Alport's syndrome, Goodpasture's syndrome, and type IV collagen.
By B. Hudson, K. Tryggvason, M. Sundaramoorthy, Eric G. Neilson. New England Journal of Medicine, 2003
923 citations recorded by the source corpus.
Subfields: Genetics, Hematology, Immunology and Allergy
View Paper: https://www.semanticscholar.org/paper/c24097b954f727185a5fe14c5d0bade20ed00cf4
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- Kenji Saito
Citations in the corpus
- Basement membranes: cell scaffoldings and signaling platforms. (2011, neutral): “When mutations develop in the genes coding for these subunits, leading to development of a GBM containing only a12a2 [IV] collagen, the GBM is thought to be destabilized leading to development of Alport syndrome (Hudson et al. 2003).”
- Mammalian collagen IV (2008, background): “However, only three specific heterotrimers (α1α1α2, α3α4α5, and α5α5α6) have so far been found in all tissues studied (Borza et al., 2001; Boutaud et al., 2000; Hudson et al., 1994, 2003).”
- The spectrum of podocytopathies: a unifying view of glomerular diseases. (2007, background): “podocyte, endothelial, and mesangial cells including the specialized a3, a4, and a5 type IV collagen chains.(16) The key organizational signaling systems required to”
- Collagen IV is essential for basement membrane stability but dispensable for initiation of its assembly during early development (2004, background): “Therefore, mutations in any of the genes coding for the α3(IV)α5(IV) chains cause tissue-specific phenotypes, associated with different forms of the Alport’s syndrome (Hudson et al., 2003; Tryggvason, 1996) or related diseases (Badenas et al., 2002; Buzza et al., 2001).”