ライフサイエンスコーパス: embryonic lethality

1 apitulate the same severe heart phenotype or embryonic lethality.

2 al, vascular and heart defects, resulting in embryonic lethality.

3 defects of Rif1-depleted ESCs and associated embryonic lethality.

4 suppresses developmental defects and rescues embryonic lethality.

5 romatin structure, DNA damage, apoptosis and embryonic lethality.

6 enotype, depletion of the stem cell pool and embryonic lethality.

7 g a molecular explanation for htt(-/-) early embryonic lethality.

8 d completely normal except for modest (~15%) embryonic lethality.

9 sed MPI defects, FOA, oocyte aneuploidy, and embryonic lethality.

10 e and severity of NTDs that led to increased embryonic lethality.

11 e (HD), while htt(-/-) mutants display early embryonic lethality.

12 oedema, haemorrhage and increased levels of embryonic lethality.

13 d specification of mesendoderm, resulting in embryonic lethality.

14 stemic knock-out of Palb2 in mice results in embryonic lethality.

15 fects, upregulation of Tbx5 target genes and embryonic lethality.

16 es including dwarfism, anophthalmia, and 80% embryonic lethality.

17 rates and litter sizes argue against induced embryonic lethality.

18 ic progenitor cells, resulting in anemia and embryonic lethality.

19 eptor agonist to pregnant dams rescued early embryonic lethality.

20 rdination results in abnormal cell shape and embryonic lethality.

21 Mendelian genotype distribution, suggesting embryonic lethality.

22 s to complex developmental defects and early embryonic lethality.

23 e genes can lead to growth abnormalities and embryonic lethality.

24 and germ-line deletion of Palb2 led to early embryonic lethality.

25 timately collapse, leading to hemorrhage and embryonic lethality.

26 d Nodal signaling, gastrulation failure, and embryonic lethality.

27 (cFlip(fl/fl) VillinCre(+) mice) resulted in embryonic lethality.

28 ic loss-of-function of YY1 resulted in early embryonic lethality.

29 deletion of many SR protein genes results in embryonic lethality.

30 on in mma-1 animals causes larval arrest and embryonic lethality.

31 h10 loss-of-function mutations lead to early embryonic lethality.

32 type; the Rala null leads to exencephaly and embryonic lethality.

33 K-Ras(G12V) from the K-Ras locus resulted in embryonic lethality.

34 Germ line deletion of RHAU led to embryonic lethality.

35 etardation, delayed hindbrain formation, and embryonic lethality.

36 ndent manner, and a mouse knock-out leads to embryonic lethality.

37 ormation of abnormal actin bundles and early embryonic lethality.

38 exocytosis and cytokinesis, leading to early embryonic lethality.

39 incompletely penetrant temperature-sensitive embryonic lethality.

40 wild type, chr12 chr23 double mutants cause embryonic lethality.

41 tion, whereas homozygous mutations result in embryonic lethality.

42 show severe defects in heart development and embryonic lethality.

43 mbined lipin-1 and lipin-2 deficiency caused embryonic lethality.

44 Higher doses of morpholino induce embryonic lethality.

45 cular chamber maturation, heart failure, and embryonic lethality.

46 ms are compatible with life and do not cause embryonic lethality.

47 at depletion of the two AIP1 isoforms causes embryonic lethality.

48 neuronal apoptosis, which eventually lead to embryonic lethality.

49 postnatal gene delivery so as to circumvent embryonic lethality.

50 s lead to strong developmental phenotypes or embryonic lethality.

51 line disruption of Dot1L in mice resulted in embryonic lethality.

52 inactivation of murine Lig3 results in early embryonic lethality.

53 total deletion of Mfrn1 in embryos leads to embryonic lethality.

54 e results in major developmental defects and embryonic lethality.

55 gene in higher vertebrates results in early embryonic lethality.

56 ic inactivation of CycK in mice causes early embryonic lethality.

57 of matrix proteins to peroxisomes can confer embryonic lethality.

58 d not be identified, due to gametophytic and embryonic lethality.

59 ng on hedgehog (Hh) signalling, and exhibits embryonic lethality.

60 ogaster crossed to uninfected females causes embryonic lethality.

61 ion in mice disrupts gastrulation and causes embryonic lethality.

62 bal Ptpn11(E76K/+) mutation results in early embryonic lethality.

63 gous Brca2 mutation typically leads to early embryonic lethality.

