CD55 _ DAF Protein
- Known as:
- CD55 _ DAF Protein
- Catalog number:
- 10101-H02H
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- CD55 _ DAF Protein
Related genes to: CD55 _ DAF Protein
- Gene:
- CD55 NIH gene
- Name:
- CD55 molecule (Cromer blood group)
- Previous symbol:
- DAF
- Synonyms:
- CR, TC, CROM
- Chromosome:
- 1q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: CD55 _ DAF Protein
Related articles to: CD55 _ DAF Protein
- Atherosclerotic carotid stenosis is a major cause of stroke, yet the mechanisms driving plaque instability remain incompletely understood. Perivascular adipose tissue (PVAT), the fat surrounding blood vessels, has been implicated in advanced atherosclerosis progression, but its cellular contributions are largely unknown. Here we show that PVAT contains two distinct adipose-derived stem cell (ADSC, multipotent progenitor cells within fat tissue) subsets. By analyzing 169 clinical samples using single-cell RNA sequencing and flow cytometry and pathological staining, we identify CD55⁺ADSCs as elevated in patients with symptomatic carotid stenosis or prior stroke. These cells migrate into plaques, differentiate into endothelial cells and promote pathological angiogenesis and vascular remodeling through FGF2 secretion thereby destabilising plaques. A second population, CXCL14ADSCs exacerbate inflammation by recruiting immune cells via the CXCL12-CXCR4 axis. Our findings identify perivascular CD55ADSCs as a therapeutic target for atherosclerosis management. - Source: PubMed
Publication date: 2026/05/14
Chen JunyeLi KangShao JiangMei SongLai ZhichaoZhao HongmeiDuan XiaohanXue YunfeiXiao XingqiFeng YuyaoLi ZhiweiZhu ZhanShu KeqiangKong DeqiangXie YiyunXu LeyinWang ChaonanLiu YananXie ZiyanHuang YixuanZhang XinleiWang JingZhang PengLiu Bao - Memory B cell (Bmem) survival is essential for guarding against reinfection, yet processes ensuring their longevity remain unclear. As decay-accelerating factor (DAF, CD55), a negative regulator of complement activation, is requisitely downregulated on germinal center B cells and is reexpressed on Bmem, we investigated the effects of deleting DAF on murine (B1-8hi) Bmem in competitive settings. Kinetic analysis showed a progressive reduction in DAF-/- Bmem numbers over 6 wk, without affecting Bmem production, pool size, or their ability to respond to rechallenge. Following transfer into unimmunized hosts, wild-type Bmem proliferated to maintain stable Bmem pool sizes, outcompeting DAF-/- Bmem, reflecting homeostatic proliferation. Reduced proliferation and increased cell death in DAF-/- Bmem associated with transcriptional differences in metabolism and migration pathways. Wild-type Bmem proliferation increased in C3-/- hosts, and vaccination with a heterologous antigen, which induces local complement activation, locally inhibited bystander B1-8hi Bmem proliferation. Thus, complement-dependent regulation of Bmem homeostatic proliferation influences Bmem longevity and repertoire composition in mice. - Source: PubMed
Publication date: 2026/05/08
Cody Evan WNingoo MehekMonga IshaTsankov Alexander MMuramatsu HiromiPardi NorbertFribourg MiguelHeeger Peter SDominguez-Sola David - Parkinson's disease (PD) is characterized by progressive degeneration of nigrostriatal dopamine neurons and synucleinopathy, which is the accumulation of aggregated α-synuclein (α-syn). Increasing evidence implicates α-syn-associated neuroinflammation as a contributor to PD pathogenesis; however, immune mechanisms linking synucleinopathy to neurodegeneration remain incompletely defined. Activation of the complement cascade occurs in PD and other neurodegenerative disorders, but most studies report complement activation after overt neurodegeneration, making it difficult to conclude if complement is directly activated by pathological α-syn or secondarily following neurodegeneration. We used the rat α-syn preformed fibril (PFF) mode, complement assays and human postmortem PD tissue to test whether pathological α-syn directly activates complement prior to overt neurodegeneration. The α-syn PFF model exhibits a protracted pathological time course and distinct temporal separation between peak α-syn aggregation and nigrostriatal degeneration; thus we quantified complement expression, activation, and regulation during the aggregation phase. Synucleinopathy induced complement activation prior to nigrostriatal degeneration, including upregulation of components of both the classical ( ) and alternative ( ) pathways, the anaphylatoxin ( ) and phagocytic ( ) complement receptors, and activation of complement C3. During early synucleinopathy, microglia upregulated C3 which significantly correlated with synucleinopathy burden across several brain regions, including the substantia nigra pars compacta (SNc) and cortex. Concurrently, complement regulatory proteins, including CD55, CD59, neuronal pentraxin-1 (Nptx1), and the neuronal pentraxin receptor were downregulated in the synucleinopathy-affected SNc. Importantly, increased levels of C1q and iC3b along with downregulation of CD55 and NPTX1 were also observed in human postmortem PD SNc, supporting the translational relevance of our findings. Mechanistically, we demonstrate that aggregated, but not monomeric, α-syn directly binds C1q and activates the complement cascade in a C1q-dpendent manner. These data provide the first evidence that synucleinopathy triggers complement activation and dysregulation prior to neurodegeneration. - Source: PubMed
