Ask about this productRelated genes to: SIGLEC12 Blocking Peptide
- 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 Blocking Peptide
Related articles to: SIGLEC12 Blocking Peptide
- - Source: PubMed
Publication date: 2026/08/06
Berkel Caglar - Emerging evidence implicates sialic acid-binding immunoglobulin-like lectin (SIGLEC) family members as emerging immune checkpoints and as having a role in cancer progression. However, as a relatively unique SIGLEC member, SIGLEC12 has rarely been studied in cancer, and its clinical significance in pancreatic ductal adenocarcinoma (PDAC) remains largely unknown. This study aimed to investigate the expression pattern and prognostic value of SIGLEC12 in PDAC. - Source: PubMed
Publication date: 2026/06/27
An YanfeiChu YafenJia Jinbin - : Genetic generalized epilepsies (GGE) often remit in childhood, yet a subset of adults remain pharmacoresistant with substantial morbidity. The genetic basis of adult pharmacoresistant GGE is poorly defined. This descriptive study used whole-genome sequencing (WGS) to identify recurrent coding variants and pathways associated with pharmacoresistant adult GGE. : WGS was performed in ten racially diverse adults (mean age 37.2 years; range 20-52) with electroencephalographically confirmed, pharmacoresistant GGE (mean onset 13.7 years). Analysis prioritized variants present in at least 80% of participants and which were either (i) missense variants predicted deleterious with ANNOVAR or (ii) loss-of-function variants predicted high-impact from snpEff. Pathway enrichment and overlap with a commercial clinical epilepsy gene panel were assessed. : Filtering identified 133 unique, deleterious coding variants across 69 genes shared by at least eight participants. Four genes (APOL4, KMT2C, SON, VDR) overlapped a clinical epilepsy panel, supporting the capacity of WGS to recover clinically relevant loci. Prioritized loci implicated gastrointestinal and metabolic regulators (e.g., MUC6, PNLIPRP2), chemosensory receptors (OR10D3, OR8U1, TAS2R19), neuroimmune mediators (LILRA2, SIGLEC12, OAS2), and ion transporters (KCNJ12, P2RX5, RHBG), consistent with multifactorial mechanisms of pharmacoresistance. : This exploratory WGS study focused exclusively on adults with pharmacoresistant GGE, revealing shared high-impact variants and convergent pathways spanning absorption/metabolism, vitamin D signaling, immunity, and ion transport. Findings broaden the genetic landscape of pharmacoresistant GGE while motivating validation in larger, multiethnic cohorts. - Source: PubMed
Publication date: 2026/05/14
Kidder Benjamin LXu JianGeng RuiDlugas HunterVavilikolanu AnushaChen WeiWasade Vibhangini S - - 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