Ret Proto-Oncogene antibody (Extracellular Domain)
Quick Overview for Ret Proto-Oncogene antibody (Extracellular Domain) (ABIN289533)
Target
See all Ret Proto-Oncogene (RET) AntibodiesReactivity
Host
Clonality
Conjugate
Application
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Binding Specificity
- Extracellular Domain
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Purification
- Purified
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Immunogen
- Ret antibody was raised in goat using NSO derived murine ret extracellular domain as the immunogen.
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Application Notes
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ELISA: 0.5-1 μg/mL, IHC-F: 5 μg/mL, IHC-P: 10-15 μg/mL, WB: 0.1-0.2 μg/mL
Optimal conditions should be determined by the investigator. -
Restrictions
- For Research Use only
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Format
- Lyophilized
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Reconstitution
- Reconstitute with PBS.
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Concentration
- Lot specific
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Buffer
- Lyophilized from PBS, pH 7.2 containing 5 % trehalose.
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Handling Advice
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Avoid repeated freeze/thaw cycles.
Dilute only prior to immediate use. -
Storage
- -80 °C
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Storage Comment
- Aliquot and store at -70 °C or lower.
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: "Distinct adhesion-independent functions of β-catenin control stage-specific sensory neurogenesis and proliferation." in: BMC biology, Vol. 13, pp. 24, (2015) (PubMed).
: "Pro-survival role for Parkinson's associated gene DJ-1 revealed in trophically impaired dopaminergic neurons." in: PLoS biology, Vol. 8, Issue 4, pp. e1000349, (2010) (PubMed).
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- Ret Proto-Oncogene (RET)
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Alternative Name
- Ret
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Background
- The Ret proto-oncogene (c-Ret) is a receptor tyrosine kinase that functions as a multicompetent receptor complex in conjunction with other membrane-bound ligand-binding GDNF family receptors. Ligands that bind the Ret receptor include the glial cell line-derived neurotropic factor (GDNF) and its congeners neurturin, persephin and artemin. Alterations in the corresponding Ret gene are associated with diseases including papillary thyroid carcinoma, multiple endocrine neoplasia (type 2A and 2B), familial medullary thyroid carcinoma and a congenital developmental disorder known as Hirschsprung’s disease. The Tyr905 residue located in the Ret kinase domain plays a crucial role in Ret catalytic and biological activity. Substitution of Phe for Tyr905 dramatically inhibits Ret autophosphorylation activity.
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Pathways
- RTK Signaling, Dopaminergic Neurogenesis, Regulation of Cell Size, Tube Formation
Target
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