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Investigations of the tpi1 knockout mutant led to the discovery of a second tpi gene (tpi2) in this organism.
By contrast we find that expressing a dominantly active Rab11 mutant led to compromised growth in mice.
This mutant led to increased production of not only resveratrol but also the flavonoid naringenin, when introduced in their corresponding biosynthetic pathways.
At the cellular levels, expressing Sin1-R81T, opposing to the phospho-mimetic Sin1-T86E/T398E mutant, led to comparable levels of cleaved caspase 3 to cells expressing Sin1-WT upon etoposide or cisplatin challenge, subsequently conferring cellular resistance to these agents.
We demonstrate that inactivation of ADP-glucose pyrophosphorylase in a Chlamydomonas starchless mutant led to a 10-fold increase in TAG, suggesting that shunting of photosynthetic carbon partitioning from starch to TAG synthesis may represent a more effective strategy than direct manipulation of the lipid synthesis pathway to overproduce TAG.
Surprisingly, infection with the mutant led to a faster killing in the systemic model of infection.
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These results suggest that one functional Rab10 allele is enough for murine embryo development and adults' survival, but that a double mutant leads to embryonic lethality.
The R1648H mutant leads to an increase in Na+ current contributing both to the spiking phase of the burst and to the afterdepolarizing potential (ADP) in between spikes.
These results demonstrate that FGFR4 expression, particularly a constitutively-activated mutant, leads to significant reduction in TNFα-stimulated IKK kinase activity when assayed in vitro.
It is interesting that the A127T paxillin mutant leads to increased angiogenesis phenotype (as previously published by our group).
Nevertheless, the Ile58Thr mutant leads to packing defects in the two four-helix bundles at the tetrameric interface, and the mutant enzyme is found predominantly as a dimer.
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