C5AR1
- Known as:
- C5AR1
- Catalog number:
- 003100A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- C5AR1
Related genes to: C5AR1
- Gene:
- C5AR1 NIH gene
- Name:
- complement C5a receptor 1
- Previous symbol:
- C5R1
- Synonyms:
- C5A, C5AR, CD88
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-04
- Date modifiied:
- 2016-08-10
Related products to: C5AR1
Related articles to: C5AR1
- Complement proteins (C1q-C5) participate in immune surveillance and inflammation, but their roles in osteoblast biology and fracture healing remain generally undefined. Emerging evidence suggests that complement activation may exert both pro‑regenerative and pro‑inflammatory effects, depending on receptor engagement and physiological context. - Source: PubMed
Publication date: 2026/09/24
Counts Patrick RBaer Tori MViswanath OmarGanti Latha - Corneal hyperglycemia is associated with epithelial dysfunction characterized by impaired inflammation, oxidative stress, neuropathy and innate immune mechanisms, as observed in diabetic corneal keratopathy. Therefore, the aim of the study was to investigate at cellular level the effects of moderate to severe acute and chronic challenges of glucose on human primary cultures of corneal epithelial cells (CECs). Human CECs (Innoprot, Spain) were exposed to single or repeated 15 mM or 30 mM High Glucose (HG)-supplemented media (CEC Medium containing plain 5 mM glucose), every 2 days from first stimulations and harvested at day 1 (single/acute challenge) or at days 3 and 5 (repeated/chronic challenge). Mannitol was used as osmotic control and cell sustainability were monitored by trypan blue exclusion test and MTT. Conditioned media were subjected to protein analysis while monolayers were processed for relative real-time RT-PCR. Few selected mediators belonging to the inflammatory, complement, innate receptor, oxidative, DNA enzymes and neurotrophic pathways were tested, and protein levels were assayed on selected mediators (IL-6, IL-8, CFH and C5b-9; ELISA). HG exposure induced a time- and concentration-dependent decrease in CEC metabolic activity, without a comparable reduction in cell number. Acute HG exposure promoted an inflammatory response characterized by increased , , and transcripts, together with an early modulation of complement components and increased expression of and (regulators). Chronic HG exposure induced a marked shift toward complement activation, with increased , , , and transcripts and reduced and expression, with a progressive accumulation of CFH and C5b-9 proteins in a positive relationship. Chronic HG also increased IL-6 and IL-8 protein release and induced a coordinated upregulation of , and , particularly at 30 mM HG. Antioxidant, DNA enzymes and neurotrophic pathways were differentially modulated over time, with an early response followed by chronic upregulation and reduction, progressive / expression, and a biphasic / transcriptional profile. Overall, these findings support a proposed biphasic model of the CEC response to hyperglycemia, characterized by an initial adaptive molecular response followed by progressive dysregulation under prolonged exposure. This early molecular profile might represent an adaptive response to acute metabolic stress, although further studies are required to confirm this functional protective significance. - Source: PubMed
Publication date: 2026/09/21
Dinice LuciaBalzamino Bijorn OmarEsposito GrazianaSquitti RosannaDi Zazzo AntonioMicera Alessandra - Urothelial carcinoma, the second most common urological malignancy, can arise in both the lower and upper urinary tract, with approximately 90-95% arising in the bladder, while urothelial carcinomas of the upper urinary tract account for only 5-10%. Treatment options depend on many factors, such as grade and risk factors, but include surgery, chemotherapy, and immunotherapy. Due to the unique pathological and molecular characteristics of each patient, some therapies are ineffective, and the need for targeted therapies and precision medicine is growing. The interactions of malignant cells within the tumor microenvironment can be decisive for the course of therapy. These interactions include components of the complement system, which is a highly conserved part of the innate immune system. The role of the complement system, especially the anaphylatoxin receptors C5aR1 and C5aR2, in cancer is complex. C5aR1 appears to be tumor-promoting by inhibiting the T cell response and modulating the TME, while C5aR2 plays an ambivalent role and was shown to counteract tumor development in some mouse models while in other types of cancer it stimulated tumor growth and led to chemoresistance. In urothelial carcinomas, C5aR1 has been described as a prognostic factor, while C5aR2 has not been considered to date. Here, we briefly summarize our current knowledge of the complex functions of C5a receptors in cancer. In particular, this is the first focused summary of data on C5a receptors in urothelial carcinomas. - Source: PubMed
Publication date: 2026/09/07
Lütje Lea SophieGruner CarolineKarsten Christian MarcelMerseburger Axel StuartRoesch Marie Christine - The complement system has functions beyond host defense, including roles in development and reproduction. However, the role of complement C5 in fertilization and early embryonic development remains unclear. Here, we investigated the reproductive phenotype of C5-deficient mice on a BALB/c background. C5 mice were fertile and showed no obvious reproductive abnormalities under standard laboratory housing conditions. However, offspring from C5 × C5 mating showed a significant deviation from the expected Mendelian distribution, with an increased proportion of female C5 offspring, whereas male offspring showed no comparable distortion. In vitro fertilization reproduced this skewed ratio which was detectable at the blastocyst stage, suggesting that the underlying mechanism operates during fertilization or preimplantation development. Parent-of-origin analysis further suggested a contribution of maternal C5. During preimplantation development, C5, C5a receptor 1 (C5ar1), and C5a receptor 2 (C5ar2) mRNA levels showed distinct dynamic expression profiles. These findings revealed an unexpected sex- and genotype-dependent reproductive phenotype associated with C5 deficiency and suggest that C5-dependent signaling may contribute to genotype-dependent selection during fertilization or preimplantation development. The dynamic expression of C5a receptors further supports a potential role for C5a signaling in early embryonic development and expands the biological role of complement beyond immune defense to include regulation of mammalian reproduction. - Source: PubMed
Publication date: 2026/09/17
Tokuhiro KeizoChi Hsi-HuaTanaka ShienaNozawai HinaFujiyoshi ShokoTsukamoto RioUeno HirokiLee Sung-IlMurayama Masanori A - Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. The resulting septic shock and multiple organ dysfunction syndrome (MODS) are the primary drivers of mortality. Heat shock factor 1 (HSF1), a master transcription factor regulating cellular stress responses, has been shown to exert protective effects during sepsis. Here, our RNA-seq analysis revealed a significant downregulation of complement C5a receptor 1 (C5aR1) in both HSF1-deficient and septic mice; however, the precise role of C5aR1 in sepsis progression remains poorly understood. In this study, we demonstrated that both C5aR1 expression on peripheral blood neutrophils and plasma soluble C5aR1 levels are significantly reduced in patients with sepsis. Neutrophil C5aR1 was also markedly decreased in septic mice and inversely correlated with disease severity. Functionally, overexpression of C5aR1 alleviated tissue injury and reduced organ bacterial burden in septic mice. Mechanistically, EMSA and dual-luciferase reporter assays confirmed that HSF1 directly binds to the heat shock element (HSE) within the C5aR1 promoter to positively regulate its transcription. Collectively, our study systematically characterizes the alterations of C5aR1 at the membrane, soluble, and transcriptional levels in sepsis and elucidates a novel molecular mechanism by which HSF1 modulates neutrophil C5aR1 to enhance antimicrobial defense and mitigate multi-organ injury, providing fresh insights into potential diagnostic and therapeutic strategies for sepsis. - Source: PubMed
Publication date: 2026/09/15
Song KaiyuanTan SichuangWang NianSong RuoyuHu QikangChen HuanWu YongbinXiao XianzhongZhang HualiTan Sipin