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MEK1 Antibody (Center S217/221) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q02750 |
|---|---|
| Clone Names | 1112605 |
| Gene ID | 5604 |
|---|---|
| Other Names | 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, MAP2K1, MEK1, PRKMK1 |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | MAP2K1 (HGNC:6840) |
|---|---|
| Synonyms | MEK1, PRKMK1 |
| Function | Dual specificity protein kinase which acts as an essential component of the MAP kinase signal transduction pathway. Binding of extracellular ligands such as growth factors, cytokines and hormones to their cell-surface receptors activates RAS and this initiates RAF1 activation. RAF1 then further activates the dual-specificity protein kinases MAP2K1/MEK1 and MAP2K2/MEK2. Both MAP2K1/MEK1 and MAP2K2/MEK2 function specifically in the MAPK/ERK cascade, and catalyze the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in the extracellular signal-regulated kinases MAPK3/ERK1 and MAPK1/ERK2, leading to their activation and further transduction of the signal within the MAPK/ERK cascade. Activates BRAF in a KSR1 or KSR2-dependent manner; by binding to KSR1 or KSR2 releases the inhibitory intramolecular interaction between KSR1 or KSR2 protein kinase and N-terminal domains which promotes KSR1 or KSR2-BRAF dimerization and BRAF activation (PubMed:29433126). Depending on the cellular context, this pathway mediates diverse biological functions such as cell growth, adhesion, survival and differentiation, predominantly through the regulation of transcription, metabolism and cytoskeletal rearrangements. One target of the MAPK/ERK cascade is peroxisome proliferator-activated receptor gamma (PPARG), a nuclear receptor that promotes differentiation and apoptosis. MAP2K1/MEK1 has been shown to export PPARG from the nucleus. The MAPK/ERK cascade is also involved in the regulation of endosomal dynamics, including lysosome processing and endosome cycling through the perinuclear recycling compartment (PNRC), as well as in the fragmentation of the Golgi apparatus during mitosis. |
| Cellular Location | Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Cytoplasm, cytoskeleton, microtubule organizing center, spindle pole body. Cytoplasm. Nucleus Membrane; Peripheral membrane protein. Note=Localizes at centrosomes during prometaphase, midzone during anaphase and midbody during telophase/cytokinesis (PubMed:14737111). Membrane localization is probably regulated by its interaction with KSR1 (PubMed:10409742) |
| Tissue Location | Widely expressed, with extremely low levels in brain. |
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Provided below are standard protocols that you may find useful for product applications.
Background
The protein encoded by this gene is a member of the dualspecificity protein kinase family, which acts as amitogen-activated protein (MAP) kinase kinase. MAP kinases, alsoknown as extracellular signal-regulated kinases (ERKs), act as anintegration point for multiple biochemical signals. This proteinkinase lies upstream of MAP kinases and stimulates the enzymaticactivity of MAP kinases upon wide variety of extra- andintracellular signals. As an essential component of MAP kinasesignal transduction pathway, this kinase is involved in manycellular processes such as proliferation, differentiation,transcription regulation and development.
References
Liang, Q., et al. J. Immunol. 185(10):5704-5713(2010)Yokoyama, T., et al. Blood 116(15):2768-2775(2010)Klemke, M., et al. EMBO J. 29(17):2915-2929(2010)Shang, C., et al. Med. Sci. Monit. 16 (6), BR168-BR173 (2010) :Sasaki, H., et al. J Thorac Oncol 5(5):597-600(2010)
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