Absence of bacterially induced RELMβ reduces injury in the dextran sodium sulfate model of colitis
J. Clin. Invest. Laila D. McVay, et al. 116:2914 doi:10.1172/JCI28121 [Go to this article.]

Figure 1
Characterization of the RELMβ knockout. (A) Schematic diagram of the knockout strategy. The phosphoglycerate kinase–Neo (PGK-Neo) cassette was used to disrupt 2323 bp of the RELMβ gene locus, replacing the promoter region and the first 2 exons. (B) Genomic PCR using primers shown in A. Amplification of a 295-bp product by primers A and B indicate the wild-type allele (lower band), whereas a 413-bp product amplified by primers A and C indicates the null allele (upper band). LA, ladder. (C) Immunoblot of RELMβ using protein isolated from the stool of wild-type and RELMβ-knockout mice. (D) Quantification of mRNA expression for RELM isoforms and goblet cell–specific genes using RNA isolated from the proximal colon of RELMβ^+/+, RELMβ ^+/–, and RELMβ^–/– mice (n = 3; mean ± SD).