04-797
Anti-phospho-MAP Kinase 1/2 (Erk1/2)(Thr185/Tyr187) Antibody, clone AW39
clone Aw39, Upstate®, from rabbit
Synonym(s):
Mitogen-activated protein kinase, Extracellular signal-regulated kinase, protein tyrosine kinase ERK2
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
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General description
Erk (Extracellular signal-Related Kinase) is a family of two, highly homologous proteins denoted as Erk1 (p44, MAPK3) and Erk2 (p42, MAPK1) that both function in the same pathway. The two proteins are often referred to collectively as ERK1/2 or p44/p42 MAP kinase. The Erk pathway is considered the classical, canonical MAPK (Mitogen-Activated Protein Kinase) signaling pathway. It is an evolutionarily conserved pathway that controls and is a critical regulator the growth and survival through the promotion of cell proliferation and the prevention of apoptosis. Erk is involved in the control of many fundamental cellular processes including cell proliferation, survival, differentiation, apoptosis, motility and metabolism. Erk is activated by growth factor stimulation of receptor tyrosine kinases (RTKs) and/or integrin stimulation. This activates the Ras-Raf-MEK,-Erk pathway that results in MEK, a dual kinase (a Ser/Thr and a Tyr kinase), phosphorylation and activation of ERK1/2 (p44/044) on the TxY motif (Thr202/Tyr204 and Thr185/Tyr187 for Erk1 and Erk2, respectively).
Specificity
Predicted to cross-react with many species based on sequence homology.
Recognizes phosphorylated MAP Kinase 1 and 2 (Erk 1&2).
Immunogen
KLH-conjugated, synthetic peptide corresponding to amino acids surrounding the pTEpY motif of human phospho-MAP Kinase 1/2 (Erk1/2), in which the Thr and Tyr residues are phosphorylated. The immunizing sequence is highly conserved among species.
Application
Research Category
Signaling
Signaling
Research Sub Category
MAP Kinases
MAP Kinases
Western Blot Analysis:
A 1:2,000-1:8,000 dilution of this lot detected phospho-MAP Kinase 1/2 (Erk1/2) in RIPA lysates from NGF stimulated PC-12 cells (Figure A).
Beadlyte Phospho-Specificity Assay:
1:500-1:4,000 dilutions of a previous lot detected active but not unactive MAP Kinase/Erk2 conjugated to Luminex microspheres. (Figure B).
A 1:2,000-1:8,000 dilution of this lot detected phospho-MAP Kinase 1/2 (Erk1/2) in RIPA lysates from NGF stimulated PC-12 cells (Figure A).
Beadlyte Phospho-Specificity Assay:
1:500-1:4,000 dilutions of a previous lot detected active but not unactive MAP Kinase/Erk2 conjugated to Luminex microspheres. (Figure B).
Quality
Routinely evaluated by immunoblot on RIPA lysates from NGF stimulated PC-12 cells
Target description
MAPK1 (~44 kDa) and MAPK2 (~42 kDa).
Linkage
Replaces: 05-797
Physical form
Cultured supernantant in 0.05% sodium azide
Format: Purified
Storage and Stability
Maintain for 2 years at -20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
Analysis Note
Control
RIPA cell lysate from NGF stimulated PC-12 cells
RIPA cell lysate from NGF stimulated PC-12 cells
Other Notes
Concentration: Variable
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Sandra L Krueckl et al.
Cancer research, 64(23), 8620-8629 (2004-12-03)
Apoptosis and inhibition of mitosis are primary mechanisms mediating androgen ablation therapy-induced regression of prostate cancer (PCa). However, PCa readily becomes androgen independent, leading to fatal disease. Up-regulated growth and survival signaling is implicated in development of resistance to androgen
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