KIDINS220 Antibody (C-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q9ULH0 |
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Clone Names | 100528166 |
Gene ID | 57498 |
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Other Names | Kinase D-interacting substrate of 220 kDa, Ankyrin repeat-rich membrane-spanning protein, KIDINS220, ARMS, KIAA1250 |
Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
Name | KIDINS220 |
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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. |
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Provided below are standard protocols that you may find useful for product applications.
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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