#Lectin Microarray

[cdbioglyco]

CD BioGlyco has rich experience in lectin microarray assay. Our multiple technology platforms and well-trained researchers can provide customers with various forms of sample testing. We have confidence to be your essential research assistant in the field of glycobiology.

[report-1]

 Glycobiology Instruments Market Size, Type, segmentation, growth and forecast 2023-2030

 Glycobiology Instruments Market

The Glycobiology Instruments Market is expected to grow from USD 1.80 Billion in 2022 to USD 3.60 Billion by 2030, at a CAGR of 9.10% during the forecast period.

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 Glycobiology Instruments Market Size

Glycobiology instruments refer to the equipment used to study glycans, which are complex macromolecules found on the surface of cells and proteins. The global glycobiology instruments market is segmented by type, application, and region. The types of instruments include mass spectrometry instruments, chromatography instruments, arrays, and others. Applications for these instruments include academic research institutes, pharmaceutical and biotechnology companies, and clinical laboratories. The market players in this industry include Merck KGaA, Agilent Technologies, Thermo Fisher Scientific, New England Biolabs, Shimadzu Corporation, Asparia Glycomics, and S-BIO. Regulatory and legal factors specific to this market include the need for validation and standardization in glycobiology analysis, as well as the importance of adhering to ethical and safe research practices. The glycobiology instruments market is expected to grow in the coming years, driven by advances in scientific research and the increasing demand for personalized medicine.

 Glycobiology Instruments Market Key Player

Merck KGaA

Agilent Technologies

Thermo Fisher Scientific

New England Biolabs

Shimadzu Corporation

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 Glycobiology Instruments Market Segment Analysis

The Glycobiology Instruments market is a niche industry that caters to the research and development of carbohydrates and their interactions with various biological systems. The target market for Glycobiology Instruments includes research organizations, pharmaceutical and biotechnology companies, academic institutions, and government agencies. The demand for Glycobiology Instruments is driven by the increasing need for understanding the role of carbohydrates in biological systems, drug discovery, and the development of new diagnostic tools.

One of the major factors driving revenue growth in the Glycobiology Instruments market are technological advancements in the field of Glycobiology research. The development of advanced technologies for carbohydrate analysis, such as lectin arrays, glycan microarrays, and mass spectrometry, has paved the way for more accurate and efficient analysis of carbohydrates. This has greatly boosted the demand for Glycobiology Instruments in the market.

Another factor driving revenue growth in this industry is the increasing demand for personalized medicine. Glycobiology research has already found applications in the development of personalized medicine, where carbohydrates are used as biomarkers for disease diagnosis and treatment. This trend is expected to continue and drive demand for Glycobiology Instruments.

The latest trends in the Glycobiology Instruments market include the development of high-throughput Glycobiology platforms that can analyze a vast number of carbohydrate samples simultaneously. The emergence of new analytical platforms, such as mass spectrometry and capillary electrophoresis, is also driving the Glycobiology Instruments market forward.

However, the Glycobiology Instruments market also faces several challenges. One of the major challenges is the high cost of Glycobiology Instruments, which limits its usage to well-funded research institutions and pharmaceutical companies. Another challenge is the lack of standardization in Glycobiology research, which can lead to inconsistencies in research results. The lack of skilled professionals in the field of Glycobiology is also a major challenge for the industry.

The main findings of the report indicate that the Glycobiology Instruments market is expected to grow at a steady pace in the coming years, driven by the increasing demand for personalized medicine and technological advancements in the field of carbohydrate analysis. The report recommends that manufacturers focus on developing cost-effective Glycobiology Instruments to expand the market reach and increase adoption across all research organizations. The report also recommends that manufacturers partner with academic institutions and research organizations to encourage standardization in Glycobiology research and attract skilled professionals to the field.

This report covers impact on COVID-19 and Russia-Ukraine wars in detail.

