Gelsolin (GSN) protein plays a key role in inflammation, cell movement, apoptosis, and cancer progression. It can prevent the fibrillization of β-amyloid protein (Aβ) and defibrillate its produced fibrils. Mutations of the GSN gene can result in hereditary amyloidosis (HA). The deposition of amyloid fibrils formed from the gelsolin protein in many organs and tissues is characterized by familial amyloidosis, Finnish type (FAF), or AGel amyloidosis (AGel).
物理的形状
Solution in phosphate buffered saline, pH 7.4
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Frontiers in medicine, 9, 869409-869409 (2022-05-17)
Fibrinogen A alpha-chain amyloidosis (AFib amyloidosis) is the most common form of hereditary renal amyloidosis in the United Kingdom and Europe, but has rarely been reported in Asia. In this study, we reported two AFib amyloidosis patients in China, reviewing
Proceedings of the National Academy of Sciences of the United States of America, 116(28), 13958-13963 (2019-06-28)
In the disease familial amyloidosis, Finnish type (FAF), also known as AGel amyloidosis (AGel), the mechanism by which point mutations in the calcium-regulated actin-severing protein gelsolin lead to furin cleavage is not understood in the intact protein. Here, we provide
Frontiers in aging neuroscience, 12, 581524-581524 (2020-11-17)
Amyloid protein deposition is a common mechanism of hereditary amyloidosis (HA) and Alzheimer's disease (AD). Mutations of gelsolin (GSN), cystatin C (CST3), transthyretin (TTR), and integral membrane protein 2B (ITM2B) genes can lead to HA. But the relationship is unclear