Recombinant Human LAIR2 /CD306 Protein
- Known as:
- Recombinant Human LAIR2 /CD306 Protein
- Catalog number:
- la-800
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human LAIR2 /CD306 Protein
Related genes to: Recombinant Human LAIR2 /CD306 Protein
- Gene:
- LAIR2 NIH gene
- Name:
- leukocyte associated immunoglobulin like receptor 2
- Previous symbol:
- -
- Synonyms:
- CD306
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human LAIR2 /CD306 Protein
Related articles to: Recombinant Human LAIR2 /CD306 Protein
- Familial prostate cancer (PCa) accounts for nearly 20% of all PCa cases and is associated with increased genetic susceptibility and earlier disease onset. However, early detection and risk stratification in genetically predisposed individuals remain challenging. Circulating cell-free DNA (cfDNA) provides a minimally invasive source of tumor-derived genomic and epigenomic information. Integrating multi-omic cfDNA analyses may enhance the discovery of biomarkers relevant to familial PCa biology. We conducted a pilot feasibility study employing whole-genome, strand-specific sequencing of cfDNA from eight patients with familial PCa. A unified analytical pipeline was used to jointly profile genomic alterations and epigenomic features. Variant calling, methylation mapping, and allele-specific methylation (ASM) analysis were performed to identify somatic mutations, characterize epigenetic dysregulation, and explore potential interactions between genetic and epigenetic mechanisms. Sequencing revealed 18,878 genetic variants, including 2276 potentially pathogenic alterations. We identified 26 recurrent high-impact mutations, such as stop-gain and start-loss variants, in genes including , , and . Epigenomic profiling demonstrated widespread gene-specific hypermethylation, consistent with transcriptional repression in these loci. ASM events were detected in , , , , and , suggesting coordinated interactions between somatic variation and epigenetic regulation in familial PCa. This proof-of-concept study highlights the feasibility and potential of integrating whole-genome and epigenome profiling of cfDNA to decode the molecular architecture of familial prostate cancer. By jointly capturing genomic alterations and epigenetic signatures, including allele-specific methylation, this multi-omic liquid biopsy approach supports a high-resolution exploration of biologically relevant molecular features. Moreover, this integrated profiling strategy provides a minimally invasive and clinically scalable tool that may substantially improve risk assessment. These findings offer a promising foundation for future validation studies in larger cohorts, with the aim of advancing multi-omic cfDNA analysis as a next-generation technology in the field of precision oncologic epigenetics. - Source: PubMed
Publication date: 2026/04/03
Truda AnnaCordella AngelaDe Leo IleniaDi Palo ArmandoIorio RobertaMarino SimonaLa Rocca RobertoCollà Ruvolo ClaudiaPotenza NicolettaRavo MariaMarchese Giovanna - The reasons for the aggressive clinical phenotype of signet ring cell carcinoma (SRCC) have not been fully elucidated. Previous studies suggest similarities in the genotype of colorectal and gastric SRCC and a clear distinction from non-SRCC. The immune microenvironments of gastric and colorectal SRCC have not been comprehensively examined. We isolated RNA from formalin-fixed, paraffin-embedded (FFPE) sections of 34 tumor specimens, 10 colorectal SRCC, 24 gastric SRCC, 4 non-SRCC colorectal (CCC), and 3 gastric adenocarcinoma (GCC) samples. The PanCancer Immune Profiling Panel was used to evaluate the expression of 770 immune-related genes. We compared the expression profiles of colorectal and gastric SRCC and non-SRCC adenocarcinoma. We found that the immune-related gene expression profiles (GEPs) of colorectal SRCC (CR-SRCC) and gastric SRCC (G-SRCC) were distinct from the non-SRCC. A total of 127 genes were upregulated and 32 downregulated in CR-SRCC compared to CCC. Only two genes (CCL27 and LAIR2 reached statistical significance (-adj < 0.05)) among the differentially expressed genes in G-SRCC compared to GCC. None of the clinically relevant immune checkpoints were significantly differentially expressed in SRCC vs. non-SRCC. Overall, we noted a relative abundance of CD8+ cells in CR-SRCC and G-SRCC and relative overexpression of genes involved in innate immune response including the complement pathway. Finally, we identified IL13RA2 as a potential biomarker and therapeutic target candidate for CR-SRCC. The immune microenvironments of CR-SRCC and G-SRCC are distinct from non-SRCC. Broadly, both CR-SRCC and G-SRCC are characterized by a complex immune microenvironment that features cytotoxic cells and innate immune activity that may facilitate immune evasion. - Source: PubMed
