BST2
- Known as:
- BST2
- Catalog number:
- Y214491
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BST2
Related genes to: BST2
- Gene:
- BST2 NIH gene
- Name:
- bone marrow stromal cell antigen 2
- Previous symbol:
- -
- Synonyms:
- CD317, tetherin
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-17
- Date modifiied:
- 2016-07-29
Related products to: BST2
Related articles to: BST2
- We constructed a gene coexpression network to uncover central key genes related to Sjögren's disease (SjD), and investigated the clinical significance of bone marrow stromal antigen 2 (BST2) in SjD. - Source: PubMed
Publication date: 2026/04/09
Ren TianZhou XinZhou EryeLiu CuipingWu JianChang XinChen Weichang - Despite the widespread success of combination antiretroviral therapy (cART) in suppressing plasma viremia to undetectable levels, people living with HIV-1 (PLWH) continue to face a significantly elevated risk of chronic inflammation and Serious Non-AIDS Events (SNAEs). In this narrative review, we bridge the critical gap between molecular virology, immunometabolism, and clinical pathology by examining the complex interface of intrinsic immunity and viral persistence. We analyzed the evolutionary "arms race" between conserved host restriction factors, including TRIM5α, APOBEC3G, SAMHD1, BST-2, MX2, and SERINC, and the sophisticated viral evasion mechanisms that facilitate reservoir establishment. We further examined the role of bacterial translocation and gut barrier dysfunction in perpetuating systemic inflammation, emphasizing how HIV-1-mediated depletion of mucosal Th17 cells and disruption of tight junction proteins create a "leaky gut" that permits microbial product translocation despite suppressive therapy. Among viral proteins that may contribute to residual pathology during suppressive cART, we focused on the HIV-1 matrix protein p17, which has been proposed to function as a secreted "viral cytokine" from latent reservoirs, acting through CXCR1/CXCR2 receptors and the RACK1-JAK1-STAT1 pathway. Although primarily characterized in in vitro and ex vivo models, emerging data suggested that p17 may sustain systemic immune activation and metabolic reprogramming; however, its relative contribution compared with other viral proteins (Tat, Nef, gp120) in virologically suppressed patients remains to be fully delineated in human studies. Furthermore, we examined how HIV-1 hijacks cellular bioenergetics by shifting host cells from oxidative phosphorylation to aerobic glycolysis. We present an integrative model that connects restriction factor biology, p17-mediated chronic inflammation, immunometabolic dysregulation, and gut barrier dysfunction into a unified pathogenic framework, distinguishing established mechanisms from working hypotheses. Last, we assessed emerging therapeutic strategies, including CRISPR/Cas9-mediated enhancement of restriction factors, modulation of the mTOR pathway, and novel "Shock and Kill" approaches, stratified by development stage and demonstrated endpoints, offering potential pathways toward a functional cure. - Source: PubMed
Publication date: 2026/03/10
Nitsotolis ThomasAssimakopoulos Stelios FKouriannidi ElliLagadinou MariaPapalexandrou AlexiaIoannou PetrosMarangos MarkosMilionis HaralamposChristaki Eirini - Triple negative breast cancer (TNBC) poses a significant clinical challenge in imaging and therapy due to absence of conventional targets such as estrogen, progesterone, and HER2 receptors. The aim of this study is to identify potential targets for TNBC through comprehensive transcriptomic analyses and validation in TNBC cell lines and tissues. - Source: PubMed
Publication date: 2026/02/04
Lee HyunjongKim GiroKim MinaKim Jung LimJung Kyung-HoLee Kyung-Han - Senescent cells contribute to degenerative processes in multiple tissues, including the retina. In the retinal pigment epithelium (RPE), their accumulation is closely associated with retinal aging and disease progression. Eliminating senescent RPE cells has shown therapeutic potential, but conventional senolytics often lack the specificity required to spare non-senescent cells, raising safety concerns. To overcome this, we performed integrated transcriptomic analyses of male mouse-derived RPE cells under natural aging and chemically induced senescence conditions. These analyses identified Bst2 as a membrane-localized marker selectively upregulated in senescent RPE cells, with minimal expression in young controls. Based on this discovery, we developed a modular, antibody-pluggable drug delivery platform-B-Z-PON-comprising mesoporous silica nanoparticles functionalized with a recombinant Fc-binding domain and conjugated with anti-Bst2 antibodies. This nanocarrier selectively accumulates in Bst2-expressing senescent RPE cells, enabling targeted drug delivery and sparing healthy retinal cells. In vivo administration of ABT-263-loaded B-Z-PON in aged and senescence-induced retinal degeneration models resulted in the selective ablation of senescent cells, restoration of RPE function, and improved visual outcomes. Together, our study integrates senescence-specific marker discovery with precision nanomedicine, establishing a versatile platform for targeted senotherapy. These findings offer a promising therapeutic approach for retinal aging disorders, such as age-related macular degeneration. - Source: PubMed
Publication date: 2026/03/18
Oh Jun YongChae Jae-ByoungLee Hyo KyungPark Chul-WooBae MinseoKim GyuriOh YujeongYang GyeongseokKim SangpilOk Hae WonKim DohyunKim ChaekyuLee SeminJang JiwonChung HyewonRyu Ja-Hyoung - Glioblastoma multiforme (GBM) is a lethal primary brain cancer with limited treatment options. Systemic and local immunosuppression induced by GBMs contributes to malignancy aggressiveness and resistance to immune checkpoint blockade (ICB) therapy. Herein, we demonstrated that a novel oncolytic virus, M1 (OVM), reversed GBM-driven systemic immunosuppression and promoted T lymphocyte infiltration within the tumor microenvironment (TME). Intravenous administration of OVM suppressed glioma progression in a spleen-dependent manner. Mechanistically, OVM enhanced B-cell-T-cell interactions in the spleen through the formation of immune synapses. A subset of B cells positive for bone marrow stromal cell antigen 2 (Bst2) was enriched in the splenic marginal zone following OVM treatment and exhibited superior capacity for antigen cross-presentation. These splenic Bst2 B cells activated cognate CD8 T cells to mediate adaptive antitumor immunity against intracranial gliomas. Moreover, OVM treatment synergized with anti-PD-1 therapy and further extended the survival of glioma-bearing animals. Collectively, our findings highlight the therapeutic potential of intravenous OVM for GBM management and reveal a novel immunomodulatory mechanism underlying oncolytic virotherapy. - Source: PubMed
Publication date: 2026/03/04
Han YuGuo CuiChen ChaoxinYang WenzhuoLi HonghuiHe ChangjiaDeng JialinChen ZhijieLiu WenfengChen JiehongZhong YingqianYan CaixinXu CuiyingLiang XuanmingZhong ShengChen FurongLi DepeiLi CongHu WanmingChen ZhengheMou YonggaoChen ZhongpingYan GuangmeiLim MichaelZhu WenboSai Ke