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As homozygous deletion in PKD1 or PKD2 in mice causes embryonic death, examination of touch sensitivity in PKD-deficient mice will require a conditional knockout [55].
Second, while the homozygous deletion of Dkk1 in mice causes embryonic lethality, the deletion of only one Dkk1 allele results in an osteosclerotic phenotype, and the opposite is observed in transgenic mice over-expressing Dkk1 [27], [27].
- Knockout p38α in mice causes embryonic lethality at E10.5 due to abnormal placenta development and erythropoiesis.
Loss-of-function of Evi in mice causes embryonic lethality due to disruption of axial patterning (Fu et al, 2009).
For example, deletion of TRF1 or TIN2 in mice causes embryonic lethality independent of telomerase dependent telomere length regulation [ 9, 10].
Germline Smad2 deletion in mice causes embryonic lethality [ 19- 22]; heterozygous Smad2 mice are viable, fertile, and no spontaneous tumors develope in their lifespan.
Similar(48)
Deletion of MM gene in mice caused embryonic lethality at 10.5 days [10], whereas deletion of MII2 gene led to embryonic lethality at 11.5 days [11], suggesting that both MM and MII2 have important and non-redundant roles in development.
Genetic manipulations to disrupt Capns1 constitutively or conditionally in mice cause embryonic lethality and cardiac hypertrophy, respectively, indicating that calpains are indispensable both to heart-specific functions and to life itself.
Unfortunately, null mutants in both HGF/SF and c-met genes in mice cause embryonic lethality because of placental insufficiency and developmental defects in the liver and muscle [ 31].
Using a gene targeting strategy to ablate Pten gene function in the mouse causes embryonic lethality between days 6.5 to 9.5 of gestation [8], [9], [10], [11].
Inactivation of the paternal allele in the mouse causes embryonic growth retardation.
Related(15)
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mice causes severe
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