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Market Segmentation (by Application):

Academic Research Institutes

Pharmaceutical and Biotechnology Companies

Clinical Laboratories

Information is sourced from www.reportprime.com

[cancersfakianakis1]

Cancers, Vol. 11, Pages 261: Loss of Stromal Galectin-1 Enhances Multiple Myeloma Development: Emphasis on a Role in Osteoclasts

Cancers, Vol. 11, Pages 261: Loss of Stromal Galectin-1 Enhances Multiple Myeloma Development: Emphasis on a Role in Osteoclasts

Cancers doi: 10.3390/cancers11020261

Authors: Joséphine Muller Elodie Duray Margaux Lejeune Sophie Dubois Erwan Plougonven Angélique Léonard Paola Storti Nicola Giuliani Martine Cohen-Solal Ute Hempel Victor L. Thijssen Yves Beguin Roy Heusschen Jo Caers

Multiple myeloma osteolytic disease is caused by an uncoupled bone-remodelling process with an increased osteoclast activity. Disease development relies on interactions between myeloma cells and bone marrow stromal cells. Recent findings suggest a role for glycan-binding proteins in myeloma microenvironment. Here, we investigated lectins involved in osteoclastogenesis and their role in myeloma bone disease. Microarray data analysis showed a lower expression of galectin-1 (gal-1) in mature osteoclasts compared to monocytic progenitor cells, confirmed at the RNA and protein levels in osteoclast cultures. Confocal microscopy showed that gal-1 localised predominantly in the sealing zone of mature osteoclasts. Although equal differentiated-osteoclast numbers, gal-1−/− osteoclasts showed a higher resorption activity compared to wild-type controls. Micro-computed tomography showed an aberrant bone phenotype with decreased bone densities in gal-1−/− mice. In vivo, tumour progression was faster in gal-1−/− mice and associated with a marked bone loss. Additionally, myeloma cells were found to decrease gal-1 expression in osteoclasts. Our results demonstrate that galectin-1 regulates osteoclast activity with an increased resorption by gal-1−/− osteoclasts and decreased bone densities in gal-1−/− mice. We observed an enhanced tumour development in gal-1−/− mice compared to wild-type mice, suggesting that galectin-1 has a functional role in stromal cells in myeloma microenvironment.

https://ift.tt/2Ep6nIt

[itsmedicinesfakianakis]

GSE77676 The Distinct Transcriptional and Metabolic Profiles Associate with Empathy in Spiritual/Religious Trained Buddhists: A Pilot Study of Shingon Esoteric Buddhism Priests

Contributors : Junji Ohnishi ; Shigeko Sakamoto ; Miyo Hori ; Seiji Nakamura ; Tomoko Sasaoka ; Eriko Ohnishi ; Masakazu Tanatsugu ; Kazuo Murakami ; Satoshi Ayuzawa Series Type : Expression profiling by array Organism : Homo sapiens

The microarray analyses revealed that the “priest-type” transcripts included up-regulated genes of type I interferon innate anti-viral responses (MX1, RSAD2, IFIT1, IFIT3, IFI27, IFI44L, and HERC5), and down-regulated genes of C17orf97 (ligand of arginyltranseferase 1), hemoglobin γA (HBG1), keratin associated protein (KRTAP10-12), and sialic acid Ig-like lectin 14 (SIGLEC14) at baseline.

from # All Medicine by Alexandros G. Sfakianakis via alkiviadis.1961 on Inoreader http://ift.tt/2vXb8Fa from OtoRhinoLaryngology - Alexandros G. Sfakianakis via Alexandros G.Sfakianakis on Inoreader http://ift.tt/2wDu2l4

[neurogenpapers]

Viscumins functionally modulate cell motility-associated gene expression.

PubMed: Related Articles Viscumins functionally modulate cell motility-associated gene expression. Int J Oncol. 2017 Feb;50(2):684-696 Authors: Schötterl S, Hübner M, Armento A, Veninga V, Wirsik NM, Bernatz S, Lentzen H, Mittelbronn M, Naumann U Abstract In Europe extracts from Viscum album L., the European white-berry mistletoe, are widely used as a complementary cancer therapy. Viscumins (mistletoe lectins, ML) have been scrutinized as important active components of mistletoe and exhibit a variety of anticancer effects such as stimulation of the immune system, induction of cytotoxicity, reduction of tumor cell motility as well as changes in the expression of genes associated with cancer development and progression. By microarray expression analysis, quantitative RT-PCR and RT-PCR based validation of microarray data we demonstrate for the Viscum album extract Iscador Qu and for the lectins Aviscumine and ML-1 that in glioma cells these drugs differentially modulate the expression of genes involved in the regulation of cell migration and invasion, including processes modulating cell architecture and cell adhesion. A variety of differentially expressed genes in ML treated cells are associated with the transforming growth factor (TGF)-β signaling pathway or are targets of TGF-β. ML treatment downregulated the expression of TGF-β itself, of the TGF-β receptor II (TGFBR2), of the TGF-β intracellular signal transducer protein SMAD2, and of matrix-metalloproteinases (MMP) MMP-2 and MMP-14. Even if the changes in gene expression differ between Aviscumine, Iscador Qu and ML-1, the overall regulation of motility associated gene expression by all drugs showed functional effects since tumor cell motility was reduced in a ML-dependent manner. Therefore, ML containing compounds might provide clinical benefit as adjuvant therapeutics in the treatment of patients with invasively growing tumors such as glioblastomas. PMID: 28101577 [PubMed - in process] http://dlvr.it/N93Ch3

