Ask about this productRelated genes to: SIGLEC12 antibody
- Gene:
- SIGLEC12 NIH gene
- Name:
- sialic acid binding Ig like lectin 12 (gene/pseudogene)
- Previous symbol:
- SIGLECL1
- Synonyms:
- SLG, S2V, Siglec-XII, Siglec-12, Siglec-L1
- Chromosome:
- 19q13.41
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-28
- Date modifiied:
- 2016-01-20
Related products to: SIGLEC12 antibody
Related articles to: SIGLEC12 antibody
- - Source: PubMed
Publication date: 2026/02/22
Berkel Caglar - Altered bile acid profiles in the follicular fluid have been implicated in the pathogenesis of PCOS. Whether certain bile acids modulate the lytic death of ovarian granulosa cells following regulated cell death mechanisms such as pyroptosis and necroptosis in the context of PCOS is unknown. We here treated ovarian granulosa cells (KGN cell line) with different concentrations of three bile acids (GCDCA, TCA, and GCA) in vitro, and then comparatively analyzed the levels of IL-18, LDH, and PGE2 released from these cells by performing ELISA experiments, in order to determine if these bile acids lead to the loss of plasma membrane integrity in granulosa cells. We found that GCDCA (glycochenodeoxycholic acid) at a concentration of 2500 nmol/L significantly increases the release of LDH from KGN cells in vitro. At this concentration, GCDCA treatment resulted in higher than 30% increased release of LDH from granulosa cells. This bile acid-induced increases in LDH release from granulosa cells were specific to GCDCA, because two other bile acids (TCA (taurocholic acid) and GCA (glycocholic acid)) failed to significantly induce the release of LDH from KGN cells. Further mechanistic studies are needed to determine which plasma membrane rupture mechanisms are mostly involved in LDH release from granulosa cells upon GCDCA treatment. For instance, NINJ1-KO and SIGLEC12-KO KGN cells should be used to see in which case GCDCA fails to induce the release of LDH from granulosa cells, and to identify molecular players involved in bile acid-induced lytic cell death-associated membrane rupture in granulosa cells in the context of PCOS. - Source: PubMed
Publication date: 2026/02/19
Avcioglu Sukran YagmurBerkel Caglar - - Source: PubMed
Publication date: 2025/12/22
Berkel Caglar - Siglec-XII, encoded by SIGLEC12, is a unique sialic acid-binding immunoglobulin-like lectin. It lacks a highly conserved R122 residue for sialic acid recognition in humans. Although it is upregulated in bladder cancer (BCa), its role in tumorigenesis remains largely unexplored. This study aims to investigate the expression patterns of SIGLEC12 in BCa and its correlation with disease features. : An integrated analysis of transcriptomic data and clinical profiles was conducted using various databases and tools, including UALCAN, GEPIA, TIMER, CAMOIP, and CPADs. The analyses encompassed SIGLEC12 expression, survival rates, immune infiltration levels, promoter methylation, and correlation with drug response. : SIGLEC12 expression was higher in both low-grade papillary and high-grade invasive non-papillary BCa. Higher SIGLEC12 expression resulting from low promoter hypomethylation was detected at the stage II-IV of BCa, and was unrelated to disease stages and metastatic stages. Elevated SIGLEC12 expression correlated with increased immune cell infiltration, higher expression of oncogenic and immune checkpoint blockade-related genes, and drug resistance signatures. Mutation analysis confirmed the absence of the canonical R122 missense mutation, indicating that the structural integrity and potential functionality of Siglec-XII are preserved in BCa. : SIGLEC12 may have sialic acid recognition functions and serve as a potential early biomarker of BCa. - Source: PubMed
Publication date: 2025/10/22
Rathore VarshaLin Wan-Wan - Ovarian cancer remains one of the most lethal gynecological malignancies with limited understanding of its genetic architecture and causal mechanisms. While genome-wide association studies have identified numerous susceptibility loci, the causal relationships between gene expression and ovarian cancer risk remain poorly understood. - Source: PubMed
Publication date: 2025/11/25
Yang QinZeng ZuruiWang JieWei Xiangcai