TRAIL-R deficiency in mice enhances lymph node metastasis without affecting primary tumor development
J. Clin. Invest. Anne Grosse-Wilde, et al. 118:100 doi:10.1172/JCI33061 [Go to this article.]

Figure 1
Generation of Trail-r^–/– mice. (A) Strategy to target exon 2 of the Trail-r gene. (i) Functional protein domains of TRAIL-R encoded by the Trail-r WT allele (ii). SP, signal peptide; CRD, cysteine-rich domain; TM, transmembrane domain; DD, death domain. Locations of the external (ext) 3′ and 5′ and the internal (int) probes and of genotyping primers mTR-a (a), mTR-b (b), and mTR-d (d) are indicated. (iii) Targeting construct. Open triangle, FRT sites; gray triangles, loxP sites; tkneo, selection cassette; DTA, diphtheria-toxin A-cassette. (iv) Null allele. (B) Southern blot analysis of targeted G418-selected ES cell clone after correct homologous recombination. (C) Constitutive deletion of exon 2 of Trail-r in different tissues. PCR analysis of genomic DNA of tail, lymph node, kidney, lung, heart, and brain of Trail-r^–/–, Trail-r+^/–, and Trail-r^+/+ mice using primers a, b, and d is shown. The primers a and b amplified a 300-bp fragment of the Trail-r WT allele, and primers a and d amplified a 235-bp fragment of the Trail-r–null allele.