ライフサイエンスコーパス: growth retardation

1 OR small for gestational age OR intrauterine growth retardation).

2 iabetes, lipodystrophy, hepatosteatosis, and growth retardation.

3 PCNT) that lead to severe pre- and postnatal growth retardation.

4 poplasia, immunodeficiency, and intrauterine growth retardation.

5 with birth defects, mental disabilities and growth retardation.

6 bitor, 26B, triggered massive cell death and growth retardation.

7 tic architecture and show pre- and postnatal growth retardation.

8 s with epithelial metastatic progression and growth retardation.

9 ith combination PIT showed significant tumor growth retardation.

10 ions such as pre-eclampsia and intra-uterine growth retardation.

11 ith microcephaly, cerebellar hypoplasia, and growth retardation.

12 potrophy and insufficiency, leading to fetal growth retardation.

13 vation, a mechanism that could contribute to growth retardation.

14 s of the lower limbs, inability to walk, and growth retardation.

15 levated risk of cancer, telangiectasias, and growth retardation.

16 yond postnatal day 28, they exhibited marked growth retardation.

17 likely to have contributed directly to their growth retardation.

18 al deficits including seizures, tremors, and growth retardation.

19 lation, and lead to small fetuses with organ growth retardation.

20 f Hrpt2 after E8.5 resulted in apoptosis and growth retardation.

21 osed splotch embryos, probably via embryonic growth retardation.

22 ient embryos exhibit developmental delay and growth retardation.

23 LIG4 syndrome, showing immunodeficiency and growth retardation.

24 rylation of Erk in neural tissues and led to growth retardation.

25 The mutation causes dominant postnatal growth retardation.

26 rly embryogenesis can result in intrauterine growth retardation.

27 xhibits oral leukoplakia and blistering, and growth retardation.

28 volved in the BMI1-dependent cancer-specific growth retardation.

29 irth weight, preterm birth, and intrauterine growth retardation.

30 lar malformations, urogenital anomalies, and growth retardation.

31 ride content diarrhea, volume depletion, and growth retardation.

32 ) hazard villages suffered from intrauterine growth retardation.

33 ing human pregnancy failure and intrauterine growth retardation.

34 Four of the 5 patients also had postnatal growth retardation.

35 n various human disorders, such as perinatal growth retardation.

36 dysmorphism, cardiac defects, and postnatal growth retardation.

37 e genes lead to important, sometimes lethal, growth retardation.

38 se4 accumulation in rcy1Delta cells leads to growth retardation.

39 hy, which manifests as joint deformities and growth retardation.

40 erse health effects, including cretinism and growth retardation.

41 surviving animals exhibiting a lifelong 20% growth retardation.

42 ce results in pre-eclampsia and intrauterine growth retardation.

43 , and extracutaneous abnormalities including growth retardation.

44 getic dysfunctional phenotypes, including 1) growth retardation, 2) cold intolerance, 3) reduced exer

45 mice Lig4(R278H/R278H) (Lig4(R/R)) includes growth retardation, a decreased life span, a severe cell

46 ditional expression of RPS19R62W resulted in growth retardation, a mild anemia with reduced numbers o

47 6 related patients with autosomal recessive growth retardation, adrenal insufficiency, and a selecti

48 rowth impairment might have resulted in less growth retardation after pediatric kidney transplantatio

49 FACC1KO mice showed prenatal growth retardation; after weaning, however, their weight

50 xpression of ANAC017 in Arabidopsis leads to growth retardation, altered leaf development with decrea

51 ation with pathogenic BCS1L variants include growth retardation, aminoaciduria, cholestasis, iron ove

52 sing the CtIP(E157K) protein alone exhibited growth retardation, an increase in the G(1) population,

53 er NDT2 in HEK293 cells resulted in dramatic growth retardation and a metabolic shift from oxidative

54 ckout leads to increased R-loop levels, cell growth retardation and accumulation of gammaH2AX, a mark

55 These data indicate that the patients' growth retardation and adrenal insufficiency likely refl

56 We demonstrate that ART treatment induces growth retardation and an accumulation of ubiquitinated

57 isruption of these oncogenic pathways led to growth retardation and apoptotic cell death of the Tax2-

58 -deficient mice were found to display severe growth retardation and are unable to survive beyond post

59 ex3c homozygous mutant mice causes postnatal growth retardation and background-dependent perinatal le

60 X-linked hypophosphatemia (XLH) leads to growth retardation and bone deformities, which are not f

61 e characterized by severe pre- and postnatal growth retardation and by mutually exclusive mutations i

62 r that is invariably characterized by severe growth retardation and cancer predisposition.

