Structure, expression profile, and chromosomal location of a mouse
gene homologous to human DNA-PK
interacting protein (KIP) gene
Genome Research Group, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan
Division of Biology and Oncology, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan
Biotechnology and Medical Engineering Field, Aisin Cosmos R&D Co., Ltd., 5-2-11 Sotokanda, Chiyoda-ku, Tokyo 101-0021, Japan
Laboratory of Animal Genetics, School of Bioagricultural Sciences, Nagoya University, Furocho, Chikusa-ku, Nagoya 464-8601, Japan
Received: 19 August 1998 / Accepted: 29 October 1998
The deduced structure of mouse Kip showing the striking homol-
ogy to human DNA-PK
interacting protein KIP is reported. A
cDNA for the protein was isolated from a mouse fetal kidney
cDNA library, and an open reading frame (ORF) of 191 amino
acids was identified. The predicted mouse Kip rotein was 95%
identical to the human counterpart. Northern blot analysis indi-
cated that mouse Kip mRNA is ubiquitously expressed in adult
tissues as well as in embryos. The gene was localized to mouse
Chromosome (Chr) 7D3 by fluorescence in situ hybridization.
DNA-dependent protein kinase (DNA-PK) is a nuclear protein
serine/threonine kinase present in a wide variety of vertebrate spe-
cies. DNA-PK has a role in the repair of double-strand DNA
breaks and in the related process of V(D)J recombination during
lymphoid development (Jackson and Jeggo 1995; Jeggo et al.
1995). DNA-PK consists of three components: one is a large poly-
peptide corresponding to the catalytic subunit p450 (DNA-PK
the other two components are DNA binding proteins called Ku (ku
p70 and ku p86/XRCC5; Anderson and Carter 1996; Jackson
1996; Lees-Miller 1996). The catalytic subunit DNA-PK
to the phosphatidylinositol-3 kinase family (Hartley et al. 1995)
that includes ATM (Savitsky et al. 1995), FRAP (Brown et al.
1994; Sabatini et al. 1994), and ATR/FRP1 (Cimprich et al. 1996;
Enoch and Norbury 1995).
The severe combined immune deficiency (SCID) mouse indi-
cated that the product of the scid gene plays a critical role in both
V(D)J recombination and DNA double-strand break repair (Blunt
et al. 1995; Kirchgessner et al. 1995; Peterson et al. 1995). A
nonsense mutation in the DNA-PK
at the C-terminal end in the
SCID mouse was demonstrated (Blunt et al. 1996; Danska et al.
1996) and finally proved to be the only mutation in the protein
(Araki et al. 1997), showing DNA-PK
gene is the scid gene.
Correspondence to: T. Saito
The nucleotide sequence data reported in this paper have been submitted to
DDBJ/EMBL/GenBank databases under the accession number AB006463.
Fig. 1. Nucleotide sequence and deduced amino acid sequence of mouse
Kip cDNA. The predicted amino acids are showed along the open reading
frame indicated with uppercases. The amino acid sequence of human KIP
is also aligned under the mouse sequence for comparison. Only the differ-
ent residues between the species are indicated, and the same residues are
represented with dots. An asterisk denotes the termination codon. The
potential calcium-binding domains known as EF-hand are underlined. The
nucleotide sequence reported here will appear in DDBJ, EMBL, and Gen-
Bank nucleotide sequence databases under accession number AB006463.
Fig. 2. Northern blot analysis of mouse Kip mRNA. Northern blot filters
containing adult mouse tissues and mouse embryo poly (A)+ RNAs (2
g/lane) were purchased from Clontech Laboratories, Inc. (Palo Alto, CA,
USA), and hybridization and washing were performed following the manu-
facturer’s instruction. The 0.7-kb cDNA fragment containing the entire
open reading frame was labeled with [a-
P] dCTP and used as a hybrid-
ization probe. Size markers (left) are in kilobases.
Mammalian Genome 10, 315–317 (1999).
© Springer-Verlag New York Inc. 1999