[cancersfakianakis1]

Alterations in the glycome after HDAC inhibition impact oncogenic potential in epigenetically plastic SW13 cells

Abstract

Background

Defects in the type and degree of cellular glycosylation impact oncogenesis on multiple levels. Although the type of glycosylation is determined by protein sequence encoded by the genome, the extent and modifications of glycosylation depends on the activity of biosynthetic enzymes and recent data suggests that the glycome is also subject to epigenetic regulation. This study focuses on the ability of HDAC inhibition to alter glycosylation and to lead to pro-oncogenic alterations in the glycome as assessed by metastatic potential and chemoresistance.

Methods

Epigenetically plastic SW13 adrenocortical carcinoma cells were treated with FK228, an HDAC inhibitor with high affinity for HDAC1 and, to a lesser extent, HDAC2. In comparing HDAC inhibitor treated and control cells, differential expression of glycome-related genes were assessed by microarray. Differential glycosylation was then assessed by lectin binding arrays and the ability of cellular proteins to bind to glycans was assessed by glycan binding arrays. Differential sensitivity to paclitaxel, proliferation, and MMP activity were also assessed.

Results

Treatment with FK228 alters expression of enzymes in the biosynthetic pathways for a large number of glycome related genes including enzymes in all major glycosylation pathways and several glycan binding proteins. 84% of these differentially expressed glycome-related genes are linked to cancer, some as prognostic markers and others contributing basic oncogenic functions such as metastasis or chemoresistance. Glycan binding proteins also appear to be differentially expressed as protein extracts from treated and untreated cells show differential binding to glycan arrays. The impact of differential mRNA expression of glycosylation enzymes was documented by differential lectin binding. However, the assessment of changes in the glycome is complicated by the fact that detection of differential glycosylation through lectin binding is dependent on the methods used to prepare samples as protein-rich lysates show different binding than fixed cells in several cases. Paralleling the alterations in the glycome, treatment of SW13 cells with FK228 increases metastatic potential and reduces sensitivity to paclitaxel.

Conclusions

The glycome is substantially altered by HDAC inhibition and these changes may have far-reaching impacts on oncogenesis.

http://bit.ly/2RsYXMF

[cancersfakianakis1]

Glycosyltransferase gene expression identifies a poor prognostic colorectal cancer subtype associated with mismatch repair deficiency and incomplete glycan synthesis

Purpose: We aimed to discover glycosyltransferase gene (glycogene)-derived molecular subtypes of colorectal cancer (CRC) associated with patient outcomes. Experimental Design: Transcriptomic and epigenomic datasets of non-tumor, pre-cancerous, cancerous tissues and cell lines with somatic mutations, mismatch repair status, clinicopathological and survival information, were assembled (n=4223) and glycogene profiles were analyzed. Immunohistochemistry for a glycogene, GALNT6, was conducted in adenoma and carcinoma specimens (n=403). The functional role and cell surface glycan profiles were further investigated by in vitro loss-of-function assays and lectin microarray analysis. Results: We initially developed and validated a 15-glycogene signature that can identify a poor-prognostic subtype, which closely related to deficient mismatch repair (dMMR) and GALNT6 downregulation. The association of decreased GALNT6 with dMMR was confirmed in multiple datasets of tumors and cell lines, and was further recapitulated by immunohistochemistry, where approximately 15% tumors exhibited loss of GALNT6 protein. GALNT6 mRNA and protein was expressed in premalignant/preinvasive lesions but was subsequently downregulated in a subset of carcinomas, possibly through epigenetic silencing. Decreased GALNT6 was independently associated with poor prognosis in the immunohistochemistry cohort and an additional microarray meta-cohort, by multivariate analyses, and its discriminative power of survival was particularly remarkable in stage III patients. GALNT6 silencing in SW480 cells promoted invasion, migration, chemoresistance and increased cell surface expression of a cancer-associated truncated O-glycan, Tn-antigen. Conclusions: The 15-glycogene signature and the expression levels of GALNT6 mRNA and protein each serve as a novel prognostic biomarker, highlighting the role of dysregulated glycogenes in cancer-associated glycan synthesis and poor prognosis.