63 revealed that caspase-2 deficiency enhanced growth retardation and caused synthetic perinatal lethal

64 of DBA, the disease is also characterized by growth retardation and congenital anomalies that are pre

65 of DBA, the disease is also characterized by growth retardation and congenital malformations, in part

66 Snx13-null embryos had significant overall growth retardation and defects in neural tube closure, b

67 addition, similar to patients, AT pigs show growth retardation and develop motor deficit phenotypes.

68 during oxidative stress can ultimately cause growth retardation and developmental defects.

69 th preterm delivery, low birth weight, fetal growth retardation and developmental defects.

70 d IGFBP-1 mediates hypoxia-induced embryonic growth retardation and developmental delay by binding to

71 significantly alleviated the hypoxia-induced growth retardation and developmental delay.

72 , null mutant (Spca1(-/-)) embryos exhibited growth retardation and did not survive beyond gestation

73 ckout mice were born normally, but displayed growth retardation and died prematurely.

74 Kif3a deficiency caused cranial base growth retardation and dysmorphogenesis, which were evid

75 9.1(-/-) mouse embryos exhibit intra-uterine growth retardation and have small placentas due to a red

76 n in insulin-like growth factor 1, postnatal growth retardation and hepatic steatosis.

77 embryos survive gestation but exhibit severe growth retardation and impaired erythropoiesis, and loss

78 These mice have severe preweaning growth retardation and incomplete catch-up growth.

79 Early Ott1-deficient embryos show growth retardation and incomplete closure of the notocho

80 mice are marked by decreased survival rates, growth retardation and increased variability in body wei

81 loss of NAA50 expression resulted in severe growth retardation and infertility in two Arabidopsis tr

82 IAV-driven vascular storm included placental growth retardation and intrauterine growth restriction,

83 Global Et2 knockout mice exhibited severe growth retardation and juvenile lethality.

84 Surviving mutants exhibited growth retardation and late-onset dilated cardiomyopathy

85 ncy including methylmalonic acidemia, severe growth retardation and lethality.

86 highly sensitive to salinity stress causing growth retardation and loss in productivity.

87 he fetus including physical and intellectual growth retardation and malformations.

88 OB precursor cells (OPC) in mice results in growth retardation and markedly decreased bone mass with

89 sorder characterized by extreme intrauterine growth retardation and multiple organ abnormalities.

90 ally, GH supplementation was able to correct growth retardation and muscle weakness.

91 oral administration of taurine rescued their growth retardation and osteoporosis phenotypes.

92 genetic model results in severe postweaning growth retardation and osteoporosis, and the severity an

93 n factor involved in brain development, show growth retardation and other abnormalities consistent wi

94 ay an inflammatory phenotype associated with growth retardation and paw swelling.

95 Inactivation of tensin3 resulted in growth retardation and postnatal lethality in one third

96 lacking Fgf8a-containing spliceforms exhibit growth retardation and postnatal lethality, and the phen

97 family helicase BLM that is associated with growth retardation and predisposition to cancer.

98 expressing human TDP-43 in neurons exhibited growth retardation and premature death that are characte

99 consequently, neonatal Pgc-1(c) mice exhibit growth retardation and profound anemia.

100 fter E13.5, YB-1(-/-) embryos exhibit severe growth retardation and progressive mortality, revealing

101 ures with the human syndromes in its overall growth retardation and reduced brain size.

102 n of one-carbon-carrying folates, as well as growth retardation and reduced cellular proliferation.

103 ficiency caused condylar disorganization and growth retardation and reduced polymorphic cell layer pr

104 g adult mice by tamoxifen injections induced growth retardation and severe deformities in knee joints

105 They also exhibit growth retardation and severe postnatal osteopenia stemm

106 everity of anemia, abnormal iron metabolism, growth retardation and shortened lifespan.

107 t the decidual-placental interface and fetal growth retardation and subsequent demise.

108 th; however, soon after weaning they exhibit growth retardation and the adult mice are hypophagic, le

109 enotype, and correlated with the severity of growth retardation and the in vitro cellular phenotype.

110 ossly normal at 2 weeks of age but exhibited growth retardation and were significantly smaller than c

111 ing those of the heart and the renal tract), growth retardation, and a recognizable facial gestalt (i

112 pose tissue and brown adipose tissue, severe growth retardation, and bone defects.

113 tochondrial biosynthesis and clearance, cell growth retardation, and cellular senescence of DC fibrob

114 clinically characterized by mild hypotonia, growth retardation, and delayed motor milestones.

115 exhibited a reduced amount of WAT, postnatal growth retardation, and early death before weaning.

116 in mice lead to partial embryonic lethality, growth retardation, and elevated level of circulating pr

117 of normal vascular patterning, severe fetal growth retardation, and embryonic death at E9.5 to 10, a

118 the risk of status dystonicus, intrauterine growth retardation, and endocrinopathies.