Publication date: 2026/04/30
Khan HinaGifford MaryKordbacheh ArashBury AsherPanoushek SpencerCole-Strauss AllysonKemp Christopher JLuk Kelvin CSteece-Collier KathyKuhn Nathan CKanaan Nicholas MSortwell Caryl EPatterson Joseph RBenskey Matthew J - Lenvatinib is the primary targeted drug for hepatocellular carcinoma(HCC). However, the development of drug resistance significantly hinders its therapeutic efficacy. The present study aimed to identify new target molecules of lenvatinib-resistant HCC, and improve the treatment of liver cancer. A lenvatinib-resistant HCC cell line, Bel7404(named Bel7404-R), was established, and the protein expression profile of the Bel7404-R cell line and changes in functional enrichment were analyzed. The expression of the identified lenvatinib-resistant critical protein B4GALT4 was validated, and its correlation with immune infiltration and drug resistance was analyzed. Apoptosis and ferroptosis of HCC cell were observe by Calcein-AM/PI staining and transmission electron microscopy. The results indicated that Bel7404-R cells significantly enhanced colony formation and decreased apoptosis ratio compared with parental Bel7404 cells. 111 upregulated and 170 downregulated proteins in the Bel7404-R cells. Notably, upregulated proteins included B4GALT4, CD55, RFTN1, and SHROOM3, whereas downregulated proteins included GRHPR, CLU, TPM2, TMEM185B and TRPM2. B4GALT4 was significantly overexpressed in Bel7404-R cells and identified as a central protein in the molecular regulatory network of these cells. Knockdown of B4GALT4 expression inhibited the levels of PKM2, LDHA and PI3K/AKT signaling, while stimulating the expression of cleaved-Caspase-3. B4GALT4 could protect the integrity of mitochondria and inhibit ferroptosis. The protein expression profile of Bel7404-R cells were significantly different from those of the parental HCC cells. B4GALT4 was identified as a critical molecule for HCC resisting to lenvatinib, and B4GALT4 can be used as a new therapeutic target for lenvatinib-resistant liver cancer. - Source: PubMed
Publication date: 2026/05/07
Wu XueqinPan YinglianPu JianghanFeng SirenLiu KunWu GangLin BoYin QiushiZhu MingyueLi Mengsen - CD55 is an immune regulator that inhibits T cell activation and also binds to CD97, a molecule involved in immune cell migration and signaling. While CD55 expression is reduced in chronic beryllium disease (CBD), its functional role in disease pathogenesis remains unclear. We hypothesized that CD55 downregulation in peripheral blood mononuclear cells (PBMCs) contributes to heightened beryllium (Be)-specific immune responses in CBD. To test this, we characterized CD55 expression and function in PBMCs from individuals with CBD and beryllium sensitization (BeS), as well as in a human Be-specific T cell model. CD55, sCD55, and CD97 mRNA expression were quantified by qRT-PCR in PBMCs from CBD (n = 25), BeS (n = 36), and control (n = 7) subjects. BeSO4 stimulation was used to assess CD55, STAT1, JAK2, and TNF-α expression over time in CBD PBMCs (n = 8). Serum sCD55 was measured by ELISA in an independent cohort. Functional studies using anti-CD55 neutralizing antibodies and the JAK2 inhibitor TG101348 evaluated effects on TNF-α production and lymphocyte proliferation (BeLPT) in PBMCs, and IL-2 production in a Jurkat-Be cell model. CD55, sCD55, and CD97 were significantly downregulated in CBD PBMCs compared to BeS (P < .001). Serum sCD55 was also reduced in CBD (P < .05). BeSO4 stimulation further downregulated CD55 and upregulated STAT1. CD55 blockade increased TNF-α production and BeLPT responses in CBD (P < .001) and BeS (P < .05); these effects were reversed by JAK2 inhibition. In the Be-cell model, CD55 inhibition enhanced IL-2 production (P < .01), attenuated by JAK2 blockade. These findings suggest that CD55 downregulation amplifies Be-induced immune responses in CBD via JAK2/STAT1 signaling. - Source: PubMed
Publication date: 2026/04/09
Li LiLiu SucaiLei ZheMacaluso JoshuaGuo ShujinMacphail KristynMroz Margaret MRestrepo Clara IYang Ivana YMaier Lisa A