https://ift.tt/2skkW9Z

[cancersfakianakis1]

A Novel Therapeutic Strategy for Pancreatic Cancer: Targeting Cell Surface Glycan Using rBC2LC-N Lectin-Drug Conjugate (LDC)

Various cancers, including pancreatic ductal adenocarcinoma (PDAC), remain intractable even with costly tumor-targeting antibody drugs. Because the outermost coatings of cancer cells are composed of cell-specific glycan layers (glycocalyx), lectins, proteins with glycan-binding potential, were evaluated for possible use as drug carriers in PDAC treatment. A human PDAC cell line with well-to-moderately differentiated properties (Capan-1) was subjected to lectin microarray analysis to identify specific lectin–glycan pairs. The selected lectin was fused with a bacterial exotoxin for the construction of a lectin–drug conjugate (LDC), and its safety and antitumor effects were evaluated. A specific affinity between a recombinant bacterial C-type lectin (rBC2LC-N) and Capan-1 was identified, and its positivity was confirmed in 69 human samples. In contrast to the belief that all lectins mediate harmful hemagglutination, rBC2LC-N did not cause hemagglutination with human erythrocytes and was safely administered to mice. The 50% inhibitory concentration of LDC to Capan-1 (1.04 pg/mL = 0.0195 pmol/L) was 1/1,000 lower than that reported for conventional immunotoxins. The intraperitoneal administration of LDC reduced the tumor weight from 390 to 130.8 mg (P < 0.01) in an orthotopic model and reduced the number of nodules from 48 to 3 (P < 0.001) and improved survival from 62 to 105 days in a peritoneal dissemination model (P < 0.0001). In addition, the effect of LDC was reproduced in nodules from patient-derived PDAC xenografts through intravenous injection. Herein, we show the concept of utilizing lectins as drug carriers to target glycans on the cancer cell surface, highlighting new insights into cancer treatments. Mol Cancer Ther; 17(1); 183–95. ©2017 AACR.

http://ift.tt/2lD1rGl

[cancersfakianakis1]

A novel therapeutic strategy for pancreatic cancer: targeting cell surface glycan using rBC2LC-N lectin-drug conjugate (LDC).

Various cancers, including pancreatic ductal adenocarcinoma (PDAC), remain intractable even with costly tumour-targeting antibody drugs. Because the outermost coatings of cancer cells are composed of cell-specific glycan layers (glycocalyx), lectins, proteins with glycan-binding potential, were evaluated for possible use as drug carriers in PDAC treatment. A human PDAC cell line with well-to-moderately differentiated properties (Capan-1) was subjected to lectin microarray analysis to identify specific lectin-glycan pairs. The selected lectin was fused with a bacterial exotoxin for the construction of a lectin-drug conjugate (LDC), and its safety and anti-tumour effects were evaluated. A specific affinity between rBC2LC-N (a recombinant bacterial C-type lectin) and Capan-1 was identified, and its positivity was confirmed in 69 human samples. In contrast to the belief that all lectins mediate harmful haemagglutination, rBC2LC-N did not cause haemagglutination with human erythrocytes and was safely administered to mice. The 50% inhibitory concentration of LDC to Capan-1 (1.04 pg/ml=0.0195 pmol/l) was 1/1000 lower than that reported for conventional immunotoxins. The intraperitoneal administration of LDC reduced the tumour weight from 390 mg to 130.8 mg (P<0.01) in an orthotopic model, and reduced the number of nodules from 48 to 3 (P<0.001) and improved survival from 62 to 105 days in a peritoneal dissemination model (P<0.0001). In addition, the effect of LDC was reproduced in nodules from patient-derived PDAC xenografts through intravenous injection. Herein, we show the concept of utilizing lectins as drug carriers to target glycans on the cancer cell surface, highlighting new insights into cancer treatments.

