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Article

Segregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains.

G3 (Bethesda, Md.) - 17 Dec 2014

Shin Dai-Lun, Pandey Ashutosh K, Ziebarth Jesse Dylan, Mulligan Megan K, Williams Robert W, Geffers Robert, Hatesuer Bastian, Schughart Klaus, Wilk Esther

Abstract excerpt

Current model DBA/2J (D2J) mice lack CD94 expression due to a deletion spanning the last coding exon of the Klrd1 gene that occurred in the mid- to late 1980s. In contrast, DBA/2JRj (D2Rj) mice, crosses derived from DBA/2J before 1984, and C57BL/6J (B6) mice lack the deletion and have normal CD94...

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Identifiers

PMID: 25520036
DOI: 10.1534/g3.114.015164
PMCID: PMC4321031

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-25520036-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

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