GAS6 Blocking Peptide (Center)
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q14393 |
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Gene ID | 2621 |
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Other Names | Growth arrest-specific protein 6, GAS-6, AXL receptor tyrosine kinase ligand, GAS6, AXLLG |
Target/Specificity | The synthetic peptide sequence is selected from aa 262-275 of HUMAN GAS6 |
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 | GAS6 (HGNC:4168) |
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Synonyms | AXLLG |
Function | Ligand for tyrosine-protein kinase receptors AXL, TYRO3 and MER whose signaling is implicated in cell growth and survival, cell adhesion and cell migration. GAS6/AXL signaling plays a role in various processes such as endothelial cell survival during acidification by preventing apoptosis, optimal cytokine signaling during human natural killer cell development, hepatic regeneration, gonadotropin-releasing hormone neuron survival and migration, platelet activation, or regulation of thrombotic responses. |
Cellular Location | Secreted. |
Tissue Location | Plasma. Isoform 1 and isoform 2 are widely expressed, isoform 1 being expressed at higher levels than isoform 2 in most tissues. Isoform 2 is the predominant form in spleen |
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Provided below are standard protocols that you may find useful for product applications.
Background
Ligand for tyrosine-protein kinase receptors AXL, TYRO3 and MER whose signaling is implicated in cell growth and survival, cell adhesion and cell migration. GAS6/AXL signaling plays a role in various processes such as endothelial cell survival during acidification by preventing apoptosis, optimal cytokine signaling during human natural killer cell development, hepatic regeneration, gonadotropin-releasing hormone neuron survival and migration, platelet activation, or regulation of thrombotic responses.
References
Manfioletti G.,et al.Mol. Cell. Biol. 13:4976-4985(1993).
Munoz X.,et al.Hum. Mutat. 23:506-512(2004).
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Dunham A.,et al.Nature 428:522-528(2004).
Maree A.O.,et al.Submitted (OCT-2002) to the EMBL/GenBank/DDBJ databases.
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