Recombinant Human KIRREL1 /NEPH1 Protein
- Known as:
- Recombinant Human KIRREL1 /NEPH1 Protein
- Catalog number:
- ki-697
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human KIRREL1 /NEPH1 Protein
Related genes to: Recombinant Human KIRREL1 /NEPH1 Protein
- Gene:
- KIRREL1 NIH gene
- Name:
- kirre like nephrin family adhesion molecule 1
- Previous symbol:
- KIRREL
- Synonyms:
- NEPH1
- Chromosome:
- 1q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-22
- Date modifiied:
- 2018-04-11
Related products to: Recombinant Human KIRREL1 /NEPH1 Protein
Related articles to: Recombinant Human KIRREL1 /NEPH1 Protein
- Gastric cancer (GC) is a leading cause of cancer-related mortality characterized by aggressive metastasis and limited therapeutic options. Kin of IRRE-like protein 1 (KIRREL1) is an emerging cell surface protein whose specific oncogenic role in GC remains largely unknown. Therefore, the intention of this study was to comprehensively investigate the clinical relevance, biological functions, and underlying molecular mechanisms of KIRREL1 in GC progression. The expression and prognostic value of KIRREL1 were evaluated using data from The Cancer Genome Atlas (TCGA) and in vitro experiments. Gain- and loss-of-function studies were performed in GC cell lines to assess the effects of KIRREL1 on proliferation, 5-FU chemosensitivity, migration, and invasion. Western blotting was used to examine the regulation of epithelial-mesenchymal transition (EMT) markers. KIRREL1 was significantly upregulated in GC tissues and cell lines, and its high expression was strongly correlated with poor progression-free, disease-specific, and overall survival in patients. Functionally, KIRREL1 overexpression promoted GC cell proliferation, migration, and invasion, whereas its knockdown had the opposite effects. Furthermore, KIRREL1 knockdown sensitized GC cells to 5-FU treatment. Mechanistically, KIRREL1 was found to positively regulate the expression of the key EMT markers Vimentin, MMP2, and MMP9. Our findings identify KIRREL1 as a novel oncogene that actively promotes GC proliferation, 5-FU chemoresistance, and metastasis via the EMT pathway. Importantly, this establishes KIRREL1 as both a robust prognostic biomarker and a targetable driver of malignancy. Future clinical perspectives should explore the development of specific KIRREL1 inhibitors to overcome chemoresistance and suppress metastatic dissemination. - Source: PubMed
Publication date: 2026/05/19
Lv HuohuaLiu JunJiang LufeiNie ZhiWenWang Yaoxin - Gastric cancer (GC) is the fifth most common type worldwide, representing a public health problem. Among the genes related to this tumorigenesis, the family of matrix metalloproteinases (MMPs), essential regulators of the extracellular matrix (ECM), stand out for their involvement in the development and progression of GC. Therefore, we aimed to evaluate MMP gene expression variation, its relationship with clinicopathological factors and its transcriptome-wide associations. To this end, RNAseq, correlation network, and biological pathway enrichment analyses were performed on tumor samples from GC and peritumoral samples from patients treated at a reference center in the Northern region of Brazil. Among the 22 investigated MMPs, seven genes (MMP2, MMP3, MMP10, MMP12, MMP14, MMP15, and MMP16) were upregulated in cancer, while MMP8 was downregulated. Increased expression of seven of the eight differentially expressed MMPs was found in early stages of the disease compared to Tumor, Node, Metastasis (TNM) stage IV. MMP16 showed higher expression in the diffuse-type gastric adenocarcinoma. An increased expression of MMP10 was observed in the EBV/TCGA group. A significant reduction in survival was noticed in those patients with lower expression of MMP8, MMP12, and MMP14. Transcriptomic correlation analyses demonstrated that differentially expressed MMPs interact with genes likely involved in cell adhesion, ECM organization, and immune response, such as COL1A2, CDH11, KIRREL1, PPP1R14D, CEACAM8, ZNF423, and PRRX1. The enrichment of biological pathways suggests involvement in processes such as ECM organization, collagen and proteoglycan degradation, suggesting that these genes possibly are involved in carcinogenic dynamics, supporting the role of MMPs in tumor ECM reorganization. - Source: PubMed
