Ask about this productRelated genes to: LENG9 antibody
- Gene:
- LENG9 NIH gene
- Name:
- leukocyte receptor cluster member 9
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-28
- Date modifiied:
- 2016-06-01
Related products to: LENG9 antibody
Related articles to: LENG9 antibody
- Environmental factors such as temperature, salinity, illumination intensity, and photoperiod exert profound influences on the physiology and reproduction of aquatic crustaceans. In this study, female mud crabs (Scylla paramamosain) were exposed to combined high-temperature and strong illumination stress (30 °C, 6000 lx) or maintained under control conditions (25 °C, 600 lx) for 30 days. To elucidate the impact of combined high-temperature and strong illumination stress on ovarian development, we conducted integrated analyses of transcriptomic data (RNA-Seq) from the hepatopancreas and ovary, alongside lipidomic profiles of the hepatopancreas and hemolymph. The hepatopancreas exhibited downregulation of lipid synthesis genes (e.g., Fasn, SCD5) and upregulation of lipid catabolism genes (e.g., BBOX1, Pnlip), which was associated with reduced lipid storage. Enrichment of sphingolipid signaling and autophagy pathways in hemolymph, along with elevated phosphatidylethanolamine species, indicated activation of protective mechanisms to maintain systemic balance. The ovary contained 1,457 differentially expressed genes, including upregulated stress-related genes (e.g., Lrp1b, Tcab1) and downregulated reproduction-related genes (e.g., Igf1r, LENG9), reflecting a trade-off between reproductive suppression and stress adaptation. In conclusion, these findings provide new insights into the adaptation of the mud crab to dual environmental stressors through coordinated molecular adjustments, offering valuable information for aquaculture management in response to sudden weather changes. - Source: PubMed
Publication date: 2025/12/24
Lu LiWang TaoWang XiaopengLiu LiangjieLiu AnYe Haihui - The relationship between dental fluorosis and alterations in the salivary proteome remains inadequately elucidated. This study aimed to investigate the salivary proteome and fluoride concentrations in urine and drinking water among Thai individuals afflicted with severe dental fluorosis. Thirty-seven Thai schoolchildren, aged 6-16, were stratified based on Thylstrup and Fejerskov fluorosis index scores: 10 with scores ranging from 5 to 9 (SF) and 27 with a score of 0 (NF). Urinary and water fluoride levels were determined using an ion-selective fluoride electrode. Salivary proteomic profiling was conducted via LC-MS/MS, followed by comprehensive bioinformatic analysis. Results revealed significantly elevated urinary fluoride levels in the SF group (p = 0.007), whereas water fluoride levels did not significantly differ between the two cohorts. Both groups exhibited 104 detectable salivary proteins. The NF group demonstrated notable upregulation of LENG9, whereas the SF group displayed upregulation of LDHA, UBA1, S100A9, H4C3, and LCP1, all associated with the CFTR ion channel. Moreover, the NF group uniquely expressed 36 proteins, and Gene Ontology and pathway analyses suggested a link with various aspects of immune defense. In summary, the study hypothesized that the CFTR ion channel might play a predominant role in severe fluorosis and highlighted the depletion of immune-related salivary proteins, suggesting compromised immune defense in severe fluorosis. The utility of urinary fluoride might be a reliable indicator for assessing excessive fluoride exposure. - Source: PubMed
Publication date: 2024/08/07
Gavila PatcharapornAjrithirong PenpitchaChumnanprai SupojKalpongnukul NuttiyaPisitkun TrairakChantarangsu SoranunSriwattanapong KanokwanTagami JunjiPorntaveetus Thantrira - Cutaneous T-cell lymphomas (CTCLs) are a kind of non-Hodgkin lymphoma that originates from skin, which is difficult to treat with traditional drugs. Human histone deacetylase inhibitors (HDACi) targeted therapy has become a promising treatment strategy in recent years, but some patients can develop resistance to the drug, leading to treatment failure. There are no public reports on whether alternative splicing (AS) and RNA binding proteins (RBP) affect the efficacy of targeted therapy. Using data from the Gene Expression Omnibus (GEO) database, we established a co-change network of AS events and RBP in CTCLs for the first time, and analyzed the potential regulatory effects of RBP on HDACi-related AS events. The dataset GSE132053, which contained the RNA sequence data for 17 HDACi samples, was downloaded and clean reads were aligned to the human GRCh38 genome by hierarchical indexing for spliced alignment of the transcripts, allowing four mismatches. Gene expression levels were evaluated using exons per million fragments mapped for each gene. Student's t-tests were performed to evaluate the significance of changes in ratios for AS events, and regulated alternative splicing events (RASEs) were defined as events with values less than 0.05. To sort the differentially expressed genes functional categories, Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways were identified using the KOBAS 2.0 server. The regulatory mechanisms of the RASEs and RBPs were evaluated using Pearson's correlation coefficient. Seven indirect events of HDACi resistance or sensitivity were identified: NIR_5151_RP11-977G19.10, NIR_4557_IRAG2, NIR_11870_SUMO1, NIR_5347_ING4, NIR_17935_DNAJC2, NIR_17974_CBLL1, and NIR_422_SLC50A1. The potential regulatory relationships between RBPs and HDACi-sensitive RASEs were also analyzed. and significantly affected NIR_11870_SUMO1, suggesting a potential regulatory relationship. Additionally, may regulate NIR_5347_ING4, may regulate NIR_17935_DNAJC2, and and may regulate NIR_422_SLC5A1. Overall, our findings establish a theoretical foundation for the precise targeted treatment of CTCLs with HDACi. - Source: PubMed
Publication date: 2022/09/06
Yu ShirongZhang JingzhanDing YuanKang XiaojingPu Xiongming - MHCY is a second major histocompatibility complex-like gene region in chickens originally identified by the presence of major histocompatibility complex class I-like and class II-like gene sequences. Up to now, the MHCY gene region has been poorly represented in genomic sequence data. A high density of repetitive sequence and multiple members of several gene families prevented the accurate assembly of short-read sequence data for MHCY. Identified here by single-molecule real-time sequencing sequencing of BAC clones for the Gallus gallus Red Jungle Fowl reference genome are 107 MHCY region genes (45 major histocompatibility complex class I-like, 41 c-type-lectin-like, 8 major histocompatibility complex class IIβ, 8 LENG9-like, 4 zinc finger protein loci, and a single only zinc finger-like locus) located amid hundreds of retroelements within 4 contigs representing the region. Sequences obtained for nearby ribosomal RNA genes have allowed MHCY to be precisely mapped with respect to the nucleolar organizer region. Gene sequences provide insights into the unusual structure of the MHCY class I molecules. The MHCY class I loci are polymorphic and group into 22 types based on predicted amino acid sequences. Some MHCY class I loci are full-length major histocompatibility complex class I genes. Others with altered gene structure are considered gene candidates. The amino acid side chains at many of the polymorphic positions in MHCY class I are directed away rather than into the antigen-binding groove as is typical of peptide-binding major histocompatibility complex class I molecules. Identical and nearly identical blocks of genomic sequence contribute to the observed multiplicity of identical MHCY genes and the large size (>639 kb) of the Red Jungle Fowl MHCY haplotype. Multiple points of hybridization observed in fluorescence in situ hybridization suggest that the Red Jungle Fowl MHCY haplotype is made up of linked, but physically separated genomic segments. The unusual gene content, the evidence of highly similar duplicated segments, and additional evidence of variation in haplotype size distinguish polymorphic MHCY from classical polymorphic major histocompatibility complex regions. - Source: PubMed
Goto Ronald MWarden Charles DShiina TakashiHosomichi KazuyoshiZhang JibinKang Tae HyukWu XiweiGlass Marla CDelany Mary EMiller Marcia M - Approximately 25% of prostate cancer (PCa) cases experience biochemical recurrence (BCR) following radical prostatectomy (RP). The patients with BCR, especially with BCR ≤2 year after RP (early BCR), are more likely to develop clinical metastasis and castration resistance. Now decision-making regarding BCR after RP relies solely on clinical parameters. We thus attempted to establish an early BCR-risk prediction model by combining a molecular signature with clinicopathological features for guiding clinical decision-making. In this study, an 8-gene signature was derived, and these eight genes were and . The Kaplan-Meier analysis revealed a significantly prolonged BCR-free survival in the patients with low-risk scores compared to those with high-risk scores in both training and validation datasets. Harrell's concordance index and time-dependent receiver operating characteristic analysis demonstrated that this gene signature tended to outperform three commercial panels at early BCR prediction. Moreover, this signature was also proven as an independent predictor of BCR-free survival. A nomogram, incorporating the gene signature and clinicopathologic features, was constructed and excellently predicted 1-, 2- and 3-year BCR-free survival of localized PCa patients after RP. Gene set enrichment analysis, tumor immunity, and mRNA expression profiling analysis showed that the high-risk group was more prone to the immunosuppressive microenvironment and impaired DNA damage response than the low-risk group. Collectively, we successfully developed a novel 8-gene signature as a powerful predictor for early BCR after RP and created a prognostic nomogram, which may help inform the clinical management of PCa. - Source: PubMed
Publication date: 2022/07/15
Guo JinanZhao ChenhuiZhang XinzhouWan ZhongChen TingtingMiao JiashunCai JinpingXie WenchuanChen HaoHuang MengliZhao XiaochenWei WeiShen Qi