NOD2通過IRF4抑制RICK和TRAF6的K63多聚泛素化而減輕結腸炎癥
發(fā)布時間:2018-11-22 18:04
【摘要】:正現(xiàn)已證實,半胱氨酸天冬氨酸酶(caspase)活化和募集結構域15(recruitment domain 15,CARD15)基因(克羅恩病的主要危險因素)的多態(tài)性可導致核苷酸結合寡聚化結構域2(nucleotide-binding oligomerization domain 2,NOD2)功能喪失。然而,這種功能喪失是如何導致克羅恩病的易感性增加,其分子機制尚不清楚。已知人類樹突狀細胞中活化的NOD2可通過其配體胞
[Abstract]:It has been proved that the polymorphism of (caspase) activation and recruitment domain 15 (recruitment domain 15 CARD15 (the main risk factor for Crohn's disease) of cysteine aspartate enzyme may lead to nucleotide binding oligodeoxynucleotide domain 2 (nucleotide-binding oligomerization domain 2). NOD2) loss of function. However, how this loss of function leads to increased susceptibility to Crohn's disease is unclear. Activated NOD2 in human dendritic cells is known to pass through its ligands
【分類號】:R574.62
[Abstract]:It has been proved that the polymorphism of (caspase) activation and recruitment domain 15 (recruitment domain 15 CARD15 (the main risk factor for Crohn's disease) of cysteine aspartate enzyme may lead to nucleotide binding oligodeoxynucleotide domain 2 (nucleotide-binding oligomerization domain 2). NOD2) loss of function. However, how this loss of function leads to increased susceptibility to Crohn's disease is unclear. Activated NOD2 in human dendritic cells is known to pass through its ligands
【分類號】:R574.62
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