Product Description
MAPK15 Antibody | 62-984 | ProSci
Host: Rabbit
Reactivity: Human
Homology: N/A
Immunogen: This MAPK15 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 32-61 amino acids from the N-terminal region of human MAPK15.
Research Area: Signal Transduction
Tested Application: WB, IHC-P
Application: For WB starting dilution is: 1:1000
For IHC-P starting dilution is: 1:10~50
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: 60 kDa
Validation: N/A
Isoform: N/A
Purification: This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis
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: Mitogen-activated protein kinase 15, MAP kinase 15, MAPK 15, Extracellular signal-regulated kinase 7, ERK-7, Extracellular signal-regulated kinase 8, ERK-8, MAPK15, ERK7, ERK8
User Note: Optimal dilutions for each application to be determined by the researcher.
BACKGROUND: The ERKs are a subfamily of the MAPKs that have been implicated in cell growth and differentiation. Extracellular signal-regulated kinase 8 (Erk8) is a large MAP kinase whose activity is controlled by serum and the c-Src non-receptor tyrosine kinase. ERK8 down-regulates transactivation of the glucocorticoid receptor through Hic-5 and can negatively regulate transcriptional co-activation of androgen receptor and GRalpha by Hic-5 in a kinase-independent manner, suggesting a broader role for ERK8 in the regulation of nuclear receptors beyond estrogen receptor alpha. Erk8 is a novel effector of RET/PTC3 and, therefore, RET biological functions.