MAP2K7 Antibody (C-Term)
Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, E |
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Primary Accession | O14733 |
Reactivity | Rat |
Host | Rabbit |
Clonality | polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 47485 Da |
Gene ID | 5609 |
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Other Names | Dual specificity mitogen-activated protein kinase kinase 7, MAP kinase kinase 7, MAPKK 7, JNK-activating kinase 2, MAPK/ERK kinase 7, MEK 7, Stress-activated protein kinase kinase 4, SAPK kinase 4, SAPKK-4, SAPKK4, c-Jun N-terminal kinase kinase 2, JNK kinase 2, JNKK 2, MAP2K7, JNKK2, MEK7, MKK7, PRKMK7, SKK4 |
Target/Specificity | This MAP2K7 antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between 325-360 amino acids of human MAP2K7. |
Dilution | WB~~1:2000 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | MAP2K7 Antibody (C-Term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | MAP2K7 |
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Synonyms | JNKK2, MEK7, MKK7, PRKMK7, SKK4 |
Function | Dual specificity protein kinase which acts as an essential component of the MAP kinase signal transduction pathway. Essential component of the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. With MAP2K4/MKK4, is the one of the only known kinase to directly activate the stress-activated protein kinase/c-Jun N-terminal kinases MAPK8/JNK1, MAPK9/JNK2 and MAPK10/JNK3. MAP2K4/MKK4 and MAP2K7/MKK7 both activate the JNKs by phosphorylation, but they differ in their preference for the phosphorylation site in the Thr-Pro-Tyr motif. MAP2K4/MKK4 shows preference for phosphorylation of the Tyr residue and MAP2K7/MKK7 for the Thr residue. The monophosphorylation of JNKs on the Thr residue is sufficient to increase JNK activity indicating that MAP2K7/MKK7 is important to trigger JNK activity, while the additional phosphorylation of the Tyr residue by MAP2K4/MKK4 ensures optimal JNK activation. Has a specific role in JNK signal transduction pathway activated by pro-inflammatory cytokines. The MKK/JNK signaling pathway is also involved in mitochondrial death signaling pathway, including the release cytochrome c, leading to apoptosis. Part of a non-canonical MAPK signaling pathway, composed of the upstream MAP3K12 kinase and downstream MAP kinases MAPK1/ERK2 and MAPK3/ERK1, that enhances the AP-1-mediated transcription of APP in response to APOE (PubMed:28111074). |
Cellular Location | Nucleus. Cytoplasm. |
Tissue Location | Ubiquitous; with highest level of expression in skeletal muscle. Isoform 3 is found at low levels in placenta, fetal liver, and skeletal muscle. |
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Background
Dual specificity protein kinase which acts as an essential component of the MAP kinase signal transduction pathway. Essential component of the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. With MAP2K4/MKK4, is the one of the only known kinase to directly activate the stress-activated protein kinase/c-Jun N-terminal kinases MAPK8/JNK1, MAPK9/JNK2 and MAPK10/JNK3. MAP2K4/MKK4 and MAP2K7/MKK7 both activate the JNKs by phosphorylation, but they differ in their preference for the phosphorylation site in the Thr-Pro-Tyr motif. MAP2K4/MKK4 shows preference for phosphorylation of the Tyr residue and MAP2K7/MKK7 for the Thr residue. The monophosphorylation of JNKs on the Thr residue is sufficient to increase JNK activity indicating that MAP2K7/MKK7 is important to trigger JNK activity, while the additional phosphorylation of the Tyr residue by MAP2K4/MKK4 ensures optimal JNK activation. Has a specific role in JNK signal transduction pathway activated by proinflammatory cytokines. The MKK/JNK signaling pathway is also involved in mitochondrial death signaling pathway, including the release cytochrome c, leading to apoptosis.
References
Wu Z.,et al.Mol. Cell. Biol. 17:7407-7416(1997).
Lu X.,et al.J. Biol. Chem. 272:24751-24754(1997).
Foltz I.N.,et al.J. Biol. Chem. 273:9344-9351(1998).
Michael L.,et al.Biochem. Biophys. Res. Commun. 341:679-683(2006).
Yang J.,et al.Submitted (SEP-1997) to the EMBL/GenBank/DDBJ databases.
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