Glycobiology最新文献_第10页

Novel sialidase inhibitors suppress mumps virus replication and infection. 新型硅糖苷酶抑制剂可抑制腮腺炎病毒的复制和感染。

IF 3.4 3区生物学

Glycobiology Pub Date : 2024-09-30 DOI: 10.1093/glycob/cwae059

Tadanobu Takahashi, Yuuki Kurebayashi, Tadamune Otsubo, Kiyoshi Ikeda, Kobun Konagaya, Shunsuke Suzuki, Mika Yamazaki, Kenya Suzuki, Yutaka Narimichi, Akira Minami, Hideyuki Takeuchi

{"title":"Novel sialidase inhibitors suppress mumps virus replication and infection.","authors":"Tadanobu Takahashi, Yuuki Kurebayashi, Tadamune Otsubo, Kiyoshi Ikeda, Kobun Konagaya, Shunsuke Suzuki, Mika Yamazaki, Kenya Suzuki, Yutaka Narimichi, Akira Minami, Hideyuki Takeuchi","doi":"10.1093/glycob/cwae059","DOIUrl":"10.1093/glycob/cwae059","url":null,"abstract":"The prevalent human pathogen, mumps virus (MuV; orthorubulavirus parotitidis) causes various complications and serious sequelae, such as meningitis, encephalitis, deafness, and impaired fertility. Direct-acting antivirals (DAAs) targeting MuV which can prevent mumps and mumps-associated complications and sequelae are yet to be developed. Paramyxoviridae family members, such as MuV, possess viral surface hemagglutinin-neuraminidase (HN) protein with sialidase activity which facilitates efficient viral replication. Therefore, to develop DAAs targeting MuV we synthesized MuV sialidase inhibitors. It is proposed that the viral HN has a single functional site for N-acetylneuraminic acid (Neu5Ac) binding and sialidase activity. Further, the known MuV sialidase inhibitor is an analog of Neu5Ac-2,3-didehydro-2-deoxy-N-acetylneuraminic acid (DANA)-which lacks potency. DANA derivatives with higher MuV sialidase inhibitory potency are lacking. The MuV-HN-Neu5Ac binding site has a hydrophobic cavity adjacent to the C4 position of Neu5Ac. Exploiting this, here, we synthesized DANA derivatives with increasing hydrophobicity at its C4 position and created 3 novel sialidase inhibitors (Compounds 1, 2, and 3) with higher specificity for MuV-HN than DANA; they inhibited MuV replication step to greater extent than DANA. Furthermore, they also inhibited hemagglutination and the MuV infection step. The insight-that these 3 novel DANA derivatives possess linear hydrocarbon groups at the C4-hydroxyl group of DANA-could help develop highly potent sialidase inhibitors with high specificity for MuV sialidase, which may function as direct-acting MuV-specific antivirals.","PeriodicalId":12766,"journal":{"name":"Glycobiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

O-glycosylation of IgA1 and the pathogenesis of an autoimmune disease IgA nephropathy. IgA1 的 O 型糖基化与自身免疫性疾病 IgA 肾病的发病机制。

