Product Description
KIDINS220 Antibody | 58-360 | ProSci
Host: Rabbit
Reactivity: Human
Homology: N/A
Immunogen: This KIDINS220 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1518-1547 amino acids from the C-terminal region of human KIDINS220.
Research Area: Neuroscience, Signal Transduction
Tested Application: WB
Application: For WB starting dilution is: 1:1000
Specificiy: N/A
Positive Control 1: N/A
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: 197 kDa
Validation: N/A
Isoform: N/A
Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.
Clonality: Polyclonal
Clone: N/A
Isotype: Rabbit Ig
Conjugate: Unconjugated
Physical State: Liquid
Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.
Concentration: batch dependent
Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Alternate Name: Kinase D-interacting substrate of 220 kDa, Ankyrin repeat-rich membrane-spanning protein, KIDINS220, ARMS, KIAA1250
User Note: Optimal dilutions for each application to be determined by the researcher.
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.