These are not genes but must have an important role because evolution has left them virtually unchanged in both
humans and mice since our evolutionary paths parted about 75 million years ago.
Not exact matches
Since then, they have studied this protein in flies,
mice, zebrafish
and humans.
A decade ago, he replicated the entire
human leukemia disease process by introducing oncogenes into normal
human blood cells, transplanting them into xenografts (special immune - deficient
mice that accept
human grafts)
and watching leukemia develop — a motherlode discovery that has guided leukemia research ever
since.
Since then, he
and his colleagues have modified the sequences of influenza viruses to bind to a natural microRNA expressed in
humans and mice, in essence developing a virus that's knocked down by the body's natural microRNA.
Since the current work was done in
mice, O'Leary
and Zembrzycki want to confirm the link in
humans by using brain scans to measure the natural variation in the neocortical areas
and search for potential links to disease.
MLVs so dependably cause cancer in lab - bred
mice — especially leukemia
and lymphoma — that a small fraternity of scientists at the NCI
and elsewhere has fruitfully studied these viruses
since the 1960s in an effort to understand how
human cancer begins.
Since CGP3466B has already been tested in phase II clinical trials to (unsuccessfully) treat Parkinson's disease
and ALS, it is known to be safe for
humans, but the researchers caution that many more years of studies are needed to definitively show whether it is effective for preventing cocaine damage, first in
mice, then in
humans.
Fittingly, most of these genes reside in ampliconic regions of the X
and appear to have been acquired independently during the 80 million years
since mouse and human diverged from a common ancestor.
To identify false - positives
and estimate the type 1 error rate, we used the genomic positions of a set of known lineage - specific repeat families in
human and mouse,
since lineage - specific repeat insertions should not overlap ancestral elements.
Collectively, these results demonstrate that it is possible to identify locations for the majority of DNA gain
and loss events
since human and mouse divergence.
This is likely true for two reasons; 1) there would not have been much time for a large number of chromosomal rearrangements to occur between these early ancestral
human and mouse genomes, 2)
and that
since divergence with the boreoeutherian ancestor the
human genome has undergone only a small number of chromosomal rearrangements meaning that many
human telomeric regions are ancestral [58, 73].
Since genetic loss of aP2 in
mouse models
and in
humans results in lowered risk of cardiometabolic disease, the molecule offers an exciting opportunity for new intervention strategies.
Since the majority of DNA loss occurred quite early after
human and mouse diverged, their karyotypes were likely similar to the current
human karyotype.
It should be noted, however, that while a study on senescent cell ablation in genetically normal
mice would provide at least some evidence on the effect of senescent cells (
and their ablation) on promoting cancer, even such a study would likely show less effect than could be anticipated in a large mammal model,
since even normally - aging
mice rarely suffer metastatic disease to the extent of aging
humans, as sheer primary tumor volume is generally sufficient to be fatal to
mice.
«Whether the results are relevant to
human Zika infection remains to be seen,
since Zika does not normally cause disease in
mice and an immune - suppressing antibody had to be administered for the Zika infection to progress.
The researchers, who previously identified NOTCH1 as a genetic culprit in
human CAVD, created
mice that had shorter telomeres
and were also missing one copy of the NOTCH1 gene,
since mutation of NOTCH1 alone failed to induce valve disease in
mice.
SSEA1 is a possible marker to detect ES cell - derived germ cells in monkeys,
since its expression is found not only in primordial germ cells in vivo [55] but also in ES cell - derived germ cells in vitro in
mice and humans [3], [56].
Since then, the Lodish lab has identified additional FATP genes, five in
mice and six in
humans.
The main hurdles: Other researchers must replicate the work
and confirm the vessel exists in
humans,
since the study primarily examined
mouse brains.