IL-17RB Protein, Mouse (HEK293, Fc)

IL-17RB (Interleukin 17 receptor B), a protein encoded by the IL17RB gene, is a receptor for the pro-inflammatory cytokines IL17B and IL17E. IL-17RB expression is high in kidney, pancreas, liver, brain, and intestines. IL-17RB may play a role in hematopoietic cell differentiation and growth. IL-17RB is involved in inflammatory diseases and cancers^[1][2]. IL-17RB Protein, Mouse (HEK293, Fc) is produced in HEK293 cells with a C-Terminal Fc-tag. It consists of 286 amino acids (M1-G286).

IL-17RB (Interleukin 17 receptor B), a 47.9 kDa transmembrane protein (462 aa) that belongs to the IL-17 receptor family, and can be activated by IL-17B. It has been proved to be involved in inflammatory diseases and cancers. IL-17RB is expressed in various endocrine tissues and in epithelial cells in different organs such as kidney and liver and mucosal tissues^[1][2][3].
The amino acid sequence of human IL-17RB protein has low homology with mouse IL-17B protein.
IL-17RB has a SEFIR cytoplasmic domain implicated in homotypic dimerization and recruitment of signaling proteins (shared with IL-17RA) and a TRAF6-binding domain (not found in IL-17RA). IL-17B shares its receptor IL-17RB with IL-17E (also known as IL-25) that binds to the heterodimeric IL-17RA/IL-17RB complex. The binding affinity (KD) of IL-17B for IL-17RB is around 30-fold lower than that of IL-17E. It does not bind IL-17, IL-17C and IL-17F. Interleukin-17 (IL-17) plays a pivotal role in inflammatory diseases and cancers. IL-17 acts its role through IL-17 receptor (IL-17R). The IL-17R family are single transmembrane proteins that include the subtype receptors of IL-17RA to IL-17RE. Upon ligand binding, IL-17RB activates the canonical NK-κB pathway as well as ERK, JNK, and p38. Moreover, TRAF6 binds to IL-17RB independently of its ligand and participates in IL-17RB-dependent NF-κB activation^[1][2][3].
It is reported that IL-17RB expression is significantly increased in gastric cancer tissues. Moreover, overexpression of IL-17RB is strongly associated with metastasis and inversely correlates with progression-free survival in pancreatic cancer. IL-17RB can enhance thyroid cancer cell invasion and metastasis via ERK1/2 pathway-mediated MMP-9 expression^[1]. By using a rodent ortholog of IL-17BR as a probe, IL-17BR message was found to be drastically up-regulated during intestinal inflammation elicited by indomethacin treatment in rats^[2]. IL-17RB expression in human innate type 2 lymphocytes, natural killer T (NKT) cells, and Th2 cells suggests a potential role in immune cells^[3].

Mouse

HEK293

C-hFc

Q9JIP3-1 (R18-G286)

50905  [NCBI]

Approximately 56.8 kDa.

Greater than 85% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.

• [1]. Lei Ren, et al. IL-17RB enhances thyroid cancer cell invasion and metastasis via ERK1/2 pathway-mediated MMP-9 expression. Mol Immunol. 2017 Oct;90:126-135.  [Content Brief]

  [2]. Y Shi, et al. A novel cytokine receptor-ligand pair. Identification, molecular characterization, and in vivo immunomodulatory activity. J Biol Chem. 2000 Jun 23;275(25):19167-76.  [Content Brief]

  [3]. Jérémy Bastid, et al. The Emerging Role of the IL-17B/IL-17RB Pathway in Cancer. Front Immunol. 2020 Apr 21;11:718.  [Content Brief]