ERK2 Antibody (YA3933)(PBS only)
(Synonyms: ERK; p38; p40; p41; ERT1; MAPK2; PRKM1; P42MAPK; p41mapk; MAPK1)ERK2 Antibody (YA3933) is a Mouse-derived and non-conjugated IgG2a monoclonal antibody, targeting to ERK2.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, IHC-P, ICC/IF, ELISA
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Reactivity :
Human, Mouse, Monkey
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Formulation:
Supplied in PBS, pH 7.4.
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|---|
| Dilution Ratio | 1:500-1:2000 | 1:200-1:1000 | 1:200-1:1000 | 1:10000 |
Product Details
ERK2 Antibody (YA3933) is a Mouse-derived and non-conjugated IgG2a monoclonal antibody, targeting to ERK2.
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Host Mouse
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Species ReactivityHuman, Mouse, Monkey
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Observed Molecular WeightObserved band size: 41 kDaNote: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 41 kDa
Purified recombinant fragment of human ERK2 aa 219-358.
affinity purified.
Non-conjugated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS, pH 7.4.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
ERK2 (MAPK1) is a core effector kinase of the Ras/Raf/MEK/ERK signaling cascade and functions as an integration point for extracellular signals that regulate cell proliferation, differentiation, survival, transcriptional programs, and development[1][2]. Mechanistically, ERK2 is activated through MEK-dependent phosphorylation and subsequently phosphorylates numerous substrates across cellular compartments, linking growth factor stimulation to broad biological responses[3]. Because ERK signaling controls fundamental cellular processes, dysregulation of the pathway is associated with multiple pathological conditions, particularly tumorigenesis, and aberrant ERK pathway activity is observed in a substantial proportion of human cancers[4]. In experimental systems, genetic disruption studies demonstrate that ERK2 is essential for normal mammalian development, as loss of ERK2 causes embryonic lethality, highlighting the critical requirement for adequate ERK signaling output[3]. Compared with the closely related isoform ERK1 (MAPK3), ERK2 shares highly conserved activation mechanisms, substrate recognition properties, and signaling functions, and many studies support the view that biological outcomes are largely determined by total ERK activity rather than strict isoform-specific functions[3]. For experimental applications, ERK pathway inhibitors targeting RAF, MEK, or ERK have been extensively developed and are widely used to investigate ERK-dependent signaling networks, disease mechanisms, therapeutic resistance, and pathway regulation in cancer models[4][5].
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Subcellular Localization
Cytoplasm, cytoskeleton, spindle; Nucleus; Cytoplasm, cytoskeleton, microtubule organizing center, centrosome; Cytoplasm; Membrane, caveola; Cell junction, focal adhesion
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Isoforms & Post-Translational Modification
P28482 has 2 isomers: P28482-1: 41390 Da (predicted); P28482-2: 36432 Da (predicted).
Phosphorylated upon KIT and FLT3 signaling (By similarity). Dually phosphorylated on Thr-185 and Tyr-187, which activates the enzyme. Undergoes regulatory phosphorylation on additional residues such as Ser-246 and Ser-248 in the kinase insert domain (KID) These phosphorylations, which are probably mediated by more than one kinase, are important for binding of MAPK1/ERK2 to importin-7 (IPO7) and its nuclear translocation. In addition, autophosphorylation of Thr-190 was shown to affect the subcellular localization of MAPK1/ERK2 as well. Ligand-activated ALK induces tyrosine phosphorylation. Dephosphorylated by PTPRJ at Tyr-187. Phosphorylation on Ser-29 by SGK1 results in its activation by enhancing its interaction with MAP2K1/MEK1 and MAP2K2/MEK2. DUSP3 and DUSP6 dephosphorylate specifically MAPK1/ERK2 and MAPK3/ERK1 whereas DUSP9 dephosphorylates a broader range of MAPKs. Dephosphorylated by DUSP1 and DUSP2 at Thr-185 and Tyr-187 (By similarity) (PubMed:16288922);ISGylated;Ubiquitinated by TRIM15 via 'Lys-63'-linked ubiquitination; leading to activation. Deubiquitinated by CYLD -
Subunit
Binds both upstream activators and downstream substrates in multimolecular complexes. This interaction inhibits its tyrosine-kinase activity. Interacts with ADAM15, ARHGEF2, ARRB2, DAPK1 (via death domain), HSF4, IER3, IPO7, NISCH, SGK1, and isoform 1 of NEK2. Interacts (via phosphorylated form) with TPR (via C-terminal region and phosphorylated form); the interaction requires dimerization of MAPK1/ERK2 and increases following EGF stimulation (PubMed:18794356). Interacts with MAP2K1 (PubMed:32721402). Interacts with DUSP6 (PubMed:32721402, PubMed:9596579). Interacts (phosphorylated form) with CAV2 ('Tyr-19'-phosphorylated form); the interaction, promoted by insulin, leads to nuclear location and MAPK1 activation. Interacts with MORG1, PEA15 and MKNK2 (By similarity). MKNK2 isoform 1 binding prevents from dephosphorylation and inactivation (By similarity). Interacts with DCC (By similarity). The phosphorylated form interacts with PML (isoform PML-4). Interacts with STYX. Interacts with CDK2AP2. Interacts with CAVIN4 (By similarity). Interacts with DUSP7; the interaction enhances DUSP7 phosphatase activity (PubMed:9788880). Interacts with GIT1; this interaction is necessary for MAPK1 localization to focal adhesions (By similarity). Interacts with ZNF263 (PubMed:32051553). Interacts with phosphoglycerate kinase PGK1; the interaction is direct, occurs under hypoxic conditions, and promotes interaction between PGK1 and PIN1 (PubMed:26942675)
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SwissProt ID
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Synonyms
ERK; p38; p40; p41; ERT1; MAPK2; PRKM1; P42MAPK; p41mapk; MAPK1
Documentation
References
[1]. Mitogen Activated Protein Kinase 1. Sciencedirect topic.
[2]. Wikipedia.
[3]. Buscà R, et al. ERK1 and ERK2 Map Kinases: Specific Roles or Functional Redundancy? Front Cell Dev Biol. 2016 Jun 8;4:53. [Content Brief]
[4]. Timofeev O, et al. ERK pathway agonism for cancer therapy: evidence, insights, and a target discovery framework. NPJ Precis Oncol. 2024 Mar 14;8(1):70. [Content Brief]
[5]. Sah VK, et al. Advances in ERK1/2 inhibition: a medicinal chemistry perspective on structure and regulation. J Enzyme Inhib Med Chem. 2025 Dec;40(1):2555510. [Content Brief]