Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 1999 Nov 15;190(10):1541–1548. doi: 10.1084/jem.190.10.1541

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 1999 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

PMC Copyright notice

Targeted disruption of the mouse T1/ST2 gene. (A) Targeting vector and restriction map of the T1/ST2 locus. The restriction map of the wild-type allele, targeting vector, and mutated allele is shown. Open and filled boxes denote the noncoding and coding exons, respectively. The orientation of the neomycin resistance gene (neo) and the herpes simplex virus–thymidine kinase gene (HSV-TK) are indicated by the arrow. E, EcoRI; B, BamHI. (B) Southern blot analysis of offspring from the heterozygote intercrosses. Genomic DNA was extracted from mouse tails, digested with BamHI, electrophoresed, and hybridized with the probe as shown in A. The approximate size of the wild-type band is 6.8 kbp, and the mutated band is 2.2 kbp. +/+, wild-type; +/−, heterozygous mutant; −/−, homozygous mutant. (C) RT-PCR analysis of T1/ST2 mRNA. Total RNA was isolated from the bone marrow cells. PCR analysis was performed using specific primers for T1/ST2 or for β-actin (reference 38). (D) Expression of T1/ST2 on BMCMCs. BMCMCs were triple stained with FITC–anti-T1/ST2 Ab, PE–anti–c-Kit Ab, IgE/biotin–anti-IgE Ab/Streptavidin–Cy-Chrome. T1/ST2 expression was analyzed in histogram mode by gating on the IgE⁺c-Kit⁺ double positive population which was >99% of the cells analyzed.

Targeted disruption of the mouse T1/ST2 gene. (A) Targeting vector and restriction map of the T1/ST2 locus. The restriction map of the wild-type allele, targeting vector, and mutated allele is shown. Open and filled boxes denote the noncoding and coding exons, respectively. The orientation of the neomycin resistance gene (neo) and the herpes simplex virus–thymidine kinase gene (HSV-TK) are indicated by the arrow. E, EcoRI; B, BamHI. (B) Southern blot analysis of offspring from the heterozygote intercrosses. Genomic DNA was extracted from mouse tails, digested with BamHI, electrophoresed, and hybridized with the probe as shown in A. The approximate size of the wild-type band is 6.8 kbp, and the mutated band is 2.2 kbp. +/+, wild-type; +/−, heterozygous mutant; −/−, homozygous mutant. (C) RT-PCR analysis of T1/ST2 mRNA. Total RNA was isolated from the bone marrow cells. PCR analysis was performed using specific primers for T1/ST2 or for β-actin (reference 38). (D) Expression of T1/ST2 on BMCMCs. BMCMCs were triple stained with FITC–anti-T1/ST2 Ab, PE–anti–c-Kit Ab, IgE/biotin–anti-IgE Ab/Streptavidin–Cy-Chrome. T1/ST2 expression was analyzed in histogram mode by gating on the IgE⁺c-Kit⁺ double positive population which was >99% of the cells analyzed.