64 eficiency of both Jnk1 and Jnk2 causes early embryonic lethality.

65 geted disruption of the Fli1 gene results in embryonic lethality.

66 nditional FAK knockout [CFKO] mice) leads to embryonic lethality.

67 n reduced brood size and partially penetrant embryonic lethality.

68 log of TIF1 gamma, cause profound anemia and embryonic lethality.

69 letions in any of the BER proteins result in embryonic lethality.

70 cell coverage of the vasculature leading to embryonic lethality.

71 alian models, causes increased sterility and embryonic lethality.

72 n mammalian skin, are yet unknown because of embryonic lethality.

73 ar uptake of the TC-bound B12, do not confer embryonic lethality.

74 AP/TAZ leads to impaired vascularization and embryonic lethality.

75 he TRP channel TRPM7, which results in early embryonic lethality.

76 hat loss of functional Zbtb24 leads to early embryonic lethality.

77 ection of AAV9-sgRNAs, thereby circumventing embryonic lethality.

78 ce results in right ventricle hypoplasia and embryonic lethality.

79 k efficient centriole conversion and lead to embryonic lethality.

80 ut of both paralogs in mice results in early embryonic lethality.

81 tical for life, because its absence leads to embryonic lethality.

82 In mice, global deficiency causes embryonic lethality.

83 pression of spontaneous cell death, and post-embryonic lethality.

84 n addition, capzb over-expression results in embryonic lethality.

85 ntegrity, leading to osmotic sensitivity and embryonic lethality.

86 how that Slc52a3 deficiency results in early embryonic lethality.

87 s to delayed initiation of cell division and embryonic lethality.

88 strated that deletion of Ada3 leads to early embryonic lethality.

89 ortic valve, ventricular septal defects, and embryonic lethality.

90 leads to developmental retardation and early embryonic lethality.

91 the endothelium because this ablation causes embryonic lethality.

92 generation of mature blood cells, leading to embryonic lethality.

93 ed EGFR nulls, an AGR2 null also resulted in embryonic lethality.

94 postimplantation stage, which leads to early embryonic lethality.

95 leads to chromosome segregation defects and embryonic lethality.

96 egregating variants modify the penetrance of embryonic lethality.

97 HR gene (Fancd2) and Polq in mice results in embryonic lethality.

98 n disrupt the actin cytoskeleton and produce embryonic lethality, a double mutant suppresses these de

99 ice harboring an Emu-Myc transgene displayed embryonic lethality, allelic loss of Bif-1 dramatically

100 that SirT7-knockout mice suffer from partial embryonic lethality and a progeroid-like phenotype.

101 in Mcm2-deficient mice results in increased embryonic lethality and accelerated cancer formation in

102 zyme critical in microRNA biogenesis, causes embryonic lethality and activation of the p53 pathway.

103 nt and vessel formation and function lead to embryonic lethality and are important in the pathogenesi

104 ciated with significant phenotypes including embryonic lethality and cancer.

105 urthermore, Commd9 deletion in mice leads to embryonic lethality and complex cardiovascular alteratio

106 atwo, a hypomorphic allele of Trim28, causes embryonic lethality and defects in convergent extension

107 Second, although loss of 53BP1 rescues the embryonic lethality and HR defects in BRCA1-deficient mi

108 the morula stage and demonstrating elevated embryonic lethality and involvement of TSPO in embryonic

109 ulates features of Meckel syndrome including embryonic lethality and multiorgan defects.

110 omeostasis but additionally results in early embryonic lethality and neural tube closure defects.

111 Cwc27 mutant mouse models, with significant embryonic lethality and severe phenotypes in the complet

112 To avoid early embryonic lethality and study NFP function in later card

113 did not affect ILK localization to FAs, the embryonic lethality and the in vitro migration defects a

114 on of the X-linked Cosmc gene in mice causes embryonic lethality and Tn antigen expression.

115 -specific knockouts also did not exhibit any embryonic lethality and were viable to adulthood.

116 utants have impaired mitochondrial function, embryonic lethality, and agenesis of the liver.

