Mouse MERTK / MER Protein (GST Tag)

Produkt-Information von MERTK / MER Protein

QC Testing von MERTK / MER Protein

Purity	> 96 % as determined by SDS-PAGE	SDS-PAGE: MERTK / MER protein
Endotoxin	< 1.0 EU per μg of the protein as determined by the LAL method
Stability	Samples are stable for up to twelve months from date of receipt at -70℃
Predicted N terminal	Met
Molecular Mass	The recombinant mouse MERTK/GST chimera consists of 532 amino acids and has a calculated molecular mass of 61.7 kDa. The recombinant protein migrates as an approximately 58 kDa band in SDS-PAGE under reducing conditions.
Formulation	Lyophilized from a 0.2μm filtered solution of 20mM Tris,500mM NaCl,pH 7.4, 10%gly. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.

Usage Guide von MERTK / MER Protein

Verwandte Produkte & Themen von MERTK / MER Protein

Enzyme>>Protein Kinase>>Receptor Tyrosine Kinase>>MERTK/Mer

Signal Transduction>>Protein Kinase>>Receptor Tyrosine Kinase>>MERTK/Mer

Cancer>>Growth Factor & Receptor>>Receptor Tyrosine Kinase>>MERTK/Mer

Immunology>>Innate Immunity>>Natural Killer Cell (NK Cell)>>MERTK/Mer

Beschreibung von MERTK / MER Protein

Mouse Tyrosine-protein kinase Mer, also known as Proto-oncogene c-Mer, Receptor tyrosine kinase MerTK and MERTK, is a single-pass type I membrane protein which belongs to the protein kinase superfamily, Tyr protein kinase family and AXL/UFO subfamily. MERTK / MER contains two fibronectin type-III domains, two Ig-like C2-type (immunoglobulin-like) domains and one protein kinase domain. MERTK / MER is not expressed in normal B- and T-lymphocytes but is expressed in numerous neoplastic B- and T-cell lines. Defects in MERTK / MER are the cause of retinitis pigmentosa type 38 (RP38) which is a retinal dystrophy belonging to the group of pigmentary retinopathies. MERTK / MER retinitis pigmentosa is characterized by retinal pigment deposits visible on fundus examination and primary loss of rod photoreceptor cells followed by secondary loss of cone photoreceptors. Patients typically have night vision blindness and loss of midperipheral visual field. As their condition progresses, they lose their far peripheral visual field and eventually central vision as well.

References

1. Gal A. et al., 2000, Nat Genet. 26: 270-1.
2. Hillier LW. et al., 2005, Nature. 434:724-31.
3. Shimojima M. et al., 2006, J Virol. 80: 10109-162.
4. Oppermann FS. et al., 2009, Mol Cell Proteomics 8: 1751-642.

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