Not exact matches
The resulting
cells mimicked the genetic
mutation seen in actual Werner syndrome patients, so the
cells began to age more rapidly
than normal.
Test tube experiments showed that white blood
cells with the
mutation responded more strongly to Il - 4
than did
normal cells.
Since genes in our chromosomes are very, very much better protected from
mutations than the mitochondrial DNA is, we can rely on the chromosomal copies carrying on working in very nearly all our
cells for much longer
than a currently
normal lifetime.
The
mutations that cause the disease make a protein called PABPN1 longer and stickier
than normal, and the mutated protein appears to form clumps in muscle
cells.