117 s, but instead causes proliferation defects, embryonic lethality, and dysregulation of ESC signaling

118 ral cell migration, differentiation, partial embryonic lethality, and hemorrhaging were observed afte

119 of the genes coding for RNase H2 results in embryonic lethality, and in humans, RNase H2 hypomorphic

120 crossing suggested that CEK4 knockout causes embryonic lethality, and microscopy analysis of the abor

121 efects in dystroglycan glycosylation, avoids embryonic lethality, and produces a phenotype resembling

122 y, BRCA1 deficiency in mice results in early embryonic lethality, and similarly, lack of BRCA1 in hum

123 of SRSF2 in the hematopoietic lineage caused embryonic lethality, and Srsf2-deficient fetal liver cel

124 at disruption of both CRTC2 and CRTC3 causes embryonic lethality, and that a single allele of either

125 ead to degradation of type I collagen, early embryonic lethality, and the scarcity of reported osteog

126 iosus, reduced myocardial proliferation, and embryonic lethality around E13.

127 of Gata4 in hepatic mesenchymal cells led to embryonic lethality around mouse embryonic stage 13.5, l

128 Genetic deletion of Casp8 results in embryonic lethality as a result of uncontrolled necropto

129 o known as Trp53), revealed late-gestational embryonic lethality associated with a host of phenotypes

130 ecific deletion of GPR124 in mice results in embryonic lethality associated with abnormal angiogenesi

131 iotic recombination primarily because of the embryonic lethality associated with Blm deletion.

132 iency, Paxx/Xlf double-knockout mice display embryonic lethality associated with genomic instability,

133 ctivated kinase 4 (PAK4) in the mouse causes embryonic lethality associated with heart and brain defe

134 deletion of alpha-pv in mice results in late embryonic lethality associated with hemorrhages and redu

135 ivation of Atm and H2ax in mice causes early embryonic lethality associated with substantial cellular

136 In marked contrast to the early embryonic lethality associated with the genetic disrupti

137 ormalities, homozygous deficiency results in embryonic lethality at approximately embryonic day 7.

138 ation, progressive apoptotic cell death, and embryonic lethality at E10.5.

139 shown that Foxo1 knockout in mice results in embryonic lethality at E11 because of impaired vascular

140 study showed that Sag total knockout caused embryonic lethality at E11.5-12.5 days with associated d

141 and arteriovenous malformations, leading to embryonic lethality at E12.5.

142 Disruption of Drosha in VSMCs resulted in embryonic lethality at E14.5 with severe liver hemorrhag

143 own of tbeta4 has been reported to result in embryonic lethality at E14.5-16.5, with severe cardiac a

144 tion of mouse tropomodulin3 (Tmod3) leads to embryonic lethality at E14.5-E18.5, with anemia due to d

145 rt that Sag endothelial deletion also causes embryonic lethality at E15.5 with poor vasculogenesis.

146 that ablation of the mouse Brpf1 gene causes embryonic lethality at E9.5.

147 cible p150 ADAR1 isoform and found it caused embryonic lethality at embryo day (E) 11-E12.

148 of Cdc42 in mice has been shown to result in embryonic lethality at embryonic day 6.5 (E6.5) before b

149 lacking FLRT2 in endothelial cells exhibited embryonic lethality at mid-gestation, with systemic cong

150 rturbed vascular development, hemorrhage and embryonic lethality at mid-gestation.

151 RapGEF2 deficiency led to embryonic lethality at ~ E11.5 due to severe yolk sac va

152 irected deficiencies of Cx45 in mice lead to embryonic lethality attributable to morphological and fu

153 POMT2 nulllizygosity resulted in embryonic lethality because of a defective Reichert's me

154 BMP10 deletion in mice results in embryonic lethality because of impaired cardiac developm

155 Absence of ALK5 leads to early embryonic lethality because of severe defects in vascula

156 inin in the mouse results in preimplantation embryonic lethality because pluripotent cells fail to fo

157 zygous deletion of Letm1 in mice resulted in embryonic lethality before day 6.5 of embryogenesis and

158 We find that Iop1 knock-out results in embryonic lethality before embryonic day 10.5.

159 e UTX KO mice, which lack the UTY gene, show embryonic lethality before embryonic day 11.5.

160 r specifically in cardiomyocytes resulted in embryonic lethality before embryonic day 12.5.

161 melastatin-like 7 (Trpm7) in mice results in embryonic lethality before embryonic day 7.

162 of both alleles of PRKCSH in mice results in embryonic lethality before embryonic day E11.5.

