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Similarly, trpv4−/− mice display defective osmoregulation when subjected to an osmotic challenge [16].
This idea is based on the observations that GRF2 knockout mice display defective LTP, but not LTD and GRF1 knockout mice display defective LTD but not LTP, when field excitatory postsynaptic potentials (fEPSPs) were used to measure synaptic plasticity.
While ephrinB2−/− mice display defective intersomitic vessel patterning that can be attributed to vascular specific ephrinB2 [44], these mutants were assessed after the DLAV had formed.
Cells lacking palladin have disrupted actin organization and palladin null mice display defective neural tube and ventral closure leading to embryonic death [27].
We showed previously that 1-month old Ras-GRF2 knockout mice display defective LTP when their Schafffer collateral fibers were stimulated with theta-burst stimulation (TBS) and synaptic activity was probed at CA3/CA1 synapses using extracellular field recordings [9].
Thus, our previous observation that GRF2 knockout mice display defective LTP using theta-burst/field recording, but not here using the LFS/single-cell recording protocol, suggested that Ras-GRF2 induces LTP by mediating the action of one, but not both subtypes of NMDA receptors in CA1 pyramidal neurons.
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Previous studies have shown that SIRT1-knockout mice displayed defective metabolism, and CR-mediated physiological responses (i.e., increased physical activity) were abrogated (Chen et al., 2005; Boily et al., 2008).
However, while maturation of DCs is defective in RelB deficient mice and DCs from these mice induce T cell tolerance in wild-type mice, RelB deficient mice also display defective thymic organogenesis, reduced numbers of mTECs, reduced negative selection, increased numbers of autoreactive T cells in the periphery, and multi-organ inflammation [ 19- 21].
Therefore, the CNS and neuroretina of Cln3 Δex1- mice similarly display defective lysosomes and autophagolysosome structures, both indicative of deficient lysosome-related degradative processes.
Similarly, RhoH knockout mice display a defective T cell maturation during transition from DN3 to DN4 and during positive selection.
These mice, which displayed defective apoptosis, had a reduced life span and most developed tumors.
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