Publication date: 2026/02/23
Bastos Aline CostaKhayat André SalimMoraes Emanuele Raimunda LouzadaTavares Ágatha Tereza MirandaMourão Ronald Matheus da SilvaMoreira Fabiano CordeiroCasseb Samir Mansour MoraesDemachki SamiaIshak GeraldoBarra Williams FernandesBurbano Rommel Mario Rodríguezde Assumpção Paulo Pimentel - Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide, yet the functional impact of noncoding variants on enhancer activity remains largely unexplored. In this study, we adapted and applied two high-throughput techniques, SNP-STARR-seq and Methyl-STARR-seq, to systematically evaluate the influence of 30,790 noncoding SNPs and more than 134,000 CpG sites on enhancer activity in primary and metastatic CRC cells. We identified 922 SNPs and 487 CpG-containing elements modulating enhancer activity in primary cells and found 3136 SNPs and 3008 methylation-sensitive elements with metastasis-specific regulatory effects. Multi-omics integration linked these variants to target genes, and CRISPR editing validated their roles in driving tumorigenic and metastatic phenotypes. Furthermore, we identified two CRC-specific hypermethylated loci, cg08640619 and cg25982657, as exceptional tissue-based early detection biomarkers (AUC > 0.96). Mechanistically, hypermethylation at cg08640619 disrupts RUNX2 binding, leading to inhibition of and . Our study provides a comprehensive platform for understanding how genetic and epigenetic variants disrupt transcriptional programs in CRC, offering insights into disease susceptibility and identifying potential diagnostic and therapeutic targets. - Source: PubMed
Publication date: 2026/02/20
Chen ErfeiYang QiqiDai HaoyangChen YixinZhang YihuiWang QianglongHou RongrongChen MingWang JieXie QianwenSun WenjuNing Yong-QiangFan LigangYan Jian - - Source: PubMed
Publication date: 2025/11/19
Shirai YokoMiura KenichiroHorita ShigeruIto NaokoTaneda SekikoKoike JunkiHonda KazuhoHattori Motoshi - Podocytopathies are glomerular diseases caused by initial podocyte injury or dysfunction that lead to proteinuria and often nephrotic syndrome. The term encompasses characteristic histological patterns, most commonly focal segmental glomerulosclerosis, minimal changes, membranous nephropathy, diffuse mesangial sclerosis and collapsing glomerulopathy. However, proteinuria of glomerular origin is frequently managed without biopsy; importantly, when the protein loss is mostly albumin, it is a direct readout of podocyte injury and a strong predictor of cardiovascular events, kidney failure and reduced survival. Patients present with oedema and volume disturbances and are at risk of thromboembolism, serious infections and progressive kidney dysfunction. Aetiologically, podocytopathies arise from autoimmune, genetic, mechanical (hyperfiltration), infectious, toxic or monoclonal mechanisms, which may coexist and vary by age; this unifying, mechanism-based view bridges the historically divergent paediatric (response-based) and adult (histology-based) classifications. Diagnosis integrates clinical features with emerging serology for podocyte-directed autoantibodies, targeted genetic testing and kidney biopsy when required. Diagnostic workup has to delineate the causes of podocyte dysfunction. Management combines supportive care with aetiology-guided therapy aimed at minimizing steroid exposure and preventing relapses. Current advances in the field and their effects on diagnostic and therapeutic algorithms open the path towards personalized use of traditional treatments and newly available drugs, which should improve outcomes and quality of life for patients with podocytopathies. - Source: PubMed
Publication date: 2025/12/11
Romagnani PaolaTang Sydney C WWeins AstridHuber Tobias BOsafo CharlotteAnders Hans-Joachim