, underlining its potential as a therapeutic target and biomarker across various cancer types. These findings provide valuable insights for future research and the development of personalized cancer treatment strategies.
Yan Liu, Yue Sun, Meixia Xiao, Shuang Li, Shengming Shi

2519 related Products with: Comprehensive pan-cancer analysis reveals the versatile role of GALNT7 in epigenetic alterations and immune modulation in cancer.



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#38775215   2024/05/22 To Up

Downregulation of circ-RAPGEF5 inhibits colorectal cancer progression by reducing the expression of polypeptide N-acetylgalactosaminyltransferase 3 (GALNT3).

Circular RNA (circRNA) plays a crucial role in the pathogenesis and progression of colorectal cancer (CRC). However, the current understanding of the emerging function and mechanism of circ-RAPGEF5 in CRC remains poorly understood.
Duo Cheng, Feifei Chu, Fang Liang, Nan Zhang, Jingjing Wang, Wenli Yue

2043 related Products with: Downregulation of circ-RAPGEF5 inhibits colorectal cancer progression by reducing the expression of polypeptide N-acetylgalactosaminyltransferase 3 (GALNT3).

100ul

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