Alternative titles; symbols
HGNC Approved Gene Symbol: RETNLB
Cytogenetic location: 3q13.13 Genomic coordinates (GRCh38) : 3:108,755,638-108,757,410 (from NCBI)
Holcomb et al. (2000) identified 2 mouse and 2 human cDNAs showing homology to mouse Fizz1 (Retnla), a cysteine-rich secreted protein associated with pulmonary inflammation: FIZZ2 (which the authors incorrectly labeled FIZZ1) and FIZZ3 (RETN; 605565). The 111-amino acid FIZZ2 protein, which shows 59% sequence identity to mouse Fizz2 and 47% identity to human FIZZ3, shares an N-terminal signal peptide and a C-terminal stretch of 10 cysteine residues with identical spacing with other FIZZ family members. Strong expression of mouse Fizz2 mRNA was found in the adult colon in the mucosal crypt epithelial cells.
Gross (2014) mapped the RETNLB gene to chromosome 3q13.13 based on an alignment of the RETNLB sequence (GenBank AF323084) with the genomic sequence (GRCh37).
Rajala et al. (2003) found that an infusion of either resistin or RELMB in rats rapidly induced severe hepatic but not peripheral insulin resistance. Increases in circulating resistin or RELMB levels markedly stimulated hepatic glucose production despite the presence of fixed physiologic insulin levels. This enhanced rate of glucose output was due to increased flux through glucose-6-phosphatase. The results supported the notion that a novel family of fat- and gut-derived circulating proteins modulates hepatic insulin action.
McVay et al. (2006) found that disrupting the Relmb gene in mice reduced the severity of colitis induced by challenge with dextran sodium sulfate (DSS) in water without altering colonic epithelial proliferation or barrier function. Recombinant Relmb activated macrophages and Tnf (191160) production in vitro and in vivo. McVay et al. (2006) proposed that loss of epithelial barrier function by DSS results in activation of the immune response by RELMB in the lumen, and that RELMB is a link among goblet cells, commensal bacteria, and the pathogenesis of inflammatory bowel disease (see IBD1; 266600).
Gross, M. B. Personal Communication. Baltimore, Md. 5/21/2014.
Holcomb, I. N., Kabakoff, R. C., Chan, B., Baker, T. W., Gurney, A., Henzel, W., Nelson, C., Lowman, H. B., Wright, B. D., Skelton, N. J., Frantz, G. D., Tumas, D. B., Peale, F. V., Jr., Shelton, D. L., Hebert, C. C. FIZZ1, a novel cysteine-rich secreted protein associated with pulmonary inflammation, defines a new gene family. EMBO J. 19: 4046-4055, 2000. [PubMed: 10921885] [Full Text: https://doi.org/10.1093/emboj/19.15.4046]
McVay, L. D., Keilbaugh, S. A., Wong, T. M. H., Kierstein, S., Shin, M. E., Lehrke, M., Lefterova, M. I., Shifflett, D. E., Barnes, S. L., Cominelli, F., Cohn, S. M., Hecht, G., Lazar, M. A., Haczku, A., Wu, G. D. Absence of bacterially induced RELM-beta reduces injury in the dextran sodium sulfate model of colitis. J. Clin. Invest. 116: 2914-2923, 2006. [PubMed: 17024245] [Full Text: https://doi.org/10.1172/JCI28121]
Rajala, M. W., Obici, S., Scherer, P. E., Rossetti, L. Adipose-derived resistin and gut-derived resistin-like molecule-beta selectively impair insulin action on glucose production. J. Clin. Invest. 111: 225-230, 2003. [PubMed: 12531878] [Full Text: https://doi.org/10.1172/JCI16521]