CTRP5 pAb
- Known as:
- CTRP5 pAb
- Catalog number:
- ASA905718100
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- CTRP5 pAb
Related genes to: CTRP5 pAb
- Gene:
- C1QTNF5 NIH gene
- Name:
- C1q and TNF related 5
- Previous symbol:
- -
- Synonyms:
- CTRP5, DKFZp586B0621, LORD
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-02
- Date modifiied:
- 2017-03-01
Related products to: CTRP5 pAb
Related articles to: CTRP5 pAb
- Post-acute sequelae of SARS-CoV-2 infection (PASC), particularly neurological manifestations, remain a significant therapeutic challenge, likely driven by persistent inflammation, immune dysregulation, and endothelial dysfunction. In a randomized, double-blind, placebo-controlled crossover trial, 10 patients with post-COVID-19 neurological symptoms received C1-esterase inhibitor (C1-INH; RUCONEST) or placebo over two eight-week phases. Longitudinal plasma proteomics (SomaScan) profiled molecular dynamics during and after C1-INH treatment. C1-INH administration was associated with distinct, phase-specific proteomic signatures, including lower levels of inflammatory-associated proteins such as CRP and IL-6, increased levels of neuroimmune and endothelial repair proteins (Neuropilin-2, CD83, C1QTNF5), and modulation of bradykinin-kinin and extracellular matrix pathways. These molecular shifts were evaluated in relation to clinical change scores during the active treatment windows. Several proteomic changes were observed at timepoint 26 after treatment cessation, describing candidate post-treatment molecular trajectories. In conclusion, these results provide exploratory mechanistic insights and support the need for validation in larger, prospective cohorts. Together, these findings prioritize immune and vascular pathways for further investigation in PASC and may have relevance to other post-infectious neuroimmune conditions. - Source: PubMed
Publication date: 2026/05/19
Orr NogaCollins MaureenNovak ShawnMelamed IsaacSteinman Lawrence - We report two ethnic Chinese families affected by distinct drusenoid inherited maculopathies: Doyne Honeycomb Retinal Dystrophy (DHRD) and Late-Onset Retinal Degeneration (L-ORD)-to expand their recognized phenotypic and ethnic spectrum. - Source: PubMed
Publication date: 2026/03/15
Zhang PeijunQuinodoz MathieuOng CharlesHo Josephine Rui YingTang Rachael W CTan Tien-EnChan Choi MunMathur Ranjana STay Hwee GoonRivolta CarloFenner Beau J - Primary biliary cholangitis (PBC) is a chronic autoimmune liver disease lacking reliable biomarkers for diagnosis or prognosis. To identify plasma complement biomarkers that improve diagnosis and prognosis of PBC. We analyzed large-scale proteomic data from the UK Biobank, concentrating on complement components linked to PBC. A total of 44 PBC patients, including 13 baseline cases and 31 incident cases, were evaluated alongside matched controls based on demographic factors. Proteomic analysis revealed significantly elevated levels of complement proteins, including complement receptor 1 (CR1), complement component 1q subcomponent A chain (C1QA), complement component 1q subcomponent-like 2 (C1QL2), complement component 7 (C7), and component 9 (C9) in PBC patients (P < 0.05). Among these, C1QA, C1QL2, C7, and CR1 demonstrated strong diagnostic potential. Elevated levels of CR1, complement receptor 1 (CR2), C1QA, C1QL2, and C7 were linked to increased risk of PBC onset (P < 0.05). Further analysis revealed that CR1, CR2, C1q and tumor necrosis factor-related protein 1 (C1QTNF1), C1q and tumor necrosis factor-related protein 5 (C1QTNF5), and C7 were associated with more severe liver outcomes (P < 0.05), while lower levels of complement component 5 (C5) and complement C1r subcomponent-like protein (C1RL) correlated with worse outcomes (P = 0.002). Notably, CR1 had the highest predictive accuracy for adverse outcomes (AUC = 81.85), outperforming traditional liver fibrosis markers such as the Fibrosis-4 (FIB-4) index (AUC = 76.33). Complement components, particularly CR1, may serve as valuable biomarkers for diagnosing PBC and predicting its severity. - Source: PubMed
Publication date: 2025/11/21
Ma XiaolinDong HangHan JunmingHan MingZhang TengZhou MengFan XiudeLiu LunaWang Zhen - It was recently proposed that the c.538C>G; p.(Q180E) missense variant in the gene leads to autosomal dominant gyrate atrophy-like choroidal dystrophy (adGALCD). AdGALCD has a phenotypic overlap with other chorioretinal dystrophies but exhibits not the typical characteristics of late-onset retinal degeneration (L-ORD). Here, we report a 70-year-old female simplex patient with adGALCD. - Source: PubMed
Publication date: 2025/05/14
Yang-Seeger DenisePauleikhoff Laurenz J BAtiskova YevgeniyaThiele SarahSpitzer Martin SBirtel Johannes - Posterior microphthalmia and nanophthalmia are related genetic conditions that disrupt ocular growth. Here, we conducted a biometric analysis of mouse models to assess shared features of these diseases. Three known microphthalmia alleles (Mfrp, Prss56, and Adipor1) and two prospective alleles (C1qtnf5 and Prss56) were introgressed onto the C57BL/6J (B6) genetic background and compared to B6 mice at 1 through 12 months of age. Biometric parameters obtained using optical coherence tomography were analyzed statistically to identify strain differences. Fundus imaging and histological analyses were performed to assess ocular morphology. Mfrp, Prss56, and Prss56 mice had significantly shorter axial and posterior lengths, and longer anterior chamber depth compared to controls at all ages studied. Adipor1 mice exhibited similar, but less severe, biometric changes. Axial length was not significantly changed in C1qtnf5 mice, but reduced anterior chamber depth and increased lens thickness were observed at one month of age. Lens and corneal thicknesses were otherwise unchanged in the models as compared to B6 controls. Corneal radius of curvature, examined at 4 months of age, was significantly decreased in all models relative to controls. Micropthalmia was observed independent of retinal degeneration (Mfrp, Adipor1) or retinal thickening (Prss56 mutants). Prss56 mutants developed retinal folds that were absent from other mutants and controls. We conclude that, in mice, Mfrp, Prss56, and Adipor1 mutations yield similar microphthalmia phenotypes involving both the anterior and posterior eye. Changes to anterior chamber depth, lens thickness, and corneal curvature in C1qtnf5 mice suggest a role of C1qtnf5 in anterior ocular growth. - Source: PubMed
Publication date: 2025/03/26
Gogna NavdeepPinkney JaiStone LisaKhorzom Mhd MustafaZhao FuxinCollin Gayle BNaggert Juergen KKrebs Mark PNishina Patsy M