ST8SIA4 Antibody (Center) Blocking Peptide
- Known as:
- ST8SIA4 Antibody (Center) Blocking Peptide
- Catalog number:
- BP9771c
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ST8SIA4 Antibody (Center) Blocking Peptide
Related genes to: ST8SIA4 Antibody (Center) Blocking Peptide
- Gene:
- ST8SIA4 NIH gene
- Name:
- ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 4
- Previous symbol:
- SIAT8D
- Synonyms:
- PST, PST1
- Chromosome:
- 5q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-11
- Date modifiied:
- 2016-10-05
Related products to: ST8SIA4 Antibody (Center) Blocking Peptide
Related articles to: ST8SIA4 Antibody (Center) Blocking Peptide
- The regulatory networks between microRNAs and target genes in blood and cerebrospinal fluid (CSF) are still not fully clarified in relapsing-remitting multiple sclerosis (RRMS). We aimed to clinically validate candidate hub-genes and hub-miRNAs, previously identified in our bioinformatic analysis and determine whether disease-associated expression patterns differed between blood and CSF compartments. - Source: PubMed
Publication date: 2026/06/28
Denkçeken TubaOnur ElifKarabacak Sevim EdaEkmekyapar Fırat YaseminKılıçparlar Cengiz EmineAltunışık Erman - - Source: PubMed
Publication date: 2026/06/14
Sökmen Okan - Diabetic retinopathy (DR) represents a significant public health challenge, with the potential to cause blindness and escalate healthcare costs, yet current diagnostic and therapeutic approaches remain insufficient. This study investigated the role of glycosylation-related differentially expressed genes (GRDEGs) in DR to identify novel biomarkers and therapeutic targets. Through analysis of Gene Expression Omnibus (GEO) datasets using differential expression analysis, functional enrichment, and machine learning, we identified 39 GRDEGs-including RPS23, VCAN, and ST8SIA4-that play significant roles in DR pathogenesis. These genes were enriched in biological processes such as wound healing and sphingolipid metabolism, as well as cancer-related pathways. Immune infiltration analysis revealed distinct patterns and correlations between immune cell types and GRDEGs, suggesting immune microenvironment involvement in DR progression. External validation using an independent blood dataset demonstrated moderate discriminatory performance (AUC 0.7-0.9), though this cross-tissue comparison should be interpreted as exploratory evidence of partial gene expression consistency rather than confirmation of biological mechanisms or clinical utility. Given the limited sample size and group imbalances in the discovery cohort, these results constitute proof-of-concept findings requiring validation in larger, balanced populations. Future research should focus on functional validation of identified GRDEGs and integration of the molecular recognition model into clinical workflows to enable proactive DR management. - Source: PubMed
Publication date: 2026/05/18
Wu QiongMa Pan Pan - Major depressive disorder (MDD) is the leading cause of disability worldwide and shows marked sex differences in prevalence and symptomatology. The dorsolateral prefrontal cortex (DLPFC) and hippocampus are key regions implicated in MDD, yet the role of extracellular matrix (ECM) dysregulation in these areas remains unclear. The ECM supports neural plasticity and synaptic stability through chondroitin sulfate proteoglycans (CSPGs), remodeling enzymes, and adhesion molecules, and its disruption has been linked to psychiatric disorders. In this study, we examined postmortem DLPFC and hippocampal tissue from 20 individuals with MDD and 20 controls to assess expression of ECM-related genes (BCAN, NCAN, VCAN, ADAMTS1, ADAMTS8, CSGALNACT1, SEMA3A, TNR, ST8SIA4). Protein levels of ADAMTS8, SEMA3A, and ST8SIA4 were further examined by Western blotting. We observed that ADAMTS8 expression was significantly reduced in the DLPFC of individuals with MDD, indicating potential impairments in ECM remodeling. Sex-stratified analyses revealed decreased SEMA3A expression in males with MDD and a trend toward reduced ST8SIA4 expression in females. At the protein level, SEMA3A was increased in the DLPFC but decreased in the hippocampus when both sexes were analyzed together, suggesting region-specific or post-transcriptional regulation. Notably, SEMA3A protein levels were significantly increased in males within the DLPFC, with a trend toward decrease in males in the hippocampus. ST8SIA4 protein expression was also reduced in the DLPFC in MDD. These findings identify alterations in ECM-related gene and protein expression in MDD, supporting a role for impaired ECM remodeling and synaptic plasticity in the disorder and highlighting the ECM as a promising therapeutic target. - Source: PubMed
Publication date: 2026/06/02
Klimczak PRivero OMolto M DUnzueta-Larrinaga PAlcaide JGramuntell YMorentin BUrigüen LCallado L FNacher J - Polysialic acid (polySia) is a linear polymer of sialic acid, which usually modifies N-glycans on the neural cell adhesion molecule (NCAM) mostly in the brain and is involved in the development of brain. PolySia is also associated with several diseases, including mental disorders and cancers. ST8Sia2 and ST8Sia4 are believed to be the only polysialyltransferases that synthesize polySia on NCAM (NCAM polysialylation). These enzymes are also autopolysialylated. In this study, we first found that ST8Sia5L, a ganglioside-specific sialyltransferase, has an activity to synthesize polysialic acid on ST8Sia5 itself, but does not exhibit the NCAM polysialylation activity. Notably, in silico and biochemical analyses revealed that ST8Sia5L contains a new polysialic acid-trapping motif (PSTM) that is essential for polySia elongation, instead of the conventional polysialyltransferase domain (PSTD) found in ST8Sia2 and ST8Sia4. We also found that autopolysialylated ST8Sia5L is secreted from the cells. To identify the autopolysialylation sites involved in secretion, we performed N-glycosylation site disruption experiments, and found that N92 and N277 in the five N-glycosylation sites are important for this phenomenon. Furthermore, the inhibitor experiments showed that certain metalloprotease(s), but not exosomal pathways, are involved in the secretion. Notably, the secreted autopolysialylated enzyme showed no ganglioside-sialylation activity; however, the activity was recovered when polySia was removed by sialidase treatment. Overall, we show that autopolysialylation of ST8Sia5L regulates both its secretion and the conventional sialyltransferase activity. - Source: PubMed
Publication date: 2026/05/07
Sakamoto FumiyaHatanaka RinaHane MasayaWu DiKitajima KenSato Chihiro