IF 3.3 3区生物学

Glycobiology Pub Date : 2024-09-30 DOI: 10.1093/glycob/cwae060

Jan Novak, R Glenn King, Janet Yother, Matthew B Renfrow, Todd J Green

{"title":"O-glycosylation of IgA1 and the pathogenesis of an autoimmune disease IgA nephropathy.","authors":"Jan Novak, R Glenn King, Janet Yother, Matthew B Renfrow, Todd J Green","doi":"10.1093/glycob/cwae060","DOIUrl":"10.1093/glycob/cwae060","url":null,"abstract":"IgA nephropathy is a kidney disease characterized by deposition of immune complexes containing abnormally O-glycosylated IgA1 in the glomeruli. Specifically, some O-glycans are missing galactose that is normally β1,3-linked to N-acetylgalactosamine of the core 1 glycans. These galactose-deficient IgA1 glycoforms are produced by IgA1-secreting cells due to a dysregulated expression and activity of several glycosyltransferases. Galactose-deficient IgA1 in the circulation of patients with IgA nephropathy is bound by IgG autoantibodies and the resultant immune complexes can contain additional proteins, such as complement C3. These complexes, if not removed from the circulation, can enter the glomerular mesangium, activate the resident mesangial cells, and induce glomerular injury. In this review, we briefly summarize clinical and pathological features of IgA nephropathy, review normal and aberrant IgA1 O-glycosylation pathways, and discuss the origins and potential significance of natural anti-glycan antibodies, namely those recognizing N-acetylgalactosamine. We also discuss the features of autoantibodies specific for galactose-deficient IgA1 and the characteristics of pathogenic immune complexes containing IgA1 and IgG. In IgA nephropathy, kidneys are injured by IgA1-containing immune complexes as innocent bystanders. Most patients with IgA nephropathy progress to kidney failure and require dialysis or transplantation. Moreover, most patients after transplantation experience a recurrent disease. Thus, a better understanding of the pathogenetic mechanisms is needed to develop new disease-specific treatments.","PeriodicalId":12766,"journal":{"name":"Glycobiology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11442006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141878566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Towards a thorough understanding of mammalian glycosylphosphatidylinositol-anchored protein biosynthesis. 深入了解哺乳动物糖基磷脂酰肌醇锚定蛋白的生物合成。

IF 3.4 3区生物学

Glycobiology Pub Date : 2024-09-30 DOI: 10.1093/glycob/cwae061

Taroh Kinoshita

引用次数: 0

Impact of glycan depletion, glycan debranching and increased glycan charge on HIV-1 neutralization sensitivity and immunogenicity. 聚糖耗尽、聚糖支化和聚糖电荷增加对 HIV-1 中和敏感性和免疫原性的影响

IF 3.3 3区生物学

Glycobiology Pub Date : 2024-09-30 DOI: 10.1093/glycob/cwae063

Alessio D'Addabbo, Tommy Tong, Emma T Crooks, Keiko Osawa, Jiamin Xu, Alyssa Thomas, Joel D Allen, Max Crispin, James M Binley

{"title":"Impact of glycan depletion, glycan debranching and increased glycan charge on HIV-1 neutralization sensitivity and immunogenicity.","authors":"Alessio D'Addabbo, Tommy Tong, Emma T Crooks, Keiko Osawa, Jiamin Xu, Alyssa Thomas, Joel D Allen, Max Crispin, James M Binley","doi":"10.1093/glycob/cwae063","DOIUrl":"10.1093/glycob/cwae063","url":null,"abstract":"Broadly neutralizing antibodies (bNAbs) isolated from HIV-1 infected donors are vaccine paradigms. These bNAbs recognize envelope glycoprotein trimers that carry 75-90 oligomannose and complex-type glycans. Although bNAbs and their precursors must navigate past glycans, they usually also make some glycan contacts. Glycan-modified vaccines may therefore be useful to initiate and guide bNAb development. Here, we describe two ways to modify Env glycans for possible vaccine use: 1) using a cocktail of glycosidases (termed \"NGAF3\" (Neuraminidase, β-Galactosidase, N-Acetylglucosaminidase, endoglycosidase F3 (endo F3)) to deplete complex glycans to try to minimize bNAb-glycan clashes and 2) co-expressing β-1,4-galactosyltransferase 1 (B4G) and β-galactoside α-2,6 sialyltransferase 1 (ST6) during Env biosynthesis, creating bNAb-preferred glycan structures. Mass spectrometry revealed that NGAF3 removed glycan heads at 3/7 sites occupied by complex glycans. B4G overexpression resulted in hybrid glycan development whenever complex glycans were closely spaced. The glycan at position 611 in of Env's gp41 transmembrane subunit was uniquely isolated from the effects of both endo F3 and B4G. B4G and ST6 co-expression increased hybrid and sialylated glycan abundance, reducing glycan complexity. In rabbit vaccinations, B4G + ST6 virus-like particles (VLPs) induced less frequent, weaker titer NAbs, implying that ST6-mediated increased Env charge dampens vaccine antibodies. In some cases, vaccine sera preferentially neutralized B4G + ST6-modified pseudovirus. HIV-1+ donor plasma NAbs were generally more effective against B4G + ST6 modified pseudovirus, suggesting a preference for less complex and/or α-2,6 sialylated Env trimers. Collectively, our data suggest that B4G and ST6 Env modifications are best suited for intermediate or late vaccine shots.","PeriodicalId":12766,"journal":{"name":"Glycobiology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11442005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141901455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of C-mannosylation in a receptor tyrosine kinase AXL. 受体酪氨酸激酶AXL中c -甘露糖基化的鉴定。

