CXCR4 Antibody
- Known as:
- CXCR4 Antibody
- Catalog number:
- XW-7735
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CXCR4 Antibody
Related genes to: CXCR4 Antibody
- Gene:
- CXCR4 NIH gene
- Name:
- C-X-C motif chemokine receptor 4
- Previous symbol:
- -
- Synonyms:
- LESTR, NPY3R, HM89, NPYY3R, D2S201E, fusin, HSY3RR, NPYR, CD184
- Chromosome:
- 2q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2019-04-23
Related products to: CXCR4 Antibody
Related articles to: CXCR4 Antibody
- Bullous pemphigoid (BP) often requires long-term corticosteroids with substantial adverse effects. Effective corticosteroid-sparing treatments could improve safety and quality of life for patients with BP. - Source: PubMed
Publication date: 2026/05/01
Wang Si-HangLi Si-ZheLi Yi-RanZhang JieWang YanZuo Ya-Gang - Macropinocytosis is a large-scale, actin-driven, fluid-phase form of endocytosis that can be exploited by HIV-1 for entry into primary CD4+ T cells. Herein, we show that HIV-1 actively induces macropinocytosis in resting and activated primary CD4+ T cells. HIV-1-induced T cell macropinocytosis is triggered by the interaction of soluble gp120 Env with cell surface CD4, is clathrin-independent and actin-dependent, and does not require CXCR4 or any other known HIV-1 coreceptors. Notably, Env-induced macropinocytosis requires calcium-independent phospholipase A2 (iPLA2) activity, identifying a role for a lipid-signaling axis downstream of Env-CD4 engagement. Across a gp120 panel, multiple HIV-1 clade B gp120 Envs can induce CD4+ T cell macropinocytosis. However, the magnitude of macropinocytosis does not correlate with CD4-binding strength alone and instead aligns with Env-driven changes in CD4 epitope exposure in CD4 domains distal to the Env-binding domain. Importantly, inhibitors of Env-induced macropinocytosis block HIV-1 infection of resting CD4+ T cells. Therefore, Env-induced macropinocytosis is a functionally important mechanism that promotes HIV-1 infection of this cell type. - Source: PubMed
Publication date: 2026/04/28
Manivannan PraveenSantos da Costa CristinaTang YipeiWang XinghaoSwanson JoelMurakami TomoyukiOno AkiraKing Philip D - Impaired endogenous vascular regenerative capacity, reflected by reduced circulating progenitor cell (CPC) counts, has been linked to age-related diseases, particularly adverse cardiovascular outcomes. Lower CPC counts have also been associated with accelerated age-related cognitive decline in otherwise healthy individuals, but their relationships with cognitive impairment and neuroimaging markers of vascular brain injury and neurodegeneration remain unclear. We investigated cross-sectional associations between CPC subsets, cognitive performance, and neuroimaging phenotypes, hypothesizing that lower CPC levels would be associated with worse cognition and adverse brain markers. - Source: PubMed
Publication date: 2026/05/07
Ahmed TahaGold MatthewKulshreshtha AmbarWoods EdwardRahbar AlirezaHossain MohammadKo Yi-AnMedina-Inojosa JoseHarris Kristen AHuang JingwenMaisuradze NodariOwais MuhammadSakr Shaimaa MThomas TiffanyGoldstein FeliciaLah JamesWaller EdmundCalhoun VinceQuyyumi ArshedHajjar Ihab - The HIV-1 envelope glycoprotein gp120 binds to the CD4 molecule and then undergoes conformational changes to interact with the co-receptors CCR5 or CXCR4, resulting in cellular entrance. However, certain types of cells, such as macrophages and CD4Foxp3 regulatory T cells (Tregs), have been shown to resist HIV-1 infection despite co-expressing CD4 and co-receptors. In this study, we found that tumor necrosis factor receptor type II (TNFR2) directly binds to gp120, with the binding site on gp120 in proximity to that of CD4. Intriguingly, exogenous TNFR2 had the capacity to inhibit the binding of gp120 to CD4 T cells. Furthermore, the infection of CD4CCR5 cells by pseudoviruses containing the HIV-1 envelope was inhibited by TNFR2 protein. In contrast, TNFR1, which is structurally similar to TNFR2 and shares the same ligand, failed to inhibit the infection of CD4 T cells by HIV-1 pseudoviruses. This property of TNFR2 may be harnessed in the prevention or treatment of HIV-1 infection and thus warrants future investigation. - Source: PubMed
Publication date: 2026/04/08
Gao YangChen ZhonghaoChen YiboYang YangWang YiruZhu CiLiao PingSong HeChen Xin - Hematological malignancies are characterized by pronounced metastatic potential associated with the chemokine receptor 4/stromal cell-derived factor-1α (CXCR4/CXCL12) signaling axis, high relapse rates, and a profoundly immunosuppressive tumor microenvironment, all of which severely limit the long-term efficacy of existing therapeutic strategies. Herein, we developed a CXCR4-targeted lipid nanozyme platform (Pt-LNP@E5), in which platinum nanozyme catalytic units and E5 peptide were hierarchically integrated to synergistically achieve metastasis blockade and immune microenvironment remodeling. E5 peptide-mediated CXCR4-specific recognition enabled precise tumor cell accumulation of Pt-LNP@E5 and effectively antagonized CXCR4/CXCL12-driven metastatic signaling, thereby markedly suppressing tumor cell migration and dissemination. Meanwhile, the lipid nanocarrier significantly increased the systemic circulation half-life of the platinum nanozyme and maintained catalytic activity. Within the tumor cell microenvironment, the catalytic system selectively generated reactive oxygen species, which not only induced efficient tumor cell killing but also promoted the transition of the immune microenvironment from an immunosuppressive to an activated state, thereby enhancing antitumor immune responses. These synergistic therapeutic effects were validated in two hematological malignancy models, demonstrating significant tumor growth inhibition, metastasis blockade, and immune microenvironment remodeling. In summary, Pt-LNP@E5 represents a promising strategy for the development of novel platinum-based nanomedicines with broad therapeutic potential. - Source: PubMed
Publication date: 2026/05/03
Wang MengjunZhao YitongLu MingzeYang FanGuo RongLi DapengWang YingWu HaoanXu HaiyanZhang Yu