Notch signaling and Notch signaling modifiers

被引:97
|
作者
Wang, Michael M. [1 ,2 ,3 ]
机构
[1] Univ Michigan, Dept Neurol, Ann Arbor, MI 48109 USA
[2] Vet Adm Ann Arbor Healthcare Syst, Neurol Serv, Ann Arbor, MI 48105 USA
[3] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA
关键词
Notch; DSL; Endocytosis; Notch dissociation; Notch inhibition; TSP2; LRP1; CCN3; MAGP; Dlk; DNER; Contactin; Periostin; EGFL7; INHIBITS TUMOR-GROWTH; UBIQUITIN LIGASE; EXTRACELLULAR DOMAIN; ALAGILLE-SYNDROME; HUMAN JAGGED1; STEM-CELLS; DROSOPHILA; MUTATIONS; RECEPTOR; PROTEIN;
D O I
10.1016/j.biocel.2011.08.005
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Originally discovered nearly a century ago, the Notch signaling pathway is critical for virtually all developmental programs and modulates an astounding variety of pathogenic processes. The DSL (Delta, Serrate, LAG-2 family) proteins have long been considered canonical activators of the core Notch pathway. More recently, a wide and expanding network of non-canonical extracellular factors has also been shown to modulate Notch signaling, conferring newly appreciated complexity to this evolutionarily conserved signal transduction system. Here, I review current concepts in Notch signaling, with a focus on work from the last decade elucidating novel extracellular proteins that up- or down-regulate signal potency. Published by Elsevier Ltd.
引用
收藏
页码:1550 / 1562
页数:13
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