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Recombinant Human CD300LB/LMIR5 (C-Fc) (PKSH033897)

All Size Price Qty
50μg $ 128.00
10μg $ 58.00
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For research use only.

Synonyms CD300LB, CD300b, CLM-7, CMRF35-A2, IREM-3, IREM3, TREM-5, TREM5
Species Human
Expression Host HEK293 Cells
Sequence Ile55-His187
Accession AAH28091.1
Calculated Molecular Weight 42.2 kDa
Observed Molecular Weight 50-60 kDa
Tag C-Fc
Bio-activity Not validated for activity
Purity > 95 % as determined by reducing SDS-PAGE.
Endotoxin < 1.0 EU per μg of the protein as determined by the LAL method.
Storage Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.
Shipping This product is provided as lyophilized powder which is shipped with ice packs.
Formulation Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.
Normally 5% - 8% trehalose, mannitol and 0.01% Tween 80 are added as protectants before lyophilization.
Please refer to the specific buffer information in the printed manual.
Reconstitution Please refer to the printed manual for detailed information.
Background CD300LB, also known as CD300b, LMIR5, CLM-7, and IREM-3, is a glycoprotein member of the immunoglobulin superfamily. LMIR5 is expressed on the surface of myeloid lineage cells. It forms noncovalent cis-homodimers and cis-heterodimers with other CD300 family proteins, and the composition of these dimers affects the cellular response. Antibody cross-linking of LMIR5 induces mast cell granule release and cytokine production as well as its tyrosine phosphorylation of LMIR5 (in human). LMIR5 interacts with TIM1 and TIM4 which regulate T cell activation and are themselves binding partners. TIM1 interactions with LMIR5 mediate mast cell activation and the accumulation of neutrophils at sites of TIM1 up regulation on damaged renal tubule epithelial cells. Acts as an activating immune receptor through its interaction with ITAM-bearing adapter TYROBP, and also independently by recruitment of GRB2.
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