한빛사논문
- 조회850
Jaeho Yoon1,2, Yoo-Seok Hwang1, Moonsup Lee1, Jian Sun1, Hee Jun Cho1,3, Laura Knapik1 & Ira O. Daar1,*
1National Cancer Institute, Frederick, MD 21702, USA.
2Department of Biochemistry, Institute of Cell Differentiation and Aging, College of Medicine, Hallym University, ChunCheon 200702 Kangwon-Do, Republic of Korea.
3Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Korea.
*Corresponding author
Abstract
Although Eph-ephrin signalling has been implicated in the migration of cranial neural crest (CNC) cells, it is still unclear how ephrinB transduces signals regulating this event. We provide evidence that TBC1d24, a putative Rab35-GTPase activating protein (Rab35 GAP), complexes with ephrinB2 via the scaffold Dishevelled (Dsh) and mediates a signal affecting contact inhibition of locomotion (CIL) in CNC cells. Moreover, we found that, in migrating CNC, the interaction between ephrinB2 and TBC1d24 negatively regulates E-cadherin recycling in these cells via Rab35. Upon engagement of the cognate Eph receptor, ephrinB2 is tyrosine phosphorylated, which disrupts the ephrinB2/Dsh/TBC1d24 complex. The dissolution of this complex leads to increasing E-cadherin levels at the plasma membrane, resulting in loss of CIL and disrupted CNC migration. Our results indicate that TBC1d24 is a critical player in ephrinB2 control of CNC cell migration via CIL.
논문정보
- Research article
- 2018년 08월 (BRIC 등록일 2020-06-15)
- 국내+국외 연구진
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