Ask about this productRelated genes to: SLCO1C1 antibody
- Gene:
- SLCO1C1 NIH gene
- Name:
- solute carrier organic anion transporter family member 1C1
- Previous symbol:
- SLC21A14
- Synonyms:
- OATP-F, OATP1C1, OATP1
- Chromosome:
- 12p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-09
- Date modifiied:
- 2015-11-18
Related products to: SLCO1C1 antibody
Related articles to: SLCO1C1 antibody
- Eggshell strength is a critical economic trait that declines with hen age, yet the molecular mechanisms distinguishing stable genetic determinants from age-responsive pathways remain unclear. This study implemented a multi-stage comparative framework using uterine transcriptomes from Rhode Island Red hens at peak lay (60 weeks) and late lay (90 weeks) to address this question. At each age, hens were stratified into Weak and Strong shell strength groups based on longitudinal records (5 time points for the 90-week cohort), with 5 individuals per group selected for RNA-seq analysis. Uterine transcriptomic analysis revealed a conserved core of 86 differentially expressed genes associated with shell strength at both ages, with 96.5% exhibiting concordant regulation direction and highly correlated fold-changes (r = 0.84). Weighted gene co-expression network analysis identified two pivotal modules: a stable intrinsic module (MElightcyan) at 60 weeks correlated with peak-lay strength, and an aging-amplified module (MEyellow) at 90 weeks whose correlation with strength progressively increased from mid- to late lay (r = 0.57 at 40 weeks to 0.72 at 90 weeks). Functionally, enriched pathways shifted from cellular structure (MElightcyan) to calcium signaling and hormone regulation (MEyellow) with age. Transcriptional network analysis identified 8 conserved transcription factors (including SATB1 and RXRG) orchestrating this core program. Integrative analysis prioritizing differential expression, longitudinal phenotypic correlation, and QTL mapping highlighted high-confidence candidate genes, including CNTNAP5 (peak-lay) and SLCO1C1 (late-lay). We propose a two-tiered regulatory model wherein a stable core genetic program interacts with dynamic, age-adapted effector networks to determine shell strength. This model provides a dual-strategy framework, distinguishing targets for genetic selection (core program) from pathways for precision management (age-adapted networks) to mitigate age-related decline in shell quality. - Source: PubMed
Publication date: 2026/03/18
Wang LiyuanLiu LeiBai YingWang YanhengZheng ChuanweiWang JinweiChang ShiminMao ZhiqiongLiu XiaohuiGao Yahui - Endothelial cells (ECs) are key structural and functional components of the blood-brain barrier (BBB). Mouse models are frequently used to study EC biology within the BBB, yet the extent to which human and mouse BBB ECs share conserved transcriptomic features remains unclear. Here, we systematically compare transcriptomic profiles of BBB capillary ECs from adult mice and humans. - Source: PubMed
Publication date: 2026/03/12
Miao YuyangWang JianhaoLi WeihanMäe Maarja AndaloussiJeansson MarieMuhl LarsHe Liqun - Prenatal exposure to bisphenol analogues (BPs) has been suggested to impair fetal growth and increase obesity risk in future life. However, the mechanisms remain unclear. Based on the Shanghai-Minhang Birth Cohort Study, this study aimed to investigate the associations between prenatal exposure to BPs and placental DNA methylation (DNAm) at thyroid hormone (TH)-related genes and explore whether these epigenetic modifications mediated the effects of BPs on offspring adiposity. The participants were recruited between April and December 2012 from the Minhang Maternal and Child Health Hospital in Shanghai, China. The study included 205 mother-child pairs with complete data on exposure, DNAm, and infant skinfold thickness. Maternal BPs concentrations were measured using a single spot urine sample collected in late pregnancy. Placental DNAm levels in the promoter regions were analyzed using bisulfite amplicon sequencing for five TH-related genes: SLC16A2, SLCO1C1, TTR, DIO3 and TRH. We found that prenatal exposure to BPA, BPF and BPS was associated with increased DNAm at SLC16A2, which mediated the associations between these BPs and increased infant skinfold thickness, accounting for 10-16% of the total effects. Additional associations were found between BPS and BPAF and higher methylation levels of SLCO1C1 and TTR. TCBPA was linked to increased DNAm at SLCO1C1 but decreased DNAm at DIO3. These findings suggest that placental DNAm at TH-related genes may serve as a mechanism underlying the effects of prenatal exposure to BPs and a potential mediator linking this exposure to offspring growth. - Source: PubMed
Publication date: 2026/02/10
Chen JiaxianZhang XiaohuaChen YaoLian HongchaoZhao YuanSong XiuyunSong XiuxiaJi HongleiYuan WeiMiao MaohuaWang Ziliang - Adults and children with cerebral cavernous malformations (CCMs) are at risk of experiencing lifelong complications such as hemorrhagic strokes, neurological deficits, and epileptic seizures. These complications can severely reduce quality of life. At present, there is no safe or effective therapeutic option for the long-term treatment of CCMs. - Source: PubMed
Publication date: 2025/12/11
Frias-Anaya EduardoGallego-Gutierrez HeliosBui CassandraBirrueta Janeth OchoaSteinberg JeffreyNiesman Ingrid ReynoldsGongol BrendanNguyen BrinaSawhney AaryamanMizushima ZaidaConnolly NyleKilpatrick BethanAwad Issam APatel Hemal HTrejo JoAnnMomper Jeremiah DTaddei AndreaLopez-Ramirez Miguel Alejandro - Prenatal exposure to organophosphate esters (OPEs) and polybrominated diphenyl ethers (PBDEs) has been linked to disrupted fetal thyroid hormone (TH), though the underlying mechanisms remain unclear. Based on the S-MBCS cohort, we analyzed OPE metabolite concentrations in maternal urine during early pregnancy and PBDE levels in cord plasma. Methylation of five TH regulatory genes, namely deiodinase type 3 (DIO3), solute carrier family 16 member 2 (SLC16A2), solute carrier organic anion transporter family member 1C1 (SLCO1C1), thyrotropin-releasing hormone (TRH), and transthyretin (TTR), was quantified in the placenta. We investigated the associations between prenatal exposure to PBDEs and OPEs and DNA methylation of placental TH-related genes, using samples from 240 and 327 mother-newborn pairs, respectively. We further examined sex-specific differences in these associations and assessed whether the observed epigenetic alterations mediated the relationship between exposures and TH disruption. Mediation analyses were conducted in a subset of mother-newborn pairs with available TH measurements in cord plasma. BDE-47 and ΣPBDE showed sex-specific relationships with DIO3 and SLC16A2 methylation, with a significant positive association in females and a non-significant inverse association in males. Both BDE-47 and ΣPBDEs were linked to SLCO1C1 hypermethylation. OPE metabolites were positively associated with DIO3 and TTR methylation, predominantly in females. Mediation analyses suggested that SLCO1C1 hypermethylation mediated 6.5-7.0 % of the association between ΣPBDE exposure and reduced free triiodothyronine. These findings highlight sex-specific epigenetic changes in placental TH-related genes in relation to PBDE and OPE exposure, providing novel insights into fetal thyroid disruption pathways. - Source: PubMed
Publication date: 2025/08/11
Luan MinZhu HaijunYang FenLiang HongSong XiuxiaJin LongmeiJi HongleiYuan WeiWu QihanSu XiujuanMiao Maohua