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Graf regulates hematopoiesis through GEEC endocytosis of EGFR.

Development. 2017 Nov 15;144(22):4159-4172. Epub 2017 Oct 09
Sungdae Kim 1 , Minyeop Nahm 2 , Najin Kim 1 , Yumi Kwon 3 , Joohyung Kim 4 , Sukwoo Choi 5 , Eun Young Choi 6 , Jiwon Shim 7 , Cheolju Lee 3 , Seungbok Lee 4
Sungdae Kim 1 , Minyeop Nahm 2 , Najin Kim 1 , Yumi Kwon 3 , Joohyung Kim 4 , Sukwoo Choi 5 , Eun Young Choi 6 , Jiwon Shim 7 , Cheolju Lee 3 , Seungbok Lee 4
+ et al

[No authors listed]

Author information
  • 1 Interdisciplinary Graduate Program in Genetic Engineering, Seoul National University, Seoul 08826, Korea.
  • 2 Department of Cell and Developmental Biology and Dental Research Institute, Seoul National University, Seoul 08826, Korea.
  • 3 Center for Theragnosis, Korea Institute of Science and Technology, Seoul 02792, Korea.
  • 4 Department of Brain and Cognitive Sciences, Seoul National University, Seoul 08826, Korea.
  • 5 School of Biological Sciences, Seoul National University, Seoul 08826, Korea.
  • 6 Department of Biomedical Sciences, Seoul National University, Seoul 08826, Korea.
  • 7 Department of Life Science, Hanyang University, Seoul 04763, Korea.

摘要

EGFR ligand Spitz (Spi), and is indispensable for efficient EGFR degradation and signal attenuation. Finally, Graf interacts directly with EGFR in a receptor ubiquitylation-dependent manner, suggesting a mechanism by which Graf promotes GEEC endocytosis of EGFR at high Spi. Based on our findings, we propose a model in which Graf functions to downregulate EGFR signaling by facilitating Spi-induced receptor internalization through GEEC endocytosis, thereby restraining plasmatocyte proliferation.

KEYWORDS: D-Cbl-mediated receptor ubiquitination, Drosophila, EGFR, GEEC endocytosis, Graf, Plasmatocyte proliferation

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