http://ift.tt/2yxBpZI

[itsmedicinesfakianakis]

GSE77676 The Distinct Transcriptional and Metabolic Profiles Associate with Empathy in Spiritual/Religious Trained Buddhists: A Pilot Study of Shingon Esoteric Buddhism Priests

Contributors : Junji Ohnishi ; Shigeko Sakamoto ; Miyo Hori ; Seiji Nakamura ; Tomoko Sasaoka ; Eriko Ohnishi ; Masakazu Tanatsugu ; Kazuo Murakami ; Satoshi Ayuzawa Series Type : Expression profiling by array Organism : Homo sapiens

The microarray analyses revealed that the “priest-type” transcripts included up-regulated genes of type I interferon innate anti-viral responses (MX1, RSAD2, IFIT1, IFIT3, IFI27, IFI44L, and HERC5), and down-regulated genes of C17orf97 (ligand of arginyltranseferase 1), hemoglobin γA (HBG1), keratin associated protein (KRTAP10-12), and sialic acid Ig-like lectin 14 (SIGLEC14) at baseline.

from # All Medicine by Alexandros G. Sfakianakis via alkiviadis.1961 on Inoreader http://ift.tt/2vXb8Fa from OtoRhinoLaryngology - Alexandros G. Sfakianakis via Alexandros G.Sfakianakis on Inoreader http://ift.tt/2vdNPE0

[itsmedicinesfakianakis]

IJMS, Vol. 18, Pages 1528: Conditioned Medium from Malignant Breast Cancer Cells Induces an EMT-Like Phenotype and an Altered N-Glycan Profile in Normal Epithelial MCF10A Cells

IJMS, Vol. 18, Pages 1528: Conditioned Medium from Malignant Breast Cancer Cells Induces an EMT-Like Phenotype and an Altered N-Glycan Profile in Normal Epithelial MCF10A Cells

International Journal of Molecular Sciences doi: 10.3390/ijms18081528

Authors: Jia Guo Changmei Liu Xiaoman Zhou Xiaoqiang Xu Linhong Deng Xiang Li Feng Guan

Epithelial-mesenchymal transition (EMT) is a key process in cancer development and progression. Communication (crosstalk) between cancer cells and normal (nonmalignant) cells may facilitate cancer progression. Conditioned medium (CM) obtained from cultured cancer cells contains secreted factors capable of affecting phenotypes and the behaviors of normal cells. In this study, a culture of normal breast epithelial MCF10A cells with CM from malignant breast cancer cells (termed 231-CM and 453-CM) resulted in an alteration of morphology. CM-treated MCF10A, in comparison with control cells, showed a reduced expression of the epithelial marker E-cadherin, increased expression of the mesenchymal markers fibronectin, vimentin, N-cadherin, and TWIST1, meanwhile cell proliferation and migration were enhanced while cell apoptosis was decreased. N-glycan profiles of 231-CM-treated and control MCF10A cells were compared by MALDI-TOF/TOF-MS (Matrix-Assisted Laser Desorption/ Ionization Time of Flight Mass Spectrometry) and a lectin microarray analysis. The treated cells showed lower levels of high-mannose-type N-glycan structures, and higher levels of complex-type and hybrid-type structures. Altered N-glycan profiles were also detected in 453-CM-treated and non-treated MCF10A cells by MALDI-TOF/TOF-MS, and we found that the expression of five fucosylated N-glycan structures (m/z 1406.663, 1590.471, 1668.782, 2421.141, and 2988.342) and one high-mannose structure m/z 1743.722 have the same pattern as 231-CM-treated MCF10A cells. Our findings, taken together, show that CM derived from breast cancer cells induced an EMT-like process in normal epithelial cells and altered their N-glycan profile.

from # All Medicine by Alexandros G. Sfakianakis via alkiviadis.1961 on Inoreader http://ift.tt/2hiVPkX from OtoRhinoLaryngology - Alexandros G. Sfakianakis via Alexandros G.Sfakianakis on Inoreader http://ift.tt/2tYWKNp