Ask about this productRelated genes to: ST6GALNAC5 antibody
- Gene:
- ST6GALNAC5 NIH gene
- Name:
- ST6 N-acetylgalactosaminide alpha-2,6-sialyltransferase 5
- Previous symbol:
- SIAT7E
- Synonyms:
- MGC3184, ST6GalNAcV
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-05
- Date modifiied:
- 2016-04-29
Related products to: ST6GALNAC5 antibody
Related articles to: ST6GALNAC5 antibody
- Cardiovascular diseases (CVDs) account for approximately 19.8 million deaths annually, with coronary artery disease (CAD) as a major contributor. Genetic factors play an important role in CVD development. Genetic risk can be attributed to monogenic and polygenic risk variants. Patients with rare, Mendelian monogenic CVDs have been shown to have mutations in many causative genes, including LRP6, MEF2A, CYP27A1, and ST6GALNAC5. - Source: PubMed
Publication date: 2026/08/13
Arif NaumanKhan ImranKhan Taj AliAhmad SajjadNauman FatimaAhmad GulzarIjaz MuhammadAhmad BilalHassan Syed MunawarAfaq SaimaHaq Zia Ul - Glaesserella parasuis (G. parasuis), the causative agent of Glässer's disease in pigs, relies on adhesion to host epithelial cells and induction of inflammation for pathogenesis. However, the potential role of ST6GALNAC5, a host sialyltransferase involved in glycan modification, in G. parasuis infection remains unclear. Using the porcine kidney epithelial cell line LLC-PK1, we investigated the function of the host sialyltransferase gene ST6GALNAC5 during G. parasuis infection. Infection significantly upregulated ST6GALNAC5 mRNA expression. CRISPR/Cas9-mediated knockout of ST6GALNAC5 reduced bacterial adhesion to and invasion of host cells. Compared to wild-type cells, ST6GALNAC5-KO cells exhibited higher proliferation and survival rates post-infection. Transcriptomic analysis revealed that ST6GALNAC5 knockout alone altered host cell pathways: DNA replication and cell cycle pathways were activated, while antigen processing and presentation and Toll-like receptor signaling pathways were suppressed. Consistently, upon infection, knockout cells showed significantly reduced expression of pro-inflammatory cytokines TNF-α, IL-8, IL-6, and IL-11. These findings demonstrate that ST6GALNAC5 promotes G. parasuis infection by enhancing bacterial adhesion, invasion and potentiating host inflammatory responses. Therefore, ST6GALNAC5 may serve as a potential host-directed target for controlling G. parasuis infection. - Source: PubMed
Publication date: 2026/07/14
Zhou HuanhuanChen XuexueZeng JiayiDuan ShijiaLiu HailongZeng XinqiZhang XiaoyuXu KeXie ShengsongChen Hongbo - Early identification of genetically superior animals is important for improving growth performance and accelerating genetic gain in swamp buffalo breeding programs. This study investigated the genetic relationships between growth and body structural traits and evaluated their potential use as early selection indicators in Thai swamp buffalo. Phenotypic records from 1034 animals and genotypic data from 462 buffaloes genotyped with 30,979 SNP markers were analyzed using weighted single-step genomic best linear unbiased prediction (WssGBLUP) and weighted single-step Genome-Wide Association Study (WssGWAS) approaches. Moderate to high heritability estimates were observed for growth traits (0.41-0.59), whereas body structural traits showed low to moderate heritability (0.08-0.27). Positive genetic correlations were identified between growth traits and several structural traits, particularly heart girth, hip height, and body depth. Principal component analysis identified two major components explaining 80.1% of the total phenotypic variation, with the first principal component (PC1) representing overall body size and skeletal development. PC1 also showed relatively high heritability (0.57), indicating its potential utility as a composite selection trait. Genome-wide association analysis identified significant SNPs and candidate genes associated with weaning weight and PC1, including , , , , , , and , which are involved in growth regulation, metabolism, cellular development, and stress-response pathways. These findings demonstrate that body structural traits are genetically associated with growth performance and may serve as effective early selection indicators in genomic breeding programs for Thai swamp buffalo. - Source: PubMed
Publication date: 2026/07/01
Kenchaiwong WootichaiChankitisakul VibuntitaDuangjinda MonchaiLomngam RawinanKuha KechaSintala KitsanathonPothikanit KulphatBoonkum Wuttigrai - Triple-negative breast cancer (TNBC) is associated with a high risk of brain metastases (BMs). Although systemic therapies have improved extracranial disease control, the central nervous system (CNS) remains less accessible to numerous agents. As a result, this limited drug penetration makes brain metastases (BMs) remain common in TNBC, which are a leading cause of serious symptoms. This review summarizes recent key advances in triple-negative breast cancer brain metastases (TNBC-BMs), including epidemiology, prognostic stratification, biological mechanisms of CNS tropism and treatment resistance, and evolving management strategies. We discuss potential mechanisms of brain colonization, including the FOXC1-CXCR4 axis, ST6GALNAC5-related interactions with the blood-brain barrier (BBB), and the bidirectional crosstalk between metastatic cells and the brain microenvironment, particularly astrocytes and microglia. Furthermore, we evaluate the evolving clinical management, emphasizing the transition from whole-brain radiotherapy (WBRT) toward more selective local approaches such as stereotactic radiotherapy (SRS) and hippocampal sparing techniques. Concurrently, we examine the integration of CNS active systemic therapy across specific molecular subsets. This review systematically distinguishes standard-of-care interventions from investigational strategies, ultimately underscoring critical evidence gaps within the TNBC-BM landscape. - Source: PubMed
Publication date: 2026/04/07
Yang HongliZhao YangWang YueMa XiaoyuanLing JinmeiZeng XianyiLi ZihuangLiao Guixiang - Cognitive resilience in Alzheimer's disease (AD) requires the maintenance of synaptic integrity despite progressive pathological insults. Reactive astrocytes can switch between neuroprotective and neurotoxic states, and their maladaptive transition significantly accelerates neurodegeneration, yet the molecular drivers of this shift remain elusive. Here, using published single-nucleus transcriptomic data, we identified the sialyltransferase St6galnac5 as a candidate regulator associated with reactive, pro-inflammatory astrocyte states. We further show that astrocyte-specific, AAV-mediated knockdown of St6galnac5 in female 3xTg-AD mice improves spatial learning, memory and anxiety-like behaviors. Neuropathological assessment revealed that this functional recovery was underpinned by a marked reduction in amyloid-β and tau pathologies, alongside the preservation of synaptic integrity. Consistent with a shift toward a less inflammatory astrocyte state, St6galnac5 knockdown decreased A1-associated markers and increased A2-associated markers in vitro and alleviated neurite outgrowth deficits in neuron-astrocyte co-culture. Together, our findings identify St6galnac5 as a critical molecular switch driving astrocytic dysfunction in AD, and further propose that targeted inhibition of this sialylation pathway represents a viable strategy to bolster astrocytic resilience and slow disease progression. - Source: PubMed
Publication date: 2026/03/19
Xue ChunhongChen ChenZou XiaoqiongLi ShiyingLv YehuaLiu Wei