Ask about this productRelated genes to: CD109 antibody
- Gene:
- CD109 NIH gene
- Name:
- CD109 molecule
- Previous symbol:
- -
- Synonyms:
- FLJ38569, DKFZp762L1111, CPAMD7
- Chromosome:
- 6q13
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-04
- Date modifiied:
- 2019-04-23
Related products to: CD109 antibody
Related articles to: CD109 antibody
- CD109 is a glycosylphosphatidylinositol‑anchored glycoprotein implicated in tumor progression and physiological homeostasis. Although aberrant CD109 expression has been reported in multiple malignancies, its prognostic relevance across cancer types and its potential immunomodulatory roles remain incompletely characterized. - Source: PubMed
Publication date: 2026/05/01
Li FangqiongZhang WeiGong XiaotingLiu DanYou QiLi YingZhao GuizhiWang Wei - The effective treatment of nasopharyngeal carcinoma (NPC) is challenged by an immunosuppressive tumor microenvironment (TME) and insufficient immune effector cell activation. Herein, we design a synergistic tri-modal therapeutic strategy to overcome these barriers. This platform integrates: (1) a CD109-targeted liposomal doxorubicin (S3-Lip-DOX) for precise chemotherapy and induction of immunogenic cell death (ICD); (2) non-genetically engineered natural killer (NK) cells armed with dual aptamers (targeting CD109 and PD-L1) bio-orthogonal chemistry for enhanced tumor recognition (S3-P-NK); and (3) an Fc-engineered anti-PD-L1 antibody (Atezolizumab/IgG1) that restores antibody-dependent cellular cytotoxicity (ADCC). Crucially, we uncovered a key mechanistic synergy: S3-Lip-DOX treatment, as a stress-adaptive response, upregulates PD-L1 expression on NPC cells. This finding provides a compelling rationale for the integration, turning a potential immune escape mechanism into a therapeutic vulnerability. The complete regimen, comprising S3-Lip-DOX, S3-P-NK, and Atezolizumab/IgG1, demonstrated potent synergistic antitumor effects and . This triple-combination therapy not only achieved significant tumor regression but also robustly reprogrammed the innate tumor microenvironment, evidenced by enhanced dendritic cell (DC) maturation and pro-inflammatory macrophage activation. This work establishes a mechanism-driven, modular therapeutic platform that effectively coordinates targeted chemotherapy with innate immunotherapy, holding significant translational potential for solid tumors. - Source: PubMed
Publication date: 2025/10/14
Yao ChaoyanWang LeiLiu WeidongShi NingLiao ZilingFu YuxuanOuyang JinhaoLei XuanHuang QianpingLi SiyuZhouyang YihuaZhao PinnanWang JieXu HongjuanZhou WenhuJiang XingjunGao XiangRen CaipingLuo Longlong - Skin fibrosis is characterized by excessive extracellular matrix (ECM) deposition, leading to tissue dysfunction and scarring. Transforming growth factor (TGF)-β is a central mediator of fibrosis. We previously identified CD109 as a TGF-β co-receptor and negative regulator of TGF-β signaling and fibrotic responses and showed that its epidermal overexpression reduces dermal fibrosis in vivo. However, the effects of CD109 loss in the dermis remain unclear. The current study investigates the impact of CD109 knockout (KO) on skin fibrosis using a bleomycin-induced fibrosis mouse model. Following bleomycin treatment, CD109 KO mice showed increased collagen I deposition and elevated fibronectin, CCN2, and α-smooth muscle actin expression in the skin, indicating enhanced ECM production and myofibroblast differentiation compared with wild-type mice. Additionally, CD109 KO mice displayed enhanced Smad1 and Smad2/3 phosphorylation in the skin, indicating heightened TGF-β signaling. In vitro, CD109 KO fibroblasts exhibited increased TGF-β-induced migration and collagen contraction. These findings suggest that CD109 deficiency exacerbates dermal fibrosis by promoting TGF-β/Smad signaling and myofibroblast activation. Given its dysregulation in fibrotic disorders such as scleroderma, our results identify CD109 as a key regulator of skin homeostasis by modulating ECM production and fibroblast activation, underscoring its potential as a therapeutic target in fibrotic disorders. - Source: PubMed
Publication date: 2026/03/20
Xu LiqinGarousi SetarehBatal AdelFinnson Kenneth WPhilip Anie - For older patients with competing comorbidities, optimizing oncologic therapies is of paramount importance. Circulating tumor DNA (ctDNA) is a validated prognostic factor across solid tumors and may provide a strategy to identify patients for whom safe de-escalation of certain therapies is possible. - Source: PubMed
Publication date: 2026/03/19
Carleton NeilChang Alexander CChen FangyuanPuhalla Shannon LFoldi JuliaWaltermire HunterTin AntonyCowher Michael SLupinacci KristinDiego Emilia JSabih QuratulainJohnson Ronald RMalhotra MonicaLaubenthal AmandaGorantla VikramBalic MarijaBhargava RohitJoy MarionFreeman TannerBridges CatherineKalashnikova EkaterinaRodriguez AngelLiu Minetta COesterreich SteffiLee Adrian VMcAuliffe Priscilla F - Thioester-containing proteins (TEPs) play vital roles in the innate immune responses to biotic and abiotic stresses. However, comprehensive genome-wide identification and expression analyses of the TEP gene family in Micropterus salmoides (M. salmoides) are lacking. In this study, 21 TEP genes were identified in the genome of M. salmoides, including 7 copies in A2M, two in CD109, five in C3, four in C4, and single copies of C5, A2ML1, and CPAMD8. Functional analyses and evolutionary relationships indicated a high level of homology with other teleost TEPs. Transcript sequence variants analysis identified numerous non-synonymous single nucleotide variants (nsSNVs) in TEP gene transcripts, with MsA2ML1, MsC3, and MsC4 being among the most affected. These variants, while potentially reflecting genomic diversity, require further validation to distinguish true polymorphisms from transcriptional or technical artifacts. Alternative splicing (AS) analysis has revealed multiple splicing sites and events in the TEPs of M. salmoides. Differential alternative splicing (DAS) analysis showed a significant induction of MsA2ML1 variants after infection with Aeromonas. Analysis of the gene structure and multiple sequence alignments revealed that these variants were produced through AS of the 18th exon. Both transcriptome quantification and qRT-PCR validation confirmed TEP gene responsiveness to Aeromonas infection in M. salmoides. Our study provides the first comprehensive characterization of the TEPs repertoire in largemouth bass, and reveals infection-induced AS as a novel layer of regulatory complexity in teleost innate immunity. - Source: PubMed
Publication date: 2026/02/26
Chen YupingJiang MengzhenTang ShengmeiXian YalingWen JiayiZou ZechengWang Yongsheng