Recombinant Human CD93 /C1QR1 Protein
- Known as:
- Recombinant Human CD93 /C1QR1 Protein
- Catalog number:
- cd-803
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human CD93 /C1QR1 Protein
Related genes to: Recombinant Human CD93 /C1QR1 Protein
- Gene:
- CD93 NIH gene
- Name:
- CD93 molecule
- Previous symbol:
- MXRA4, C1QR1
- Synonyms:
- C1qRP, C1qR(P), dJ737E23.1, CDw93, ECSM3
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-05
- Date modifiied:
- 2015-08-24
Related products to: Recombinant Human CD93 /C1QR1 Protein
Related articles to: Recombinant Human CD93 /C1QR1 Protein
- B cell development relies on stringent checkpoints that ensure immune competence and eliminate autoreactive clones. Transitional B cells (B220CD93), which emerge from the bone marrow, migrate to the spleen and differentiate into follicular (FO) or marginal zone (MZ) B cells, a process governed by B cell receptor (BCR) signaling strength, metabolic fitness, and survival cues. Here, we identify Folliculin Interacting Protein 1 (Fnip1) as a key regulator of this developmental transition. Using conditional Fnip1-deficient mice (), loss of Fnip1 results in a developmental arrest at the transitional B220CD93 stage, severely limiting differentiation into FO and MZ B cells and leading to accumulation of a distinct enlarged CD19, RAG negative B cells. Fnip1 modulates BCR signaling thresholds and metabolic programming by regulating the AMPK/FLCN/TFEB and CD19/PI3K/Akt/mTORC1 pathways through restricting TFEB access to the nucleus. Using the MD4/mHEL/sHEL tolerance model, we show that Fnip1 is dispensable for negative selection but is essential for maintaining peripheral tolerance. Together, our findings define Fnip1 as a metabolic gatekeeper that integrates nutrient-sensing pathways with BCR signaling to orchestrate transitional B cell fate decisions, promote peripheral tolerance, and maintain immune homeostasis. - Source: PubMed
Publication date: 2026/04/01
Park HeonCulbert RyanSakya DechenSilprasert Raynah RIritani Brian M - Chimeric antigen receptor (CAR) T cell therapy has transformed the treatment of B cell malignancies, but translation to acute myeloid leukemia (AML) has been hindered by on-target, off-tumor (OTOT) toxicity. In particular, endothelial cell (EC)-specific toxicity has limited clinical translation of promising leukemia stem cell-enriched targets such as CD93. Innovative strategies to mitigate EC damage while preserving antileukemic efficacy are needed. - Source: PubMed
Publication date: 2026/03/11
Woodring TessKletzien Otto ASchlevensky KierstinSanchez-de-Diego CristinaVishwasrao PareshMahoney LaurenKerr Sheena CRichards Rebecca M - Lung cancer (LC) remains a leading cause of cancer-related mortality worldwide, and the limited efficacy of immunotherapy due to treatment resistance underscores the urgent need for new therapeutic strategies. In the present study, CD93-targeted poly(lactic-co-glycolic acid) (PLGA) nanoparticles encapsulating resveratrol (CD93-NPs@RSV) were developed to remodel the metabolic fitness of CD8 tumor-infiltrating lymphocytes. The nanoparticles were precisely engineered and characterized using dynamic light scattering, transmission electron microscopy, and in vivo imaging, which confirmed their stability and tumor-targeting capability. Mechanistic studies revealed that CD93-NPs@RSV suppressed CD93 expression, facilitated apoptosis-inducing factor (AIF) mitochondrial translocation, and activated oxidative phosphorylation (OXPHOS), thereby enhancing T cell function in the tumor microenvironment. Transcriptomic and proteomic analyses further confirmed regulation of the CD93-AKT-PAK5-AIF signaling axis. In a Lewis LC model, CD93-NPs@RSV significantly inhibited tumor progression and displayed strong synergy with anti-PD-1 therapy, resulting in improved survival outcomes. Collectively, our study demonstrates that CD93-NPs@RSV provide a powerful nanotechnology-driven approach to reverse immunotherapy resistance by reprogramming T cell metabolism. These findings establish a promising paradigm for precision cancer immunotherapy and underscore the translational potential of targeted nanomedicine in overcoming therapeutic bottlenecks in LC. - Source: PubMed
Publication date: 2026/03/14
Jiang ZhouLi Yuning - Tumor metastasis represents a major determinant of prognosis in ovarian cancer. Accumulating evidence has demonstrated that the glycosylation of secretome proteins regulates cell communication in the tumor microenvironment, thereby affecting tumor metastasis; however, the underlying regulatory mechanisms remain unclear. In this study, we observed markedly elevated glycosylation levels in metastatic ovarian cancer and identified GALNT10 as a key glycosyltransferase that promotes EMT of ovarian cancer cells. Furthermore, GALNT10 enhances the extracellular secretion of IGFBP7 through O-GalNAc glycosylation modification at the T188 site. IGFBP7 subsequently interacts with the CD93 receptor on endothelial cells, leading to vascular remodeling characterized by abnormal vascular formation and impaired vascular maturity. Moreover, we identified the GALNT10 inhibitor Luteolin, which effectively suppresses ovarian cancer metastasis, modulates the immunosuppressive tumor microenvironment through tumor vascular-immune crosstalk, and exhibits synergistic effects with anti-PD1 therapy. Collectively, our findings indicate that GALNT10 facilitates ovarian cancer metastasis through the induction of tumor cell EMT and tumor vascular dysfunction, suggesting that GALNT10 inhibitors represent a promising avenue for the development of novel therapeutic strategies in ovarian cancer. - Source: PubMed
Publication date: 2026/02/04
Zhang YananZuha AyalaWu ZhangxinLuo AipingJin BixiaSun QinkunLi YuanLiu QiyuGuo HongyanShang Chunliang - The aberrant tumor vasculature fosters a permissive microenvironment that impedes immune effector cell infiltration and simultaneously promotes neoplastic progression. CD93 is an important target for antiangiogenic normalization therapy. Here, we found that the expression of CD93 and its ligand IGFBP7 were significantly upregulated in cancers and closely associated with various pro-angiogenic factors. Next, we identified the CD93 binding peptides (CBP). After systematic D-amino acid modification and retro-inversion, CBP-D8 peptide exhibited the highest blocking activity on CD93/IGFBP7 interaction, and potent inhibition on the migration of endothelial cells. Besides, CBP-D8 peptide significantly facilitated cytotoxic CD8 T cells and NK cells infiltration through enhanced blood perfusion and increased coverage of pericytes and vascular smooth muscle cells. More importantly, CBP-D8 peptide combined with radiotherapy significantly abrogated tumor growth and elicited systemic antitumor immune response. Our study identified a novel peptide blocking CD93/IGFBP7 interaction to normalize tumor vascular function, as well as revealed an approach to promote a favorable tumor microenvironment for the therapeutic intervention. - Source: PubMed
Publication date: 2026/01/31
Qian YuzhenZhang QiongqiongWu YahongSun YixuanCheng YingShi PeishangWang QingchaoQiu LuWang MingshuangZhao WenshanZhai WenjieLi Lingling