IF 3.4 3区生物学

Glycobiology Pub Date : 2024-09-30 DOI: 10.1093/glycob/cwae096

Kento Mori, Takehiro Suzuki, Urara Waki, Soichiro Hayashi, Shigehito Kadono, Ryota Kawahara, Minae Takeuchi, Hayato Mizuta, Naoshi Dohmae, Ryohei Katayama, Siro Simizu

{"title":"Identification of C-mannosylation in a receptor tyrosine kinase AXL.","authors":"Kento Mori, Takehiro Suzuki, Urara Waki, Soichiro Hayashi, Shigehito Kadono, Ryota Kawahara, Minae Takeuchi, Hayato Mizuta, Naoshi Dohmae, Ryohei Katayama, Siro Simizu","doi":"10.1093/glycob/cwae096","DOIUrl":"10.1093/glycob/cwae096","url":null,"abstract":"C-mannosylation is a unique type of glycosylation in which a mannose is added to tryptophan in a protein. However, the biological function of C-mannosylation is still largely unknown. AXL is a receptor tyrosine kinase, and its overexpression contributes to tumor malignancy. The role of AXL in cancer cells is broad, including invasion, drug resistance, and vasculogenic mimicry formation. Although Trp320 of AXL was predicted to be C-mannosylated, it has not been confirmed. Here, we demonstrated that Trp320 of AXL is C-mannosylated, measured by mass spectrometry of recombinant AXL purified from various cancer cells. Furthermore, re-expression of C-mannosylation-deficient AXL in human breast cancer MDA-MB-231 cells lacking AXL by the CRISPR/Cas9 system resulted in reduction of vasculogenic mimicry formation. Interestingly, phosphorylation levels of AKT in C-mannosylation-deficient AXL re-expressing cells were comparable to those of parental and wild-type AXL re-expressing cells. These results represent the first discovery of C-mannosylation in a receptor tyrosine kinase and the possibility that C-mannosylation may affect AXL function, distinct from its downstream signaling in cancer cells.","PeriodicalId":12766,"journal":{"name":"Glycobiology","volume":"34 11","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

(Key1-001) congenital disorders of glycosylation: Glycobiology at the bedside. (Key1-001)先天性糖基化紊乱：床旁的糖生物学。

IF 4.3 3区生物学

Glycobiology Pub Date : 2024-09-10 DOI: 10.1093/glycob/cwae070

Andrew C Edmondson

{"title":"(Key1-001) congenital disorders of glycosylation: Glycobiology at the bedside.","authors":"Andrew C Edmondson","doi":"10.1093/glycob/cwae070","DOIUrl":"https://doi.org/10.1093/glycob/cwae070","url":null,"abstract":"Congenital disorders of glycosylation (CDG) are a group of rare monogenic human disorders caused by defects in the genes encoding the proteins that generate, attach, and modify glycans, thus disrupting cellular glycosylation machinery. Over 200 CDG caused by disruptions of 189 different genes are currently known. The multi-system disease manifestations of the CDG disorders highlight the importance of glycosylation across the organ systems. Clinical manifestations of CDG tend to group among genes contributing to the same glycosylation pathways, suggesting shared pathophysiology related to the glycosylation disruptions. However, the underlying glycosylation disruptions and pathophysiologic mechanisms responsible for specific CDG clinical manifestations have been determined for only a few hypoglycosylated proteins. The Frontiers in CDG Consortium (FCDGC) is an international network of clinical sites, laboratories, and patient advocacy groups established in 2019 to improve clinical symptoms, quality of life, and life expectancy for individuals with CDG. FCDGC seeks to answer decades of unresolved questions, address knowledge gaps, develop and validate new biochemical diagnostic techniques and therapeutic biomarkers, and explore novel therapeutic options for CDG. Over the past 5 years, FCDGC has launched a Natural History Study with over 300 CDG patients, discovered novel biomarkers suggesting new mechanisms of disease, and launched clinical trials aiming to restore appropriate glycosylation and targeting newly identified potential mechanisms of disease. Technical advances in glycobiology are making it increasingly possible to comprehensively catalog glycoproteomic data and to probe functional impact of altered glycosylation. My laboratory applies glycoproteomic technologies to samples from human subjects and genetic model systems to identify glycosylation abnormalities and unlock new insights from translational glycobiology. Current findings and accomplishments highlight the ongoing bottlenecks and knowledge gaps at intersections of glycobiology and clinical care requiring further investigation.","PeriodicalId":12766,"journal":{"name":"Glycobiology","volume":"3 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142215791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dystroglycan-HSPG interactions provide synaptic plasticity and specificity. Dystroglycan-HSPG相互作用提供了突触的可塑性和特异性。

