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. 2002 Jan;22(2):635–643. doi: 10.1128/MCB.22.2.635-643.2002

TABLE 2.

Molecular analysis of SCAs in MT-TGFα mice

Genotype LOHa
Methylation of p16Ink4a Expression
Other lesion Gene inactivationb
p53 Ink/Arf p16 p19 p53 p19Arf p16Ink4a p53
Ink/Arf−/−
    A1 Null Y Y N
    A2 Null Y Y N
    A3 Null Y Y N
    A4 Null Y Y N
Ink/Arf+/−
    B1 NDc ND Y Y N
    B2 + Y Y N
    B3 + Y Y N
    B4 + Y Y N
    B5 + Y Y N
    B6 + ND ND ND Y Y N
    B7 + ND ND ND Y Y N
Ink/Arf+/−p53+/−
    C1 + 1 1 Y
    C2 + 1 1 Y
    C3 + + Y Y Y
    C4 + + Y Y Y
    C5 + Y Y N
    C6 + + Y Y Y
    C7 d Splice defecte Y Y N
    C8 + + ND ND ND Y Y Y
Ink/Arf+/−p53−/−
    D1 Null + Y Y Y
    D2 Null + Y Y Y
p53+/−
    E1 + 1 1 Y
    E2 + + + N Y Y
    E3 Splice defecte Y Y N
p53−/−
    F1 Null + + N Y Y
    F2 Null 1 1 Y
    F3 Null + ND ND ND N Y Y
a

In the LOH column, − indicates lack of LOH in heterozygotes or absence of deletion in +/+ animals.

b

Y, yes; N, no; 1, no lesions of Ink4a/Arf locus detected, but lack of p19Arf overexpression despite p53 nullizygosity is consistent with a defective Ink4a/Arf locus.

c

ND, not done.

d

p16Ink4a protein is detected but migrates aberrantly at 9 to 11 kDa.

e

RT-PCR analysis detects transcripts from exon 1α and 1β but no products containing exons 2 and 3, suggesting defects in splicing or truncation of message.