163 ine kinases 1 and 2 (Sphk1 and Sphk2) showed embryonic lethality between E11.5 and E12.5 due to defec

164 letion of SENP1 (SENP1 KO) causes anemia and embryonic lethality between embryonic day 13.5 and postn

165 Ablation of the KLF1 or KLF2 gene causes embryonic lethality, but double KO embryos are more anem

166 d-ligation defects and p53- and Ku-dependent embryonic lethality, but open hairpin-sealed ends normal

167 pment in mice resulted in p53 activation and embryonic lethality, but the mice with arf-bp1 deletion

168 eletion of skNAC in mice resulted in partial embryonic lethality by embryonic day 12.5, with ventricu

169 the global deletion of Etv2 and that it has embryonic lethality by embryonic day 9.5.

170 istration of a MEK inhibitor ameliorated the embryonic lethality, cardiac defects, and NS features of

171 Vinculin loss results in embryonic lethality, cardiovascular diseases, and cancer

172 have shown that MLKL deficiency rescued the embryonic lethality caused by loss of Caspase-8 or FADD.

173 TRPM7 expression, indicating that the early embryonic lethality caused by loss of hepatocystin is ma

174 al of paternal mitochondria causes increased embryonic lethality, demonstrating that PME is important

175 e mouse Hinfp(LacZ) null allele causes early embryonic lethality due to a blastocyst defect.

176 GRK2 null animals exhibit embryonic lethality due to a severe developmental heart

177 gene; the absence of ptc-3 results in a late embryonic lethality due to an apparent defect in osmoreg

178 ial-specific WNK1 gene disruption results in embryonic lethality due to angiogenic and cardiovascular

179 Unexpectedly, male UTX-null mice escape embryonic lethality due to expression of UTY, a paralog

180 INV) on the paternal X chromosome results in embryonic lethality due to failure of imprinted X inacti

181 Loss of murine Nf1 results in embryonic lethality due to heart defects, while mice wit

182 icult because global Met knockout results in embryonic lethality due to placental and liver abnormali

183 rated in EPCR knockout mice which show early embryonic lethality due to placental thrombosis.

184 etal liver, erythroid maturation arrest, and embryonic lethality due to profound anemia.

185 of Notch1 in Prox1 heterozygous mice rescued embryonic lethality due to Prox1 haploinsufficiency and

186 Its absence in mitochondria results in embryonic lethality due to the failure to amplify mitoch

187 c vasculogenesis as a primary cause of early embryonic lethality following loss of this critical bHLH

188 thelial-specific GPR124 deletion resulted in embryonic lethality from CNS-specific angiogenesis arres

189 he wild type PSTPIP1 in mice lead to partial embryonic lethality, growth retardation, and elevated le

190 report that Naa10-null mice display partial embryonic lethality, growth retardation, brain disorders

191 FOXF1-deficient embryos exhibited embryonic lethality, growth retardation, polyhydramnios,

192 e observed and heterozygous mice also showed embryonic lethality (haploinsufficient lethality) observ

193 Embryonic lethality has limited the characterization of

194 Whereas homozygous deletion of LKB1 led to embryonic lethality, heterozygous LKB1-knock-out (KO) (L

195 Hypomorphic levels of Ift80 result in embryonic lethality highlighting a key role for Ift80 in

196 hereas complete loss of Spartan causes early embryonic lethality, hypomorphic mice with low amounts o

197 us variant (such as aneuploidy) could escape embryonic lethality if the genome-wide burden of slightl

198 sed imprinted genes, is the primary cause of embryonic lethality in 70-80% of parthenogenotes immedia

199 germ line deletion of Flcn results in early embryonic lethality in animal models.

200 expressed by osteoblast-lineage cells; early embryonic lethality in Bag-1 null mice, however, has lim

201 e DNA damage response factor 53BP1 overcomes embryonic lethality in Brca1-nullizygous mice and rescue

202 ortance in development is exemplified by the embryonic lethality in cFLIP-deficient animals.

203 ytoplasmic incompatibility, which results in embryonic lethality in crosses between infected males an

204 Each gene additively augments embryonic lethality in crosses between infected males an

205 We discovered a selfish element causing embryonic lethality in crosses between wild strains of t

206 , we investigated the cellular basis of male embryonic lethality in D. melanogaster induced by Spirop

207 t the dominant inducers of RIP kinase-driven embryonic lethality in FADD-deficient mice.

208 a loss of junctional membrane complexes and embryonic lethality in germ-line junctophilin-2 (JPH2) k

209 ated thin filament length, were the cause of embryonic lethality in HSPB7 KOs.