IF 3.4 3区生物学

Glycobiology Pub Date : 2024-08-30 DOI: 10.1093/glycob/cwae051

James Melrose

{"title":"Dystroglycan-HSPG interactions provide synaptic plasticity and specificity.","authors":"James Melrose","doi":"10.1093/glycob/cwae051","DOIUrl":"10.1093/glycob/cwae051","url":null,"abstract":"Aim: This study examined the roles of the laminin and proteoglycan receptor dystroglycan (DG) in extracellular matrix stabilization and cellular mechanosensory processes conveyed through communication between the extracellular matrix (ECM) and cytoskeleton facilitated by DG. Specific functional attributes of HS-proteoglycans (HSPGs) are conveyed through interactions with DG and provide synaptic specificity through diverse interactions with an extensive range of cell attachment and adaptor proteins which convey synaptic plasticity. HSPG-DG interactions are important in phototransduction and neurotransduction and facilitate retinal bipolar-photoreceptor neuronal signaling in vision. Besides synaptic stabilization, HSPG-DG interactions also stabilize basement membranes and the ECM and have specific roles in the assembly and function of the neuromuscular junction. This provides neuromuscular control of muscle systems that control conscious body movement as well as essential autonomic control of diaphragm, intercostal and abdominal muscles and muscle systems in the face, mouth and pharynx which assist in breathing processes. DG is thus a multifunctional cell regulatory glycoprotein receptor and regulates a diverse range of biological and physiological processes throughout the human body. The unique glycosylation of the αDG domain is responsible for its diverse interactions with ECM components in cell-ECM signaling. Cytoskeletal cell regulatory switches assembled by the βDG domain in its role as a nuclear scaffolding protein respond to such ECM cues to regulate cellular behavior and tissue homeostasis thus DG has fascinating and diverse roles in health and disease.","PeriodicalId":12766,"journal":{"name":"Glycobiology","volume":"34 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11368572/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Glyco-Forum. Glyco-Forum.

IF 3.4 3区生物学

Glycobiology Pub Date : 2024-08-30 DOI: 10.1093/glycob/cwae066

引用次数: 0

Sialylated keratan sulfates on MUC5B are Siglec-8 ligands in the human esophagus. 人食管中 MUC5B 上的硅氨酰化角叉硫酸盐是 Siglec-8 配体。

IF 3.3 3区生物学

Glycobiology Pub Date : 2024-08-30 DOI: 10.1093/glycob/cwae065

T August Li, Anabel Gonzalez-Gil, Abduselam K Awol, Steven J Ackerman, Benjamin C Orsburn, Ronald L Schnaar

