KLF16 antibody - middle region (ARP30079_P050)
- Known as:
- KLF16 (anti-) - middle region (ARP30079_P050)
- Catalog number:
- arp30079_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KLF16 antibody - middle region (ARP30079_P050)
Related genes to: KLF16 antibody - middle region (ARP30079_P050)
- Gene:
- KLF16 NIH gene
- Name:
- Kruppel like factor 16
- Previous symbol:
- -
- Synonyms:
- NSLP2, BTEB4, DRRF
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-27
- Date modifiied:
- 2016-06-03
Related products to: KLF16 antibody - middle region (ARP30079_P050)
Related articles to: KLF16 antibody - middle region (ARP30079_P050)
- : Multiple myeloma (MM) is a hematologic malignancy characterized by clonal plasma cell expansion and diverse genomic rearrangements, including immunoglobulin heavy chain (IGH) translocations. Although RNA sequencing enables the comprehensive detection of IGH-associated fusions, routine molecular monitoring remains limited, particularly in non-secretory MM (NSMM), which lacks measurable serologic markers. Here, we contracted an integrated system combining RNA sequencing (RNA-seq) and reverse transcription quantitative polymerase chain reaction (RT-qPCR) to identify and validate fusion gene-based molecular markers for minimal residual disease (MRD) monitoring. The global fusion landscape was delineated by the sequencing analysis of bone marrow samples from 22 newly diagnosed patients with MM. A total of 362 fusion events were identified, of which 190 non-immunoglobulin fusions were selected for detailed characterization. Recurrent breakpoints were concentrated on chromosomes 1 and 19, and five recurrent fusions, , , , , and , were detected across nine patients. Functional enrichment analyses indicated the significant involvement of these genes in RNA splicing regulation, transcriptional misregulation in cancer-related pathways, and focal adhesion processes. Twenty-three fusion transcripts were validated using RT-PCR and Sanger sequencing, demonstrating high specificity for MM. Longitudinal monitoring revealed that the quantitative assessment of fusion transcript levels enabled earlier relapse detection than flow cytometry, including in NSMM, where conventional MRD tools are ineffective. These findings suggest that individualized fusion transcripts serve as robust molecular markers for MRD surveillance. The proposed RNA-seq-RT-qPCR pipeline offers a clinically practical strategy to enhance precision diagnosis and personalized treatment in MM. - Source: PubMed
Publication date: 2026/02/03
Ren YifeiLu YangHuang DanZhang XuehongGao BeibeiWang XijiaKui XiangjieLiu HongchenLou JiachengYan Jinsong - Colorectal cancer (CRC) is a malignant tumor originating from the epithelial cells of the colon and rectum. Interleukin enhancer binding factor 2 (ILF2), an emerging RNA-binding protein, has been implicated in the regulation of multiple cancer-related processes. However, its specific role in the pathogenesis and progression of CRC remains largely unexplored. In this study, we systematically investigated the functional role of ILF2 in CRC through multi-level experiments. ILF2 expression was first assessed in clinical CRC tissues via quantitative real-time PCR and western blot. Functional implications were further examined through gain-of-function and loss-of-function approaches. Cellular assays included CCK-8 proliferation, colony formation, Transwell migration/invasion, macrophage coculture, and flow cytometry for apoptosis, complemented by immunofluorescence staining. In vivo relevance was confirmed using xenograft models for tumor growth and metastasis. Mechanistically, Co-IP revealed a robust interaction between ILF2 and ILF3, while RIP, RNA pull-down and dual-luciferase reporter assays demonstrated direct binding of ILF3 to KLF16 mRNA, suggesting a novel regulatory axis in CRC progression. Our results demonstrated that both ILF2 mRNA and protein were significantly upregulated in colorectal cancer (CRC) tissues compared to matched peritumoral tissues. Functional assays revealed that ILF2 overexpression enhanced, whereas ILF2 knockdown suppressed, the proliferation, migration, and invasion capabilities of CRC cells in vitro. Additionally, ILF2 overexpression induced M0 macrophages to polarize toward an M2-like phenotype. Consistent with these findings, in vivo experiments indicated that ILF2 facilitated tumor growth and promoted liver metastasis in CRC. Our work suggests that ILF2 formed a complex with ILF3 to enhance the stability of KLF16 mRNA, thereby contributing to CRC progression through the regulation of KLF16. - Source: PubMed
Publication date: 2026/01/23
Mao DongSun JufengZhang XiaoweiWang ZhaopingZhang Yun - Nuclear factor erythroid 2-like 1 (Nrf1/NFE2L1) is a crucial redox-sensitive factor essential for mitochondrial homeostasis. However, its function in controlling macrophage-associated liver inflammation and fibrosis remains to be fully understood. Herein, this study was conducted to elucidate the roles of macrophage Nrf1 in regulating liver fibrosis. Expression levels were analyzed in human liver tissues collected from individuals diagnosed with or without liver fibrosis. High-fat diet feeding, carbon tetrachloride injection or bile duct ligation was performed respectively to established three mouse models of liver fibrosis. Myeloid-specific Nrf1-knockout ( ) mice were developed to investigate the role and underlying mechanisms of macrophage Nrf1 and . Macrophage Nrf1 expression was markedly reduced in liver samples from both humans and mice with liver fibrosis. The deletion of myeloid Nrf1 remarkably accelerated liver inflammation and fibrosis. Macrophages from mice exhibited enhanced M1 polarization and mitochondrial dysfunction. Mechanistically, Nrf1 directly binds to Foxo1 and inhibits its transcriptional activity. The target gene , regulated by the Nrf1-Foxo1 complex, is crucial for modulating mitochondrial function and immune response. Our study highlights the functional properties of macrophage Nrf1-Foxo1 axis in controlling mitochondrial reprogramming and liver fibrosis progression. - Source: PubMed
Publication date: 2026/01/01
Lin YuanbangBian XiyunYao YaoXu JingmanCao YingliWu QiongNing WenLi LianSheng MingweiWang Fengmei - Studies have shown that glutathione peroxidase 8 (GPX8) promotes the progression of various cancers. However, the role of GPX8 in osteosarcoma (OS) progression remains unclear. The aim of this study was to investigate the function of GPX8 in OS progression and its underlying mechanisms. - Source: PubMed
Publication date: 2025/12/02
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