MARK3 Antibody #9311
Filter:
- WB
- IP
Western blot analysis of extracts from various cell lines using MARK3 Antibody.
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 83 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Related Products
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
MARK3 Antibody detects endogenous levels of total MARK3 protein. No cross-reactivity is observed with other family members.
Species Reactivity:
Human, Mouse, Rat
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Monkey, Bovine, Dog
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide surrounding Asn500 of human MARK3. Antibodies were purified by protein A and peptide affinity chromatography.
Background
Microtubule associated proteins regulate the stability of microtubules and control processes such as cell polarity/differentiation, neurite outgrowth, cell division and organelle trafficking (1). The MARK (MAP/microtubule affinity-regulating kinases) family (MARK1-4) of serine/threonine kinases was identified based on their ability to phosphorylate microtubule-associated proteins (MAPs) including tau, MAP2 and MAP4 (2-6). MARK proteins phosphorylate MAPs within their microtubule binding domains, causing dissociation of MAPs from microtubules and increased microtubule dynamics (2-4). In the case of tau, phosphorylation has been hypothesized to contribute to the formation of neurofibrillary tangles observed in Alzheimer's disease. Overexpression of MARK leads to hyperphosphorylation of MAPs, morphological changes and cell death (4). The tumor suppressor kinase LKB1 phosphorylates MARK and the closely related AMP-kinases within their T-loops, leading to increased activity (7).
MARK3 is an ubiquitously expressed member of the MARK/EMK/Par-1 family that was identified as Cdc25C-associated protein kinase (C-TAK1) based on its association and ability to phosphorylate Cdc25C (8). MARK3 substrates include Cdc25C phosphatase, MAPK scaffold kinase suppressor of Ras1 (KSR1) (9), protein-tyrosine phosphatase H1 (PTPH1) (10), plakophilin 2 (PKP2) (11), and histone deacetylases (HDACs) (12). MARK3 phosphorylates Cdc25C on serine 216 in response to DNA damage which allows for the preferential binding of 14-3-3 proteins that control entry into mitosis (8). MARK3 has also been shown to phosphorylate HDAC7 on one of its 14-3-3 binding sites that effects both the subcellular localization and repressive function of the HDAC (12).
MARK3 is an ubiquitously expressed member of the MARK/EMK/Par-1 family that was identified as Cdc25C-associated protein kinase (C-TAK1) based on its association and ability to phosphorylate Cdc25C (8). MARK3 substrates include Cdc25C phosphatase, MAPK scaffold kinase suppressor of Ras1 (KSR1) (9), protein-tyrosine phosphatase H1 (PTPH1) (10), plakophilin 2 (PKP2) (11), and histone deacetylases (HDACs) (12). MARK3 phosphorylates Cdc25C on serine 216 in response to DNA damage which allows for the preferential binding of 14-3-3 proteins that control entry into mitosis (8). MARK3 has also been shown to phosphorylate HDAC7 on one of its 14-3-3 binding sites that effects both the subcellular localization and repressive function of the HDAC (12).
- Drubin, D.G. and Nelson, W.J. (1996) Cell 84, 335-44.
- Illenberger, S. et al. (1996) J Biol Chem 271, 10834-43.
- Drewes, G. et al. (1995) J Biol Chem 270, 7679-88.
- Drewes, G. et al. (1997) Cell 89, 297-308.
- Kato, T. et al. (2001) Neoplasia 3, 4-9.
- Trinczek, B. et al. (2004) J Biol Chem 279, 5915-23.
- Lizcano, J.M. et al. (2004) EMBO J 23, 833-43.
- Peng, C.Y. et al. (1998) Cell Growth Differ. 9, 197-208.
- Müller, J. et al. (2001) Mol. Cell 8, 983-993.
- Zhang, S.H. et al. (1997) J. Biol. Chem. 272, 27281-27287.
- Müller, J. et al. (2003) EMBO J. 22, 4431-4442.
- Dequiedt, F. et al. (2006) Mol. Cell Biol. 26, 7086-7102.
Pathways
Explore pathways related to this product.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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