T-cell survival regulator LKLF is not involved in inappropriate apoptosis of diabetes-prone BBDP rat T cells.
Diabetes-prone BB (dpBB) rats develop autoimmune insulin-dependent diabetes mellitus (IDDM) at high frequency as a consequence of a defect in T cell development, caused by a mutation in a single gene locus on rat chromosome 4 (lyp) which has recently been identified as immune-associated nucleotide 4 (ian4). A phenotype similar to dpBB rat lymphopenia has recently been described in the mouse as the result of the targeted inactivation of the gene for the transcription factor LKLF (Lung Krüppel-like factor, KLF2) in the immune system. We cloned the LKLF gene of the rat and screened a panel of rat/hamster radiation hybrid cell lines to determine its chromosomal localization. We conclude that the LKLF gene is not defective in dpBB rats and that its expression is not compromised by the lyp mutation.
Diessenbacher
Philip
P
Institute of Immunology, University Hospital, D-20246 Hamburg, Germany.
Bartels
Katrin
K
Koch-Nolte
Friedrich
F
Haag
Friedrich
F
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002470:Cell Survival; D002874:Chromosome Mapping; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics* / Q000473:pathology; D005786:Gene Expression Regulation; D005819:Genetic Markers; D051381:Rats; D011913:Rats, Inbred BB; D013601:T-Lymphocytes / Q000166:cytology / Q000473:pathology / Q000502:physiology*; D016335:Zinc Fingers
D005819:Genetic Markers