Recombinant Mouse LRRTM3 Protein, CF

Recombinant Mouse LRRTM3 Protein, CF Summary

Product Specifications

Product Datasheets

Carrier Free

CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.

In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.

Background: LRRTM3

Leucine-rich repeat transmembrane neuronal 3 (LRRTM3) is a 68 kDa type I transmembrane protein that belongs to the LRRTM family, LRR superfamily of proteins (1). Mouse LRRTM3 is 582 amino acids (aa) in length with a 30 aa signal sequence, a 390 aa extracellular region, a 21 aa transmembrane region, and a 141 aa cytoplasmic domain. Within the extracellular region, there are ten LRRs flanked by cysteine-rich domains and one potential site for N‑linked glycosylation (1, 2). The cytoplasmic region contains several tyrosine, serine, and threonine residues that have potential to be phosphorylated and thus to be involved in signal transduction (1). There is also a conserved ECEV motif that interacts with PDZ proteins (1, 3). One isoform variant exists that shows an Ile514Val transition coupled to a deletion of aa 515 ‑ 582. Mature mouse LRRTM3 shares 98% aa sequence identity with mature human LRRTM3. All LRRTM proteins are expressed in the brain with varying profiles in other tissues (3). Strong LRRTM3 expression is present prenatally at 8.5 dpc in the neural progenitors of the anterior neural plate that will form the rostral neural tube (3). Expression is also seen in the region of the presomitic mesoderm/somite boundary plus the forebrain and developing eye (3). In the adult, LRRTM3 may be expressed both on neurons and placental trophoblasts. In neurons, it has been demonstrated to positively influenced by STOX1 and subsequently to induce BACE1 cleavage of APP, thus generating A beta PP beta production and a C99 fragment (2, 4).

Related Research Areas

• Activin Family
• APP Processing and Amyloid Plaque Formation
• Developmental Factors Implicated in Neurodegeneration