کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5509431 | 1538514 | 2017 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A Sonic hedgehog coreceptor, BOC regulates neuronal differentiation and neurite outgrowth via interaction with ABL and JNK activation
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کلمات کلیدی
GliEGFNPCNgn1DCCMAP2SH3JLPBOCDcxABLJun N-terminal kinasebFGFITSJnkSH2MAPK - MAPKglioma-associated oncogene - انکوژن مرتبط با گلیومNeuronal differentiation - تمایز نورونShh - خیرSrc homology domain 2 - دامنه وابستگی Src 2Src homology domain 3 - دامنه وابستگی Src 3deleted in colorectal cancer - در سرطان کولورکتال حذف شده استdoublecortin - دوچرخهRetinoic acid - رتینوئیک اسیدNeurite outgrowth - رشد عصبیRobo - روبوEmbryonal carcinoma cell - سلول های کارسینومای Embryonalneural progenitor cell - سلول پیشرو عصبیConditioned medium - شرایط محیطیsonic hedgehog - صدای جیر جیرepidermal growth factor - عامل رشد اپیدرمیbasic fibroblast growth factor - فاکتور رشد فیبروبلاست پایهroundabout - میدانNeurogenin 1 - نوروژنین 1CDO - هرmitogen activated protein kinase - پروتئین کیناز فعال Mitogen فعال استkinase dead - کیناز مرده است
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Neurite outgrowth is a critical step for neurogenesis and remodeling synaptic circuitry during neuronal development and regeneration. An immunoglobulin superfamily member, BOC functions as Sonic hedgehog (Shh) coreceptor in canonical and noncanonical Shh signaling in neuronal development and axon outgrowth/guidance. However signaling mechanisms responsible for BOC action during these processes remain unknown. In our previous studies, a multiprotein complex containing BOC and a closely related protein CDO promotes myogenic differentiation through activation of multiple signaling pathways, including non-receptor tyrosine kinase ABL. Given that ABL and Jun. N-terminal kinase (JNK) are implicated in actin cytoskeletal dynamics required for neurogenesis, we investigated the relationship between BOC, ABL and JNK during neuronal differentiation. Here, we demonstrate that BOC and ABL are induced in P19 embryonal carcinoma (EC) cells and cortical neural progenitor cells (NPCs) during neuronal differentiation. BOC-depleted EC cells or Bocâ/â NPCs exhibit impaired neuronal differentiation with shorter neurite formation. BOC interacts with ABL through its putative SH2 binding domain and seems to be phosphorylated in an ABL activity-dependent manner. Unlike wildtype BOC, ABL-binding defective BOC mutants exhibit impaired JNK activation and neuronal differentiation. Finally, Shh treatment enhances JNK activation which is diminished by BOC depletion. These data suggest that BOC interacts with ABL and activates JNK thereby promoting neuronal differentiation and neurite outgrowth.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 30, January 2017, Pages 30-40
Journal: Cellular Signalling - Volume 30, January 2017, Pages 30-40
نویسندگان
Tuan Anh Vuong, Young-Eun Leem, Bok-Geon Kim, Hana Cho, Sang-Jin Lee, Gyu-Un Bae, Jong-Sun Kang,