210 idgestation, consistent with RTT-linked male embryonic lethality in humans.

211 th a putative role in splicing, causes early embryonic lethality in mice and that its loss in Purkinj

212 Disruption of Casp8 expression leads to embryonic lethality in mice between embryonic days 10.5

213 , a survivin-associated immunophilin, causes embryonic lethality in mice by embryonic day 13.5-14, in

214 dly, catalytically inactive prostasin caused embryonic lethality in mice lacking its cognate inhibito

215 Ubiquitous inactivation of Utf1 causes embryonic lethality in mice with a hybrid genetic backgr

216 Deletion of Lig3 results in early embryonic lethality in mice, as well as apparent cellula

217 by REMOTE-control was potent enough to cause embryonic lethality in mice, reminiscent of a genetic kn

218 both D2899A and Q2740P mutations cause early embryonic lethality in mice, without displaying dominant

219 and homozygous loss of this protein leads to embryonic lethality in mice.

220 poplasia (FDH), whereas gene deletion causes embryonic lethality in mice.

221 Disruption of Axin1 causes embryonic lethality in mice.

222 vated p53 transcriptional activity and early embryonic lethality in mice.

223 nzyme thymine DNA glycosylase (TDG) leads to embryonic lethality in mice.

224 SEL1L causes systemic ER stress and leads to embryonic lethality in mice.

225 kout is problematic as the knockout leads to embryonic lethality in mice.

226 on, causing right ventricular hypoplasia and embryonic lethality in mice.

227 or subunit, and knockout of Med31 results in embryonic lethality in mice; however, Med31 function in

228 its catalytic subunit (P4ha1(-/-)) leads to embryonic lethality in mouse, whereas P4ha1(+/-) mice ha

229 Molecular strategies that promote embryonic lethality in these agricultural pests are limi

230 developmental arrest in frogs and zebrafish, embryonic lethality in transgenic mice, and lesions in m

231 o the inhibition of cell death and increased embryonic lethality in unirradiated animals.

232 cell cycle progression and results in early embryonic lethality in vertebrates.

233 mental defects, a failure to gastrulate, and embryonic lethality, including changes in the steady sta

234 affects endogenous geminin levels; apparent embryonic lethality is observed around 3-4 hours after m

235 Although ablation of Zfp516 causes embryonic lethality, knockout embryos still show drastic

236 Interestingly, the maternal-effect embryonic lethality, larval lethality, and adult eye def

237 ent to yield homozygous mutant mice revealed embryonic lethality later than occurred with global Gata

238 though NIR deficiency in mice leads to early embryonic lethality, lymphoid-restricted deletion result

239 th syndromes (i.e. ribosomal frame-shifting, embryonic lethality, neurodegeneration and cancer) typic

240 e TGF-beta1(Lbeta3/Lbeta3) mice show neither embryonic lethality nor signs of multifocal inflammation

241 Here we show that embryonic lethality observed in abp1-1, which has been a

242 unrecognized action of Meis1 may explain the embryonic lethality observed in Meis1(-/-) mice that ari

243 their regulation might explain the observed embryonic lethality of Abi1-deficient embryos, which sur

244 PE1 in CSR has been difficult because of the embryonic lethality of APE1 ablation in mice.

245 We demonstrate that the embryonic lethality of aph-1(zu147) mutants can be suppr

246 plicated by nonspecific reagents, and by the embryonic lethality of conventional GRIP1 KO mice.

247 Due in part to the early embryonic lethality of Dnmt1 and Uhrf1 knockout mice, ro

248 In contrast to the early embryonic lethality of H2AX(-/-)XLF(-/-) mice, 53BP1(-/-

249 However, the early embryonic lethality of Hand2-null mice has precluded lin

250 n Bcl-xL has remained unclear because of the embryonic lethality of mice globally deleted for Bcl-xL.

251 a role in patterning blood formation, early embryonic lethality of mice lacking Hh signaling preclud

252 p53 deletion prevents the embryonic lethality of normal tissues lacking Mdm2, sugg

253 eEF2(G717R/G717R) mice, suggesting that the embryonic lethality of OVCA1(-/-) mice is due to diphtha

254 ntial role in development, apparent from the embryonic lethality of Pbmr1-null mice, but very little

255 etween Stx1 isoforms Stx1A and Stx1B and the embryonic lethality of Stx1A/1B double knock-out (DKO) m

256 We report the first characterization of the embryonic lethality of the Apj-/- mice.

257 Early embryonic lethality of the mouse knockout challenges inv

258 ratio (26.5%; n = 1,080 pups), indicating no embryonic lethality of this genotype.

