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KIDINS220 Antibody (C-term) Blocking Peptide

Synthetic peptide

     
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Product Information
Primary Accession Q9ULH0
Clone Names 100528166
Peptide ID 100528166
Additional Information
Gene ID 57498
Other Names Kinase D-interacting substrate of 220 kDa, Ankyrin repeat-rich membrane-spanning protein, KIDINS220, ARMS, KIAA1250
Format Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.
StorageMaintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.
PrecautionsThis product is for research use only. Not for use in diagnostic or therapeutic procedures.
Protein Information
Name KIDINS220
Synonyms ARMS, KIAA1250
Function Promotes a prolonged MAP-kinase signaling by neurotrophins through activation of a Rap1-dependent mechanism. Provides a docking site for the CRKL-C3G complex, resulting in Rap1-dependent sustained ERK activation. May play an important role in regulating postsynaptic signal transduction through the syntrophin-mediated localization of receptor tyrosine kinases such as EPHA4. In cooperation with SNTA1 can enhance EPHA4-induced JAK/STAT activation. Plays a role in nerve growth factor (NGF)- induced recruitment of RAPGEF2 to late endosomes and neurite outgrowth. May play a role in neurotrophin- and ephrin-mediated neuronal outgrowth and in axon guidance during neural development and in neuronal regeneration (By similarity). Modulates stress- induced apoptosis of melanoma cells via regulation of the MEK/ERK signaling pathway.
Cellular Location Membrane; Multi-pass membrane protein. Late endosome. Note=Localized at late endosome before or after nerve growth factor (NGF) stimulation
Tissue Location Abundant in developing and adult neural tissues as well as neuroendocrine cells and dendritic cells Overexpressed in melanoma and melanoma cell lines
Research Areas
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Background

KIDINS220 promotes a prolonged MAP-kinase signaling by neurotrophins through activation of a Rap1-dependent mechanism. Provides a docking site for the CRKL-C3G complex, resulting in Rap1-dependent sustained ERK activation. May play an important role in regulating postsynaptic signal transduction through the syntrophin-mediated localization of receptor tyrosine kinases such as EPHA4. In cooperation with SNTA1 can enhance EPHA4-induced JAK/STAT activation. May play a role in neurotrophin-and ephrin-mediated neuronal outgrowth and in axon guidance during neural development and in neuronal regeneration (By similarity). Modulates stress-induced apoptosis of melanoma cells via regulation of the MEK/ERK signaling pathway.

References

Wu, Z., et al. J. Biol. Chem. 283(42):28198-28215(2008)Sniderhan, L.F., et al. Mol. Cell. Neurosci. 38(3):404-416(2008)Li, J., et al. J. Biol. Chem. 283(5):2614-2621(2008)Liao, Y.H., et al. Cancer Res. 67(24):11547-11556(2007)Bracale, A., et al. Mol. Biol. Cell 18(1):142-152(2007)

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$ 80.00
Cat# BP16256b
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