LCK & CD55 Protein Protein Interaction Antibody Pair
- Known as:
- LCK & CD55 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0081
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- LCK & CD55 Protein Interaction Antibody Pair
Related genes to: LCK & CD55 Protein Protein Interaction Antibody Pair
- 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: LCK & CD55 Protein Protein Interaction Antibody Pair
Related articles to: LCK & CD55 Protein Protein Interaction Antibody Pair
- Cholangiocarcinoma (CCA) has a complex tumor microenvironment (TME) and poor immunotherapy response. Understanding how the adaptive immune response (AIR) affects the TME and prognosis is critical. - Source: PubMed
Publication date: 2026/07/06
Jie WangJixiang ZhouYang BaoYanting WangLing Liu - Osteoarthritis (OA) is a globally prevalent degenerative joint disorder that imposes significant socioeconomic burdens. While traditionally viewed as a localized "wear-and-tear" disease, emerging evidence supports a systemic pathogenesis involving the gut-joint axis. The oral-gut-joint pathway remains underexplored in OA pathophysiology. - Source: PubMed
Publication date: 2026/06/22
Liu YuchiGong JinhuaZhang YuyingWang HongyuFeng Haotian - Acquired resistance to oxaliplatin limits the efficacy of first-line chemotherapy in colorectal cancer (CRC), yet the stress-responsive signaling mechanisms that enable tumor cells to adapt to platinum-induced DNA damage remain incompletely understood. CD55, a glycosylphosphatidylinositol-anchored complement regulator, has recently been implicated in non-canonical cellular stress signaling beyond its classical immune-modulatory role. Here, we investigated whether stress-induced CD55 signaling contributes to oxaliplatin resistance by modulating DNA damage response and repair capacity. - Source: PubMed
Publication date: 2026/07/10
Wang TianyangZhang XiaoyanYan XiaocanWang GuiyingZhao Lianmei - Alzheimer's disease (AD) is the leading cause of dementia worldwide. The retina shares molecular pathways with the brain, yet no study has systematically linked retinal gene expression to AD risk. - Source: PubMed
Publication date: 2026/07/04
Zhang YinuoChen BrianSun HuaiguShi RuhaoLi YunDu JiawenHorimoto Andrea R V R - Intervertebral disc degeneration pathogenesis involves chronic inflammation and cell death, highlighting the need for targeted therapeutic strategies. Extracellular vesicles (EVs) have emerged as promising bioactive materials for designing therapeutic approach. In this study, we demonstrate that youthful-state EVs (Y-EVs) outperform aged donor-derived EVs (O-EVs) in resolving inflammatory cascades within nucleus pulposus (NP) cells. EVs from young rats significantly suppressed TNF--induced inflammation in NP cells by reducing pro-inflammatory cytokine secretion, inhibiting extracellular matrix catabolism, and ameliorating rat disc degeneration. Mechanistically, CD55 enrichment in Y-EVs attenuated NF-B pathway activation, thereby disrupting inflammatory transcriptional programs. CD55 knockdown abrogated the anti-inflammatory efficacy of Y-EV, confirming its functional necessity. Besides, we identified thioredoxin (TRX) as a critical suppressor of NLRP1 inflammasome activation via direct protein binding, which inhibited NP cell pyroptosis. Crucially, CD55 in Y-EVs facilitated TRX-mediated NLRP1 suppression, whereas O-EVs failed to upregulate TRX or suppress the NLRP1 inflammasome. This study highlights the age-dependent functional divergence of EV bioactivity and establishes CD55 as a key determinant of their therapeutic superiority. The TRX-NLRP1 interaction represents a novel target for disc degeneration intervention, positioning youthful-state EVs as an optimized bioactive material for disc regeneration strategies. - Source: PubMed
Publication date: 2026/07/10
Liao ZhiweiWang KunLei MingHerman BomansaanLi ShuaiYang CaoYin Huipeng