ANG2 IHC Antibody
- Known as:
- ANG2 Immunohistochemistry Antibody
- Catalog number:
- IW-PA1005
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- IHC
- Gene target:
- ANG2 IHC Antibody
Related genes to: ANG2 IHC Antibody
- Gene:
- VPS51 NIH gene
- Name:
- VPS51 subunit of GARP complex
- Previous symbol:
- C11orf3, C11orf2
- Synonyms:
- ANG2, ANG3, FFR
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-06
- Date modifiied:
- 2019-01-25
Related products to: ANG2 IHC Antibody
Related articles to: ANG2 IHC Antibody
- The role of endothelial dysfunction in tubulointerstitial fibrosis associated with chronic kidney disease (CKD) is not well understood. In this study, we demonstrate that the activation of the endothelial tyrosine kinase TIE2 alleviates renal pathology in experimental CKD in mice. TIE2 activation was achieved using a human angiopoietin-2-binding and TIE2-activating antibody (ABTAA) or through adult-induced endothelium-specific knockout of the vascular endothelial protein tyrosine phosphatase gene (Veptp). Both methods markedly protected CKD mice from endothelial dysfunction, peritubular capillary loss, tubular epithelial injury, and tubulointerstitial fibrosis. Conversely, silencing TIE2 through adult-induced endothelium-specific knockout of the Tie2 gene exacerbated CKD pathology. Additionally, we found that endothelial dysfunction promoted renal fibrosis not through endothelial-to-mesenchymal transition, as previously expected, but by inducing the expression of profibrotic PDGFB in tubular epithelial cells, a process that is inhibited by TIE2 activation. Our findings suggest that TIE2 activation via ABTAA warrants investigation as a therapy in human CKD, where there is a substantial unmet medical need. - Source: PubMed
Publication date: 2025/09/15
Pietilä RiikkaMarks-Hultström AmandaHe LiqunNanavazadeh SamiQuaggin Susan EBetsholtz ChristerJeansson Marie - Disorders of vesicular trafficking and genetic defects in autophagy play a critical role in the development of metabolic and neurometabolic diseases. These processes govern intracellular transport and lysosomal degradation, thereby maintaining cellular homeostasis. In this article, we present two siblings with a novel homozygous variant in (Vacuolar protein sorting 51) gene (c.1511C>T; p.Thr504Met), exhibiting developmental delay, a thin corpus callosum, severe intellectual disability, epilepsy, microcephaly, hearing loss, and dysphagia. This study aimed to investigate the effects of the novel gene variation at the RNA and protein level in fibroblasts derived from patients. A comparative proteomic analysis, which has not been previously elucidated, was performed to identify uncharacterized proteins associated with vesicular trafficking. Furthermore, the impact of disrupted pathways on mitochondria-lysosome contact sites was assessed, offering a thorough pathophysiological evaluation of GARP/EARP (Golgi Associated Retrograde Protein / Endosome Associated Retrograde Protein) complex dysfunction. An analysis of mRNA expression indicated decreased levels of the gene, alongside modifications in the expression of autophagy-related genes (, , , ). Western blotting demonstrated a reduction in VPS51 and autophagy-related protein levels. Proteomic profiling revealed 585 differentially expressed proteins, indicating disruptions in vesicular trafficking, lysosomal function, and mitochondrial metabolism. Proteins involved in mitochondrial β-oxidation and oxidative phosphorylation exhibited downregulation, whereas pathways related to glycolysis and lipid synthesis showed upregulation. Live-cell confocal microscopy revealed a notable increase in mitochondria-lysosome contact sites in patient fibroblasts, suggesting that VPS51 protein dysfunction contributes to impaired organelle communication. The findings indicate that the novel gene variation influences intracellular transport, autophagy, and metabolic pathways, offering new insights into its involvement in neurometabolic disorders. - Source: PubMed
Publication date: 2025/06/14
Aygun DamlaYücel Yılmaz Didem - - Source: PubMed
Publication date: 2025/04/03
Bhanudeep SinganamallaKoneti Bramhini Bhargavi - The purpose of this study was to investigate the dynamic changes in aqueous concentrations of angiopoietin (Ang)-1/2 and vascular endothelial growth factor (VEGF) during injection in treatment-naïve patients with diabetic macular edema (DME) receiving faricimab during the induction phase (3 consecutive monthly doses) and retrospectively analyze the data. - Source: PubMed
Shimura MasahikoSasaki ShotaroNonaka RyotaKashiwagi IkumiYasuda KanakoNoma HidetakaTakagi Hitoshi - Evaluate the ocular pharmacodynamics (PD) of intravitreal faricimab, a bispecific inhibitor of angiopoietin-2 (Ang-2) and vascular endothelial growth factor-A (VEGF-A), in patients with neovascular age-related macular degeneration (nAMD) or diabetic macular edema (DME). - Source: PubMed
Diack CheikhAvery Robert LCheung Chui Ming GemmyCsaky Karl GGibiansky LeonidJaminion FelixGibiansky EkaterinaSickert DeniseStoilov IvoCosson ValerieBogman Katrijn