Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cholera toxin was coupled to peroxidase to yield a highly specific marker for GM1 gangliosides. Study of embryonic brain cells in culture revealed intense binding of cholera-peroxidase by plasma membranes of both neurons and glial cells. In contrast, long-term monolayer glioblastoma cultures, including one producing C-type virus, revealed virtually no labelling of their plasma membranes. Such cells were shown to be capable of incorporating exogenously applied GM1 into their plasma membranes. Studies with fixed brain and synaptosomal fractions were in accord with results on embryonic brain cells in culture, and autoradiographic findings with 125I cholera supported observations made utilizing cholera-peroxidase. From our studies there is some indication that long-term propagation in vitro alters the plasma membrane GM1.
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PMID:Ultrastructural study of plasma membrane GM1 in neuroectodermal cells using cholera-peroxidase. 97 33

The creatine kinase isoenzymes play an important role in maintaining ATP levels in some cell types during times of high energy demand. We have previously shown in primary cell cultures from rat brain that glial cells express much higher levels of brain creatine kinase (CKB) mRNA than neurons. In a separate earlier study we observed that transcription of CKB mRNA in glial cells can be stimulated by a forskolin-mediated increase in cAMP via a pathway involving protein kinase A (PKA). In this report, we show that the level of CKB mRNA in human U87 glioblastoma cells can be increased by either prostaglandin E1 (PGE1), prostaglandin E2 (PGE2), or cholera toxin (an activator of G alpha s proteins). The induction of CKB mRNA occurs rapidly (with maximal induction after 6 h), is at the level of transcription, and is mediated specifically through PKA. In addition, the results indicate that both PGE1 and PGE2 use the same or related signal transduction pathways to increase CKB transcription. These results suggest that in glial cells CKB mRNA can be regulated by extracellular signals acting through G-protein-coupled receptors. This study may contribute to an understanding of the mechanisms underlying the previously-reported, early postnatal increase in CKB enzyme activity in rat brain. The results are also discussed with regard to the potential involvement of the expression of prostaglandins and CKB during hypoxia and ischemia.
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PMID:Prostaglandin E1, E2, and cholera toxin increase transcription of the brain creatine kinase gene in human U87 glioblastoma cells. 892 40

The present study aimed to investigate changes at the transcript level that are associated with spontaneous astrocytoma progression, and further, to discover novel targets for glioma diagnosis and therapy. GSE4290 microarray data downloaded from Gene Expression Omnibus were used to identify the differentially expressed genes (DGEs) by significant analysis of microarray (SAM). The Short Time Series Expression Miner (STEM) method was then applied to class these DEGs based on their degrees of differentiation in the process of tumor progression. Finally, EnrichNet was used to perform the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis based on a protein-protein interaction (PPI) network. A total of 4,506 DEGs were detected, and the number of DEGs was the highest in grade IV cells (2,580 DEGs). These DEGs were classified into nine clusters by the STEM method. In total, 11 KEGG pathways with XD-scores larger than the threshold (0.96) were obtained. The DEGs enriched in pathways 1 (extracellular matrix-receptor interaction), 3 (phagosome) and 6 (type I diabetes mellitus) mainly belonged to cluster 5. Pathway 2 (long-term potentiation), 4 (Vibrio cholerae infection) and 5 (epithelial cell signaling in Helicobacter pylori infection) was involved with DEGs that belonged to different clusters. Significant changes in gene expression occurred during glioma progression. Pathways 1, 3 and 6 may be important for the deterioration of glioma into glioblastoma, and pathways 2, 4 and 5 may have a role at each stage during glioma progression. The associated DEGs, including SV2, NMDAR and mGluRs, may be suitable as biomarkers or therapeutic targets for gliomas.
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PMID:Analysis of gene expression profiles associated with glioma progression. 2584 10

Cholera toxin subunit B (CTB) is the nontoxic moiety of cholera toxin. It can target the glycosphingolipid GM1 expressed in the blood-brain barrier (BBB), neovasculature, and glioblastoma cells. Thus, CTB has been utilized as a multifunctional molecule for targeted therapy of glioblastoma. Here, we describe a detailed method for preparation of CTB functionalized paclitaxel (PTX)-loaded poly (lactic-co-glycolic acid) (PLGA) nanoparticles. This unique modification can guide nanoparticles across the BBB and target glioblastoma cells. The characterization of nanoparticles such as size, zeta potential, morphology, drug loading, and encapsulation efficiency is shown in this chapter.
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PMID:Preparation of Cholera Toxin Subunit B Functionalized Nanoparticles for Targeted Therapy of Glioblastoma. 3143 23