Anti-ERK2 / MAPK1 / MAPK2 antibody

Anti-ERK2 / MAPK1 / MAPK2 antibody

• DataSheet
• Material Safety Data Sheets (MSDS)

Rabbit polyclonal to ERK2 / MAPK1 / MAPK2

ELISA, WB

Mouse ERK2 / MAPK1 / MAPK2

Erk antibody; ERK antibody; p40 antibody; p41 antibody; ERK2 antibody; ERT1 antibody; ERK-2 antibody; MAPK2 antibody; PRKM1 antibody; PRKM2 antibody; P42MAPK antibody; p41mapk antibody; p42-MAPK antibody; Erk2 antibody; MAPK2 antibody; PRKM2 antibody; Prkm1 antibody; C78273 antibody; p41mapk antibody; p42mapk antibody; AA407128 antibody; AU018647 antibody; 9030612K14Rik antibody; p38 antibody; ERK antibody; MAPK 1 antibody; MAPK 2 antibody; MAPK 2 antibody; p38 antibody; p41mapk antibody; 29030612K14Rik antibody; AA407128 antibody; AU018647 antibody; C78273 antibody; ERK antibody; Erk2 antibody; ERK2 antibody; ERK-2 antibody; ERK-2 antibody; ERT1 antibody; ERT1 antibody; MAPK 1 antibody; Mapk1 antibody; MAPK1 antibody; MAPK2 antibody; MAPK2 antibody; p40 antibody; p41 antibody; p41mapk antibody; P42MAPK antibody; p42mapk antibody; p42-MAPK antibody; p42-MAPK antibody; Prkm1 antibody; PRKM1 antibody; PRKM2 antibody; PRKM2 antibody

Rabbit IgG

Produced in rabbits immunized with purified, recombinant Mouse ERK2 / MAPK1 / MAPK2 (rh ERK2 / MAPK1 / MAPK2; P63085; Met1-Ser358). ERK2 / MAPK1 / MAPK2 specific IgG was purified by Mouse ERK2 / MAPK1 / MAPK2 affinity chromatography.

Polyclonal

0.2 μm filtered solution in PBS

This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.

MAP kinases, also known as extracellular signal-regulated kinases (ERKs), act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. ERK is a versatile protein kinase that regulates many cellular functions. Growing evidence suggests that extracellular signal-regulated protein kinase 1/2 (ERK1/2) plays a crucial role in promoting cell death in a variety of neuronal systems, including neurodegenerative diseases. It is believed that the magnitude and the duration of ERK1/2 activity determine its cellular function. Activation of ERK1/2 are implicated in the pathophysiology of spinal cord injury (SCI). ERK2 signaling is a novel target associated with the deleterious consequences of spinal injury. ERK-2, also known as Mitogen-activated protein kinase 1 (MAPK1), is a member of the protein kinase superfamily and MAP kinase subfamily. MKP-3 is a dual specificity phosphatase exclusively specific to MAPK1 for its substrate recognition and dephosphorylating activity. The activation of MAPK1 requires its phosphorylation by upstream kinases. Upon activation, MAPK1 translocates to the nucleus of the stimulated cells, where it phosphorylates nuclear targets. MAPK1 is involved in both the initiation and regulation of meiosis, mitosis, and postmitotic functions in differentiated cells by phosphorylating a number of transcription factors such as ELK1. MAPK1 acts as a transcriptional repressor which represses the expression of interferon gamma-induced genes. Transcriptional activity is independent of kinase activity. The nuclear-cytoplasmic distribution of ERK2 is regulated in response to various stimuli and changes in cell context. Furthermore, the nuclear flux of ERK2 occurs by several energy- and carrier-dependent and -independent mechanisms. ERK2 has been shown to translocate into and out of the nucleus by facilitated diffusion through the nuclear pore, interacting directly with proteins within the nuclear pore complex, as well as by karyopherin-mediated transport. ERK2 interacts with the PDE4 catalytic unit by binding to a KIM (kinase interaction motif) docking site located on an exposed beta-hairpin loop and an FQF (Phe-Gln-Phe) specificity site located on an exposed alpha-helix. These flank a site that allows phosphorylation by ERK, the functional outcome of which is orchestrated by the N-terminal UCR1/2 (upstream conserved region 1 and 2) modules.

• Houslay MD, et al. (2003) The role of ERK2 docking and phosphorylation of PDE4 cAMP phosphodiesterase isoforms in mediating cross-talk between the cAMP and ERK signalling pathways. Biochem Soc Trans. 31(Pt 6): 1186-90.
• Jivan A, et al. (2010) Reconstitution of the Nuclear Transport of the MAP Kinase ERK2. Methods Mol Biol. 661: 273-85.
• Yu CG, et al. (2010) Involvement of ERK2 in traumatic spinal cord injury. J Neurochem. 113(1): 131-42.
• Subramaniam S, et al. (2010) ERK and cell death: ERK1/2 in neuronal death. FEBS J. 277(1): 22-9.