259 f TRPM7 in mouse models has been hampered by embryonic lethality of transgenic ablations.

260 ypes in homozygotes: skin abnormalities, and embryonic lethality on normal chow diet, but not on high

261 es viability of the individual (for example, embryonic lethality) or results in profound loss of fitn

262 eas complete ATR pathway inactivation causes embryonic lethality, partial Hus1 impairment has been ac

263 While TDP-43 knockout mice show early embryonic lethality, post-natal conditional knockout mic

264 use model and found that loss of Fdxr led to embryonic lethality potentially due to iron overload in

265 Deletion of CDK2AP1 leads to early embryonic lethality, potentially through altered differe

266 ulatory complex Mediator generally result in embryonic lethality, precluding study of its physiologic

267 e perinatal lethal, in contrast to the early embryonic lethality previously reported for Rnaseh2b- or

268 Deletion of Pak4 in mice results in embryonic lethality prior to embryonic day 11.5.

269 currence of NTDs in heterozygous embryos and embryonic lethality prior to NT closure.

270 h GATA genes, but not either alone, leads to embryonic lethality prior to the onset of their expressi

271 ate, whereas deletion from mice causes early embryonic lethality, raising the question of whether La

272 ell fate into working myocardium, and causes embryonic lethality, recapitulating the phenotypes inclu

273 To circumvent the embryonic lethality resulting from Cx45 deficiency, mice

274 The embryonic lethality resulting from loss of SEC24C occurs

275 ion of Rspo3 in the Isl1 lineage resulted in embryonic lethality secondary to impaired development of

276 Since deletion of Tie1 results in embryonic lethality secondary to vascular dysfunction, w

277 te for the lack of TFPI and rescue TFPI-null embryonic lethality, Tfpi(+/-) mice lacking the platelet

278 cytes of maternal-zygotic mutants results in embryonic lethality that can be fully rescued with gdf3

279 or survival of mouse embryos, but because of embryonic lethality, their precise developmental roles r

280 Gata4(MyoDel/wt);Tbx5(+/-) mice displayed embryonic lethality, thin myocardium with reduced cell p

281 DNase II-dependent embryonic lethality was rescued by loss of STING functio

282 To bypass embryonic lethality we used Tie2CRE-mediated recombinati

283 While loss of FAK in mice results in embryonic lethality, we have deleted FAK in the adult bo

284 use complete ATR pathway inactivation causes embryonic lethality, we weakened the ATR mechanism to di

285 which if mutated (or knocked-out) result in embryonic lethality when homozygous, and initiate the st

286 nes that are widely expressed or which cause embryonic lethality when mutated.

287 tion of the editing activity of AlaRS caused embryonic lethality, whereas an intermediate reduction i

288 Ssb1/Ssb2 double knockout (DKO) caused early embryonic lethality, whereas conditional Ssb1/Ssb2 doubl

289 nstitutive knockout of Lkb1 in mice leads to embryonic lethality, whether Lkb1 is required for the gr

290 Ezh2 in developing mouse endothelium caused embryonic lethality with compromised vascular integrity

291 hat the inactivation of Cdc42 in NCCs caused embryonic lethality with craniofacial deformities and ca

292 pk as a model for Shh dysfuction) results in embryonic lethality with e12.5 embryos having exencephal

293 e show that disruption of L3mbtl2 results in embryonic lethality with failure of gastrulation.

294 of Gata6-loxP with Nkx2.5-cre produced late embryonic lethality with heart defects, whereas deletion

295 Embryonic lethality with incomplete penetrance was obser

296 deletion of ERG (Erg(cEC-KO)) in mice causes embryonic lethality with vascular defects.

297 The deletion of Cdc42 in ECs caused embryonic lethality with vasculogenesis and angiogenesis

298 specific deletion of Wnk1 in mice results in embryonic lethality, with angiogenesis and cardiac defec

299 ion of ARID1a-DNA binding in mice results in embryonic lethality, with mutant embryos manifesting pro

300 t together with Atm loss resulted in partial embryonic lethality, with the surviving double-mutant mi