Publication date: 2025/12/23
Zhang JianqingCollingwood RobinAl Diffalha SameerManna Deborah DellaPaluri Ravi KumarMejbel Haider AGbolahan Olumide - There are currently no effective pharmacological treatments for Sjögren's disease (SjD). Our study aims to identify potential therapeutic targets for the condition using druggable genome-wide Mendelian randomization (MR). - Source: PubMed
Publication date: 2025/11/27
He JialeLi KesongGuo ZilinZhou XinyaoTang Xiaopo - Patients with cutaneous T cell lymphoma (CTCL) experience high morbidity and mortality due to S. aureus skin infections and sepsis, but the underlying mechanisms remain unclear. We have previously identified high levels of LAIR2, a decoy protein for the inhibitory receptor LAIR1, in advanced CTCL. Mice lack a LAIR2 homolog, so we used Lair1 knock-out (KO) mice to model LAIR2 overexpression. In a model of S. aureus skin infection, Lair1 KO mice had significantly larger abscesses and areas of dermonecrosis compared to WT despite similar bacterial burdens. Lair1 KO exhibited a pattern of increased inflammatory responses in infection and sterile immune stimulation, with increased production of proinflammatory cytokines and myeloid chemokines, neutrophil ROS, and collagen/ECM pathway proteins, including collagens and complement factors. These findings support the notion that loss of LAIR1 signaling causes an excessive inflammatory response that exacerbates tissue damage and does not improve infection control. Underscoring the clinical relevance of our findings, CTCL skin lesions exhibited similarly increased expression in cytokine and collagen/ECM remodeling pathways, suggesting that high levels of LAIR2 promote excessive inflammatory tissue damage and compromise host defense against S. aureus infection. LAIR signaling represents a promising target for therapeutic development in CTCL and other inflammatory diseases. - Source: PubMed
Publication date: 2025/11/13
Dorando Hannah KMutic Evan CTomaszewski Kelly LKorshunova YuliaTian LingStefanov Mellisa KQuinn Chaz CVeis Deborah JBubeck Wardenburg JulianeMusiek Amy CMehta-Shah NehaPayton Jacqueline E - Rituximab (RTX) is an effective treatment for children with steroid-resistant immune thrombocytopenia (ITP), but reliable biomarkers to predict its response early are lacking. We analysed urine samples from 37 steroid-resistant ITP patients-17 RTX responders (RTX-R) and 20 RTX non-responders (RTX-NR)-along with 40 healthy controls using a discovery-validation proteomics workflow. In the discovery cohort, we identified 78 differential proteins (DPs) before treatment and 67 DPs after treatment using the data-independent acquisition (DIA) approach. The RTX-R group was associated with humoral immunity and complement activation before treatment, while the RTX-NR group showed stronger connections to cellular immunity and glycolysis. The Mfuzz analysis indicated that RTX worked by reducing the B-cell receptor pathway and lipid metabolism while enhancing platelet activation. We validated two proteins (KLK6 and FUBP1) as candidate biomarkers for predicting RTX response through parallel reaction monitoring (PRM) technology, achieving an area under the curve (AUC) of 0.98, with a sensitivity of 1.00 and specificity of 0.85. A monitoring model with HK1, FUBP1, LAIR2, CSTA and RPL12 differentiated RTX-R from RTX-NR after treatment, yielding an AUC of 1.00, sensitivity of 0.92 and specificity of 0.95. Overall, these findings enhance our understanding of RTX mechanisms and support personalized therapy development for ITP. - Source: PubMed
Publication date: 2025/08/08
Yu YuncuiXie XingjuanChen ZhenpingWei JingOuyang JuntaoLin ZheyanMa JingyaoGuo PengWu RunhuiJia LuluGui Jingang