ArticleGlycoconjugate journal2010
Transcriptional regulation of the human ST6GAL2 gene in cerebral cortex and neuronal cells.
Article in Glycoconjugate journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Golgi Drivers of Cancer.Sub-cellular biochemistry · 2026Review
- B-Cell ST6Gal1/Neuraminidase 1 Ratios Inversely Predict the Combined Remission and Low-Disease-Activity Subgroup with DAS28-MCP-1 and SDAI Scores for Rheumatoid Arthritis.International journal of molecular sciences · 2025Article
- Functional study of theHeliyon · 2024Article
- Establishment of a humanized ST6GAL1 mouse model for influenza research.Animal models and experimental medicine · 2024Article
- Glycosylation as a tracer of off-target Cre-lox activation in development.Glycobiology · 2024Article
- The alteration and role of glycoconjugates in Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Sialic-Acid-Related Enzymes of B Cells and Monocytes as Novel Markers to Discriminate Improvement Categories and to Fulfill Two Remission Definitions in Rheumatoid Arthritis.International journal of molecular sciences · 2023Article
- Review
- Deficiency in ST6GAL1, one of the two α2,6-sialyltransferases, has only a minor effect on the pathogenesis of prion disease.Frontiers in molecular biosciences · 2022Article
- Regulation of ST6GAL1 sialyltransferase expression in cancer cells.Glycobiology · 2021Review
- Modulation of hepatocyte sialylation drives spontaneous fatty liver disease and inflammation.Glycobiology · 2020Article
- Region-Specific Sialylation Pattern of Prion Strains Provides Novel Insight into Prion Neurotropism.International journal of molecular sciences · 2020Article
- Involvement of ST6Gal I-mediated α2,6 sialylation in myoblast proliferation and differentiation.FEBS open bio · 2020Article
- ST6GAL2 Downregulation Inhibits Cell Adhesion and Invasion and is Associated with Improved Patient Survival in Breast Cancer.OncoTargets and therapy · 2020Article
- Increased α2-6 sialylation of endometrial cells contributes to the development of endometriosis.Experimental & molecular medicine · 2018Article
- IgG and leukocytes: Targets of immunomodulatory α2,6 sialic acids.Cellular immunology · 2018Review
- Review
- Analyses of N-linked glycans of PrPThe FEBS journal · 2017Article
- Review
- B-cell-independent sialylation of IgG.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The second human beta-galactoside alpha-2,6-sialyltransferase (hST6Gal II) differs from hST6Gal I, the first member of ST6Gal family, in substrate specificity and tissue expression pattern. While ST6GAL1 gene is expressed in almost all human tissues, ST6GAL2 shows a restricted tissue-specific pattern of expression, mostly expressed in embryonic and adult brain. In order to understand the mechanisms involved in the transcriptional regulation of ST6GAL2, we first characterized the transcription start sites (TSS) in SH-SY5Y neuroblastoma cells. 5' RACE experiments revealed multiple TSS located on three first alternative 5' exons, termed EX, EY and EZ, which are unusually close on the genomic sequence and are all located more than 42 kbp upstream of the first common coding exon. Using Taqman duplex Q-PCR, we showed that the ST6GAL2 transcripts initiated by EX or EY are mainly expressed in both brain-related cell lines and human cerebral cortex, testifying for the use of a similar transcriptional regulation in vivo. Furthermore, we also showed for the first time hST6Gal II protein expression in the different lobes of the human cortex. Luciferase reporter assays allowed us to define two sequences upstream EX and EY with a high and moderate promoter activity, respectively. Bioinformatics analysis and site-directed mutagenesis showed that NF-kappaB and NRSF are likely to act as transcriptional repressors, whereas neuronal-related development factors Sox5, Puralpha and Olf1, are likely to act as transcriptional activators of ST6GAL2. This suggests that ST6GAL2 transcription could be potentially activated for specific neuronal functions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.