Measured by the ability of the immobilized protein to support the adhesion of MS1 mouse pancreatic islet endothelial cells. When cells are added to mouse KIRREL3 coated plates (15 μg/mL, 100 μL/well), > 40% will adhere specifically after 90 minutes at 37 ℃.

KIRREL3 Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 57.5 kDa and the accession number is Q8BR86-1.

Mouse

HEK293 Cells

SST4,NEPH2,mKIAA1867,kin of IRRE like 3 (Drosophila),2900036G11Rik,1500010O20Rik

A DNA sequence encoding the mouse KIRREL3 (Q8BR86-1) extracellular domain (Met 1-Ala 535) was expressed, with a C-terminal polyhistidine tag. Predicted N terminal: Leu 22

> 96 % as determined by SDS-PAGE

A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.

It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.

Kin of IRRE-like protein 3 (KIRREL3) also known as nin of irregular chiasm-like protein 3 or nephrin-like protein 2 (NEPH2) is a member of the nephrin-like protein family of transmembrane proteins, which includes NEPH1 (KIRREL) and NEPH3 (KIRREL2). KIRREL3/NEPH2 is expressed in the fetal and adult brain, and also in podocytes of kidney glomeruli. The cytoplasmic domains of KIRREL3/NEPH2 interact with the C-terminus of podocin, also expressed in the podocytes, cells involved in ensuring size- and charge-selective ultrafiltration. Mutations in KIRREL3/NEPH2 are associated with mental retardation autosomal dominant type 4. KIRREL3/NEPH2 expression is turned on in migrating Nucleogenesis of the pontine nucleus (PN) neurons only after they enter the presumptive nuclear region. KIRREL3/NEPH2 knockdown disrupted the nuclear organization of PN presumably by changing the migratory behavior of PN neurons inside the nuclear region. Moreover, overexpression of the cytoplasmic region of KIRREL3, which can sequester intracellular signaling of endogenous KIRREL3, resulted in similar phenotypes. Overall, these results suggest KIRREL3 is involved in the Nucleogenesis of the PN through the control of neuronal migration inside the nucleus.