Phospho-MEK1 (Ser298) Antibody (YA9822)
(Synonyms: MAP2K1; MEK1; PRKMK1; Dual specificity mitogen-activated protein kinase kinase 1; MAP kinase kinase 1; MAPKK 1; MKK1; ERK activator kinase 1; MAPK/ERK kinase 1; MEK 1)Based on 1 Customer Validation
Phospho-MEK1 (Ser298) Antibody (YA9822) is a Rabbit-derived and non-conjugated IgG Recombinant, Monoclonal antibody, targeting to Phospho-MEK1 (Ser298).
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, ICC/IF, IF-Tissue, IHC-P
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in TBS (pH7.4), 0.05% BSA, 40% Glycerol, 0.05% Sodium Azide.
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
IF-Tissue
IF-Tissue: Immunofluorescence-Tissue
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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|---|---|---|---|---|
| Dilution Ratio | 1:1000-2000 | 1:50-200 | 1:50-200 | 1:50-200 |
Product Details
Phospho-MEK1 (Ser298) Antibody (YA9822) is a Rabbit-derived and non-conjugated IgG Recombinant, Monoclonal antibody, targeting to Phospho-MEK1 (Ser298).
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Host Rabbit
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 45 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: 43 kDa
Synthetic phospho-peptide corresponding to residues surrounding Ser298 of Human MEK1aa 271-320 / 393.
Endogenous
affinity purified
Non-conjugated
Phosphorylated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in TBS (pH7.4), 0.05% BSA, 40% Glycerol, 0.05% Sodium Azide.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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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
MEK1 is a MAP kinase or ERK kinase that phosphorylates the ERK gene product and acts as an immediate upstream activator of ERK signaling[1][2]. Mechanistically, MEK1 and MEK2 phosphorylate and activate ERK1/ERK2, positioning MEK proteins as pathway gatekeepers in the RAS-RAF-MEK-ERK cascade[3][4]. This cascade regulates cell proliferation, differentiation, survival, invasion, and other ERK-dependent cellular responses[3][5]. In disease models, ERK pathway activation is prominent in cancers driven by receptor tyrosine kinase, RAS, BRAF, CRAF, MEK1, or MEK2 alterations, which promote growth factor-independent ERK1/2 activation[5]. Compared with MEK2, MEK1 shares the same ERK substrates, but Mek1- embryos die from placental defects whereas Mek2- mice survive, indicating isoform-related developmental differences and functional redundancy controlled by total MEK protein level[4]. Structurally, MEK1 and MEK2 are closely related dual-specificity tyrosine/threonine kinases with a hydrophobic allosteric pocket adjacent to the ATP-binding site[6][5]. For experimental applications, PD098059 selectively inhibited MEK without significant inhibition of MAPK itself, and allosteric MEK blockade suppressed colon tumor growth in vivo[7][8].
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Subcellular Localization
Cytoplasm, cytoskeleton, microtubule organizing center, centrosome; Cytoplasm, cytoskeleton, microtubule organizing center, spindle pole body; Cytoplasm; Nucleus; Membrane; Peripheral membrane protein
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Expression
Tissue_specificity:It is widely expressed, but present in extremely low concentrations in the brain. -
Isoforms & Post-Translational Modification
Q02750 has 2 isomers: Q02750-1: 43439 Da (predicted); Q02750-2: 40764 Da (predicted).
Phosphorylation at Ser-218 and Ser-222 by MAP kinase kinase kinases (BRAF or MEKK1) positively regulates kinase activity (PubMed:29433126, PubMed:8131746). Also phosphorylated at Thr-292 by MAPK1/ERK2 and at Ser-298 by PAK (PubMed:16129686). MAPK1/ERK2 phosphorylation of Thr-292 occurs in response to cellular adhesion and leads to inhibition of Ser-298 phosphorylation by PAK (PubMed:16129686). Autophosphorylated at Ser-218 and Ser-222, autophosphosphorylation is promoted by NEK10 following UV irradiation (PubMed:20956560);(Microbial infection) Acetylation by Yersinia YopJ prevents phosphorylation and activation, thus blocking the MAPK signaling pathway -
Subunit
Found in a complex with at least BRAF, HRAS, MAP2K1, MAPK3/ERK1 and RGS14 (By similarity). Forms a heterodimer with MAP2K2/MEK2 (By similarity). Forms heterodimers with KSR2 which further dimerize to form tetramers (By similarity). Interacts with KSR1 or KSR2 and BRAF; the interaction with KSR1 or KSR2 mediates KSR1-BRAF or KSR2-BRAF dimerization (PubMed:10409742, PubMed:29433126). Interacts with ARBB2, LAMTOR3 and RAF1 (By similarity). Interacts with MAPK1/ERK2 (PubMed:32721402). Interacts with MORG1 (By similarity). Interacts with PPARG (PubMed:17101779). Interacts with isoform 1 of VRK2 (PubMed:20679487). Interacts with SGK1 (PubMed:19447520). Interacts with BIRC6/bruce (PubMed:18329369). Interacts with KAT7; the interaction promotes KAT7 phosphorylation (By similarity). Interacts with RAF1 and NEK10; the interaction is required for ERK1/2-signaling pathway activation in response to UV irradiation (PubMed:20956560). Interacts with TRAF3IP3 (PubMed:26195727). Interacts with MOS (PubMed:34779126, PubMed:35670744)
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SwissProt ID
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Synonyms
MAP2K1; MEK1; PRKMK1; Dual specificity mitogen-activated protein kinase kinase 1; MAP kinase kinase 1; MAPKK 1; MKK1; ERK activator kinase 1; MAPK/ERK kinase 1; MEK 1
Documentation
References
[1]. Crews CM, et al. The primary structure of MEK, a protein kinase that phosphorylates the ERK gene product. Science. 1992 Oct 16;258(5081):478-80. [Content Brief]
[2]. Zheng CF, et al. Properties of MEKs, the kinases that phosphorylate and activate the extracellular signal-regulated kinases. J Biol Chem. 1993 Nov 15;268(32):23933-9. [Content Brief]
[3]. Shaul YD, et al. The MEK/ERK cascade: from signaling specificity to diverse functions. Biochim Biophys Acta. 2007 Aug;1773(8):1213-26. [Content Brief]
[4]. Aoidi R, et al. Functional redundancy of the kinases MEK1 and MEK2: Rescue of the Mek1 mutant phenotype by Mek2 knock-in reveals a protein threshold effect. Sci Signal. 2016 Jan 26;9(412):ra9. [Content Brief]
[5]. Caunt CJ, et al. MEK1 and MEK2 inhibitors and cancer therapy: the long and winding road. Nat Rev Cancer. 2015 Oct;15(10):577-92. [Content Brief]
[6]. Ohren JF, et al. Structures of human MAP kinase kinase 1 (MEK1) and MEK2 describe novel noncompetitive kinase inhibition. Nat Struct Mol Biol. 2004 Dec;11(12):1192-7. [Content Brief]
[7]. Dudley DT, et al. A synthetic inhibitor of the mitogen-activated protein kinase cascade. Proc Natl Acad Sci U S A. 1995 Aug 15;92(17):7686-9. [Content Brief]
[8]. Sebolt-Leopold JS, et al. Blockade of the MAP kinase pathway suppresses growth of colon tumors in vivo. Nat Med. 1999 Jul;5(7):810-6. [Content Brief]