DNA content in
the mutant cells increased and some of the resulting cell sizes were larger.
Not exact matches
Dr. Llovet and colleagues demonstrated that the expression of
mutant IDH in the adult liver of genetically engineered mice impairs liver
cell development and liver regeneration — a process in which the liver responds to injury — and
increases the number of
cells to form a tumor.
Meanwhile, recent human studies indicate that aging is associated with an
increase in somatic mutations in the hematopoietic system, which gives rise to blood
cells; these mutations provide a competitive growth advantage to the
mutant hematopoietic
cells, allowing for their clonal expansion — a process that has been shown to be associated with a greater incidence of atherosclerosis, though specifically how remains unclear.
In the study, exosomes, which are generated by all
cells and are naturally present in blood, were modified as «iExosomes,» capable of delivering small RNA to specifically target
mutant KRAS, resulting in disease suppression and
increased overall survival in mouse models.
No one knows exactly how this works, but the
mutant worms — known as daf - 2
mutants —
increase production of enzymes that protect
cells from oxidants.
However, this is unlikely given that the frequency of in - frame mutations remained stable over nearly four weeks in culture, that there was no significant
increase in
cell death between control cultures and those treated with X4 - ZFNs, and that the most common in - frame
mutant was not expressed on the
cell surface and thus can not maintain functionality.
«In the new study we saw huge
increases in the proliferation of the special iNKT
cells in TET2 / 3
mutant mice.
Expression of the familial PD - linked A53T or A30P
mutant ASs in
cell models results in an
increased proportion of CTTAS being produced than is the case when expressing the WT protein; consistent with this, a higher proportion of the total soluble AS in human brain tissue with AS neuropathology is CTTAS, and a higher proportion yet of the total AS in insoluble AS deposits.
Testing eight different combinations of the corrective tRNAs, each designed with or without the RP import signal, its modified aminoacyl stem, or the MTS, they found that with the inclusion of all three modifications — and only with their inclusion — expression of their constructs induced a substantial
increase in mitochondrially - encoded protein synthesis (6 -8-fold) and respiration (~ 2.5-fold) in
mutant cybrid
cells.
Moreover,
cells expressing the V617F / Y931C double JAK2
mutant showed identical sensitivity to the inhibitors as
cells expressing Y931C
mutant alone, with a 20 to 50-fold
increase in the IC50 (INCB018424 and CMP6, respectively) compared to V658F mutation - positive
cells.
In these situations, rather than eliminating the neoplastic clone, deletion of
mutant cells can paradoxically lead to their
increased turnover.
Together, this new data suggests that the missing endodermal
cells observed at the end of gastrulation (Figure 1B) are not due to initial specification or proliferation defects but instead may result from an
increase in
cell death in toddler
mutants during gastrulation.
Thus, lefty
mutants have
increased Nodal signaling resulting in
increased endodermal and mesodermal gene expression and
cell number during gastrulation (Meno et al., 1999; Rogers et al., unpublished).
Third, wild - type and toddler
mutant embryos were injected at the one
cell stage with
increasing levels of Nodal mRNA and Nodal target gene expression was measured just prior to gastrulation using qRT - PCR.
Using a
mutant version of green fluorescent protein and chromatin modifying agents, recently, in collaboration with Prof. Dénes Dudits (Institute of Plant Biology, BRC, HAS, Szeged), we have achieved significantly
increased frequency of TNE on cultured maize
cells.