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SLAM Family Receptors Distinguish Hematopoietic Stem and Progenitor Cells and Reveal Endothelial Niches for Stem Cells
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Bmi-1 dependence distinguishes neural stem cell self-renewal from progenitor proliferation
TLDR
It is shown that Bmi-1 is required for the self-renewal of stem cells in the peripheral and central nervous systems but not for their survival or differentiation but restricted neural progenitors from the gut and forebrain proliferate normally in the absence of B mi-1.
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Characterization of intracellular signals via tyrosine 1062 in RET activated by glial cell line-derived neurotrophic factor
TLDR
It is suggested that the RAS and PI3-K pathways activated by GDNF bifurcate mainly through SHC bound to tyrosine 1062 in RET, which is important for activation of CREB and NF-κB in GDNF-treated cells, respectively.
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Neural Crest Stem Cells Persist in the Adult Gut but Undergo Changes in Self-Renewal, Neuronal Subtype Potential, and Factor Responsiveness
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A Mutation at Tyrosine 1062 in MEN2A-Ret and MEN2B-Ret Impairs Their Transforming Activity and Association with Shc Adaptor Proteins*
TLDR
Investigation of the role of tyrosine residues present in the carboxyl-terminal sequence for the transforming activity of Ret with the MEN 2A or MEN 2B mutation demonstrated that tyosine 1062 represents an autophosphorylation site of the mutant Ret proteins.
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Temporally Distinct Requirements for Endothelin Receptor B in the Generation and Migration of Gut Neural Crest Stem Cells
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Hirschsprung Disease Is Linked to Defects in Neural Crest Stem Cell Function
Genes associated with Hirschsprung disease, a failure to form enteric ganglia in the hindgut, were highly up-regulated in gut neural crest stem cells relative to whole-fetus RNA. One of these genes,…
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Biological and biochemical properties of Ret with kinase domain mutations identified in multiple endocrine neoplasia type 2B and familial medullary thyroid carcinoma
TLDR
Interestingly, the level of transforming activity correlated with clinical phenotypes; high group RET with the A883F or M918T mutation and low group Ret with the E768D, V804L or S891A mutation were associated with the development of MEN 2B and FMTC, respectively.
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Mechanism of activation of the ret proto-oncogene by multiple endocrine neoplasia 2A mutations
TLDR
This result demonstrated that transport of the Ret protein to the plasma membrane is required for its transforming activity, and indicated that MEN 2A mutations induced ligand-independent dimerization of the c-Ret protein on the cell surface, leading to activation of its intrinsic tyrosine kinase.
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Identification of SNT/FRS2 docking site on RET receptor tyrosine kinase and its role for signal transduction
TLDR
The results suggest that tyrosine 1062 in RET provides a site for the interaction of multiple signaling molecules and that the balance of SHC and SNT/FRS2 binding may affect the nature of the intracellular signaling for cell proliferation, differentiation and survival induced by activated RET.
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