{"title":"Sialylated keratan sulfates on MUC5B are Siglec-8 ligands in the human esophagus.","authors":"T August Li, Anabel Gonzalez-Gil, Abduselam K Awol, Steven J Ackerman, Benjamin C Orsburn, Ronald L Schnaar","doi":"10.1093/glycob/cwae065","DOIUrl":"10.1093/glycob/cwae065","url":null,"abstract":"Human sialic acid-binding immunoglobulin-like lectins (Siglecs) are expressed on subsets of immune cells. Siglec-8 is an immune inhibitory Siglec on eosinophils and mast cells, which are effectors in allergic disorders including eosinophilic esophagitis. Inhibition occurs when Siglec-8 is crosslinked by multivalent Siglec ligands in target tissues. Previously we discovered a high-affinity Siglec-8 sialoglycan ligand on human airways composed of terminally sialylated keratan sulfate chains carried on a single protein, DMBT1. Here we extend that approach to another allergic inflammatory target tissue, human esophagus. Lectin overlay histochemistry revealed that Siglec-8 ligands are expressed predominantly by esophageal submucosal glands, and are densely packed in submucosal ducts leading to the lumen. Expression is tissue-specific; esophageal glands express Siglec-8 ligand whereas nearby gastric glands do not. Extraction and resolution by gel electrophoresis revealed a single predominant human esophageal Siglec-8 ligand migrating at >2 MDa. Purification by size exclusion and affinity chromatography, followed by proteomic mass spectrometry, revealed the protein carrier to be MUC5B. Whereas all human esophageal submucosal cells express MUC5B, only a portion convert it to Siglec-8 ligand by adding terminally sialylated keratan sulfate chains. We refer to this as MUC5B S8L. Material from the esophageal lumen of live subjects revealed MUC5B S8L species ranging from ~1-4 MDa. We conclude that MUC5B in the human esophagus is a protein canvas on which Siglec-8 binding sialylated keratan sulfate chains are post-translationally added. These data expand understanding of Siglec-8 ligands and may help us understand their roles in allergic immune regulation.","PeriodicalId":12766,"journal":{"name":"Glycobiology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11364441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

High expression of B3GALT5 suppresses the galectin-4-mediated peritoneal dissemination of poorly differentiated gastric cancer cells. 高表达 B3GALT5 可抑制由 galectin-4 介导的分化不良胃癌细胞的腹膜扩散。

IF 3.4 3区生物学

Glycobiology Pub Date : 2024-08-30 DOI: 10.1093/glycob/cwae064

Akiko Tsuchida, Kazuko Hachisu, Mamoru Mizuno, Yoshio Takada, Hiroko Ideo

{"title":"High expression of B3GALT5 suppresses the galectin-4-mediated peritoneal dissemination of poorly differentiated gastric cancer cells.","authors":"Akiko Tsuchida, Kazuko Hachisu, Mamoru Mizuno, Yoshio Takada, Hiroko Ideo","doi":"10.1093/glycob/cwae064","DOIUrl":"10.1093/glycob/cwae064","url":null,"abstract":"Peritoneal metastasis frequently accompanies metastatic and/or recurrent gastric cancer, leading to a poor prognosis owing to a lack of effective treatment. Hence, there is a pressing need to enhance our understanding of the mechanisms and molecules driving peritoneal metastasis. In a previous study, galectin-4 inhibition impeded peritoneal metastasis in a murine model. This study examined the glycan profiles of cell surface proteins and glycosphingolipids (GSLs) in cells with varying tumorigenic potentials to understand the intricate mechanisms underlying galectin-4-mediated regulation, particularly glycosylation. Detailed mass spectrometry analysis showed that galectin-4 knockout cells exhibit increased expression of lacto-series GSLs with β1,3-linked galactose while showing no significant alterations in neolacto-series GSLs. We conducted real-time polymerase chain reaction (PCR) analysis to identify candidate glycosyltransferases that synthesize increased levels of GSLs. Subsequently, we introduced the candidate B3GALT5 gene and selected the clones with high expression levels. B3GALT5 gene-expressing clones showed GSL glycan profiles like those of knockout cells and significantly reduced tumorigenic ability in mouse models. These clones exhibited diminished proliferative capacity and showed reduced expression of galectin-4 and activated AKT. Moreover, co-localization of galectin-4 with flotillin-2 (a raft marker) decreased in B3GALT5-expressing cells, implicating GSLs in galectin-4 localization to lipid rafts. D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (a GSL synthase inhibitor) also affected galectin-4 localization in rafts, suggesting the involvement of GSL microdomains. We discovered that B3GALT5 plays a crucial role in regulating peritoneal metastasis of malignant gastric cancer cells by suppressing cell proliferation and modulating lipid rafts and galectin-4 via mechanisms that are yet to be elucidated.","PeriodicalId":12766,"journal":{"name":"Glycobiology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0