c_Jun Antibody (Ab_243), pAb, Rabbit
- Known as:
- c_Jun Antibody (Ab_243), pAb, Rabbit
- Catalog number:
- A00238
- Product Quantity:
- 40ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- c_Jun Antibody (Ab_243) pAb Rabbit
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- Foregut mediastinal cysts are rare congenital anomalies arising from aberrant embryonic foregut development, with an estimated incidence of 1 in 42,000 to 1 in 100,000. These benign lesions, including bronchogenic, esophageal duplication, and neurenteric cysts, account for 12-20% of mediastinal masses. They may remain asymptomatic or cause respiratory, gastrointestinal, or neurological symptoms due to compression or complications like infection. This review aims to provide a comprehensive analysis of their embryogenesis, clinical presentation, diagnostic strategies, treatment options, and prognosis to guide clinical decision-making. - Source: PubMed
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Lei WenTripathi AlokHu Shuwen - Membranous nephropathy is a leading cause of nephrotic syndrome, driven by autoantibodies targeting podocyte antigens. Although antibodies against PLAR and THSD7A account for the majority of cases, a substantial fraction of patients remain seronegative, implying the existence of additional, unidentified autoantigens. Here, we report the identification of two novel compound heterozygous mutations in encoding Laminin α5, in a pediatric patient with severe nephrotic syndrome. Whole-exome sequencing revealed c.1355A>T (p.N452I) and c.9770A>G (p.N3257S) variants, with structural modeling indicating that p.N452I induces a conformational change in Laminin α5. This altered conformation enhanced its binding to Collagen IV networks, resulting in thickening of the glomerular basement membrane and the creation of a neo-epitope recognized by conformation-specific IgG1/IgG3 autoantibodies. These autoantibodies activated the classical complement pathway, triggering podocyte injury. A knock-in mouse model harboring the mutation recapitulated the human phenotype, exhibiting proteinuria, glomerular basement membrane thickening, and glomerular IgG deposits. Notably, rituximab treatment in the patient led to the disappearance of anti-Laminin α5 autoantibodies and sustained clinical remission. Our findings establish Laminin α5 as a novel genetic autoantigen in membranous nephropathy and suggest that screening for anti-Laminin α5 antibodies may help identify patients who could benefit from B-cell-targeted therapies. - Source: PubMed
Publication date: 2026/06/13
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Publication date: 2026/06/03
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