ERK1/2 Products

Antibodies
ERK1/2 Antibody
ERK1/2 Antibody
NB110-96887
Species: Hu, Mu, Rt
Applications: WB, Flow, ICC/IF, IHC, IHC-P
Host: Rabbit Polyclonal
ERK1/2 Antibody
ERK1/2 Antibody
NBP2-12728
Species: Hu, Mu, Rt, Ch
Applications: WB, Flow, ICC/IF, IHC, IHC-P
Host: Rabbit Polyclonal
ERK1/2 Antibody (B20-U)
ERK1/2 Antibody (B20-U)
NBP1-30128
Species: Hu, Mu, Rt, Rb
Applications: WB, ELISA, IHC, IHC-Fr, IHC-P, IP
Host: Rabbit Monoclonal
ELISA Kits
Human ERK1/2 [p Tyr204, p Thr ...
Human ERK1/2 [p Tyr204, p Thr202, ...
KA2164
Species: Hu
Human ERK1/2 [p Tyr187, p Thr ...
Human ERK1/2 [p Tyr187, p Thr202, ...
KA2163
Species: Hu
Proteins
Recombinant Human ERK1/2 Prot ...
Recombinant Human ERK1/2 Protein
P4688
Species: Hu
Applications: Func, PAGE

Description

The extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2), also called p44 and p42 MAP kinases, are members of the Mitogen Activated Protein Kinase (MAPK) family of proteins found in all eukaryotes. Because the 44 kDa ERK1 and the 42 kDa ERK2 are highly homologous and both function in the same protein kinase cascade, the two proteins are often referred to collectively as ERK1/2 or p44/p42 MAP kinase (1). They are both located in the cytosol and mitochondria (2). While the role of cytosol ERK1/2 is well studied and involved in multiple cellular functions (2), the role of mitochondrial ERK1/2 remains poorly understood. Both ERK 1 and 2 are activated by MEK1 or MEK2, by dual phosphorylation of a threonine and tyrosine residue in the activation loop (TEY motif) (1, 3). Either phosphorylation alone can induce an electrophoretic mobility shift, but both are required for activation of the kinase. This dual phosphorylation is efficiently detected by phosphorylation state-specific antibody directed to the pTEpY motif. Once activated, MAP kinases phosphorylate a broad spectrum of substrates, including cytoskeletal proteins, translation regulators, transcription factors, and the Rsk family of protein kinases (4). ERK1/2 activation is generally thought to confer a survival advantage to cells (5); however there is increasing evidence that suggests that the activation of ERK1/2 also contributes to cell death under certain conditions (5). ERK1/2 also is activated in neuronal and renal epithelial cells upon exposure to oxidative stress and toxicants or deprivation of growth factors, and inhibition of the ERK pathway blocks apoptosis (5).

Bioinformatics

Entrez Human
Human
Mouse
Rat
Uniprot Human
Human
Rat
Product By Gene ID 5595
Alternate Names
  • EC 2.7.11
  • MAPK 3
  • extracellular signal-related kinase 1
  • MAPK 1
  • P44MAPK
  • MAP kinase isoform p44
  • P44ERK1
  • MAP kinase 3
  • MAP kinase 1
  • ERT2
  • MGC20180
  • ERK-1
  • HUMKER1A
  • Mitogen-activated protein kinase 1
  • HS44KDAP
  • Microtubule-associated protein 2 kinase
  • p44mapk
  • Insulin-stimulated MAP2 kinase
  • p44erk1
  • Extracellular signal-regulated kinase 1
  • PRKM3EC 2.7.11.24
  • ERK1p44-MAPK
  • p44-ERK1
  • mitogen-activated protein kinase 3

Research Areas for ERK1/2

Find related products by research area and learn more about each of the different research areas below.

Angiogenesis
Apoptosis
Breast Cancer
Cancer
Caspases
Cell Cycle and Replication
Diabetes Research
Hypoxia
MAP Kinase Signaling
mTOR Pathway
Phospho-Specific
Protein Kinase
Signal Transduction

PTMs for ERK1/2

Learn more about PTMs related to ERK1/2.

Phosphorylation
Methylation
Cleavage
Acetylation
Dephosphorylation

Bioinformatics Tool for ERK1/2

Discover related pathways, diseases and genes to ERK1/2. Need help? Read the Bioinformatics Tool Guide for instructions on using this tool.
 
Vizit™, under license from BioVista Inc.

Related ERK1/2 Blog Posts

Check out the latest blog posts on ERK1/2.
SUCNR1/GPR91 - a potential role in renovascular hypertension
SUCNR1 is the cognate receptor for the Kreb's citric acid cycle intermediate succinate. It is of interest to scientists because it is involved in not only energy metabolism but possibly also in renovascular hypertension, a condition linked to diabe...    Read more.
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