ArticleCancer science2010
Analysis of DOK-6 function in downstream signaling of RET in human neuroblastoma cells.
Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 32 citations in OpenAlex.
- AT-rich interaction domain 5A facilitates axon regeneration through docking protein 6 in the peripheral nervous system.Burns & trauma · 2025Article
- Integrated single-nucleus sequencing and spatial architecture analysis identified distinct injured-proximal tubular types in calculi rats.Cell & bioscience · 2023Article
- The Emerging Portrait of Glial Cell Line-derived Neurotrophic Factor Family Receptor Alpha (GFRα) in Cancers.International journal of medical sciences · 2022Review
- Association between ABHD1 and DOK6 polymorphisms and susceptibility to Hirschsprung disease in Southern Chinese children.Journal of cellular and molecular medicine · 2021Article
- DOK6 promoter methylation serves as a potential biomarker affecting prognosis in de novo acute myeloid leukemia.Cancer medicine · 2019Article
- The GDNF Family: A Role in Cancer?Neoplasia (New York, N.Y.) · 2018Review
- Chromosomal breaks at FRA18C: association with reducedNPJ precision oncology · 2017Article
- mRNA expression of DOK1-6 in human breast cancer.World journal of clinical oncology · 2014Article
- Structure and physiology of the RET receptor tyrosine kinase.Cold Spring Harbor perspectives in biology · 2013Review
- Multiple endocrine neoplasias type 2B and RET proto-oncogene.Italian journal of pediatrics · 2012Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Point mutations and structural alterations of the RET tyrosine kinase gene cause multiple endocrine neoplasia type 2 (MEN 2) and papillary thyroid carcinoma, respectively. RET activation by glial cell line-derived neurotrophic factor (GDNF) is essential for the development of the enteric nervous system and the kidney. The signal through RET tyrosine kinase requires several adaptor proteins including the DOK (downstream of kinase) family of proteins. Of the seven members of the DOK protein family, DOK-1, -4, -5, and -6 have been reported to play roles in the GDNF-RET signaling pathway. Although DOK-6 has been shown to bind to RET and promote GDNF-induced neurite outgrowth in mouse Neuro2A cells, DOK-6 function in human cells remains unclear. In the present study, we investigated the role of DOK-6 in GDNF-RET signaling in human cells including neuroblastoma cells. DOK-6 was constitutively localized to the plasma membrane via its pleckstrin homology (PH) domain, and was phosphorylated following RET activation via a MEN2A mutation or GDNF stimulation. However, DOK-6 could not significantly affect downstream signaling and neurite outgrowth in human neuroblastoma cells. The binding affinity of the DOK-6 phosphotyrosine-binding (PTB) domain to RET was much lower than that of the DOK-1, DOK-4, and SHC PTB domains to RET. These findings indicate that DOK-6 is involved in RET signaling with less influence when compared with DOK-1, DOK-4, and SHC.
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