119 exhibited dwarfism, as a result of in utero growth retardation, and had low serum insulin-like growt

120 inant form of mild syndromic ID with ptosis, growth retardation, and hypotonia, and we identified an

121 vation of supv311 caused liver degeneration, growth retardation, and juvenile lethality, a phenotype

122 t explains how Giardia infection can lead to growth retardation, and may offer insights that guide fu

123 or its murine homologue Fto result in severe growth retardation, and mice globally overexpressing FTO

124 lated disorders are macrocephaly, absence of growth retardation, and more variability in the degree o

125 increased prenatal and postnatal mortality, growth retardation, and multiple tissue abnormalities.

126 against death, progression of brain injury, growth retardation, and neurobehavioral deficits after a

127 o extend our understanding of diet-dependent growth retardation, and offers a potential mechanism to

128 efective RNR often led to cell cycle arrest, growth retardation, and p53-dependent apoptosis, whereas

129 rt shape, ventricular septal defects, severe growth retardation, and postnatal lethality with no upre

130 tions such as preterm delivery, intrauterine growth retardation, and preeclampsia; however, the molec

131 boptimal response, poor treatment adherence, growth retardation, and presentation in advanced phases)

132 pilepsy, microcephaly, congenital cataracts, growth retardation, and spasticity.

133 The Pitx2-Cre/Dicer1 mutant mice demonstrate growth retardation, and the pituitaries are hypoplastic

134 astrulation, results in increased apoptosis, growth retardation, and, ultimately, embryonic death.

135 female, but not male, UGRP(-/-) mice exhibit growth retardation as do G6Pase(-/-) mice and patients w

136 e for up to several weeks although they show growth retardation as well as emphysema.

137 Only a few genetic studies of growth retardation associated with the KBD have been car

138 the short stature homeobox gene SHOX lead to growth retardation associated with Turner, Leri-Weill dy

139 alpha-Adducin-null mice show growth retardation at birth and throughout adulthood.

140 rowth suppression and of stress-induced leaf growth retardation both required the AUXIN-RESISTANT1 ge

141 ll mice display partial embryonic lethality, growth retardation, brain disorders, and maternal effect

142 ual disability with cataracts, epilepsy, and growth retardation but without rhizomelia.

143 a and vascular abnormalities, causing severe growth retardation by E9.5 and death by E10.5, early dev

144 are more sensitive than wild-type plants to growth retardation by nanomolar concentrations of MTX, a

145 utosomal recessive disorder characterized by growth retardation, cancer predisposition, and sterility

146 myopathy, neutropenia, organic aciduria, and growth retardation caused by mutations in tafazzin.

147 e show that Hsp90 inhibitors rescue the axon growth retardation caused by overexpression of the LRRK2

148 kindreds, all of whom displayed intrauterine growth retardation, chronic neutropenia, and NK cell def

149 and underlies intra-uterine (and postnatal) growth retardation, chronic neutropenia, and NK cell def

150 he association of CALM/PICALM mutations with growth retardation, cognitive defects, and Alzheimer's d

151 ty for ionizing radiation, microcephaly, and growth retardation comparable to mutations in LIG4 and X

152 chemical gradient, aha2 mutant plants show a growth retardation compared with wild-type plants.

153 showed increased levels of serum glucose and growth retardation consistent with a severe diabetic sta

154 l blood pH, but exhibit increased mortality, growth retardation, corneal edema, and tooth enamel defe

155 Significant cell growth retardation could be observed for pathogenic bact

156 en entails metabolic costs and the resulting growth retardation could generally increase tolerance ag

157 RBS) is an autosomal recessive disorder with growth retardation, craniofacial abnormalities and limb

158 found that loss of Ube3b in mice resulted in growth retardation, decreased grip strength, and loss of

159 hat knockout of p21 can partially rescue the growth retardation defect of Ola1(-/-) embryos but fails

160 pe in developing zebrafish, characterized by growth retardation, delayed hindbrain formation, and emb

161 sitivity, microcephaly, facial dysmorphisms, growth retardation, developmental delay, and a variable

162 terized by bone marrow failure, intrauterine growth retardation, developmental delay, microcephaly, c

163 ild with classic features of hypothyroidism (growth retardation, developmental retardation, skeletal

164 ied mice with a syndromic disorder marked by growth retardation, diabetes, premature death, and sever

165 enotypes observed in ACH patients, including growth retardation, disproportionate shortening of the l

166 Severe growth retardation, distorted branches and up-curled lea

167 The ABI3p:OXA2a plants displayed growth retardation due to a reduction in the steady-stat

168 d-OXA2b-complemented plants displayed severe growth retardation due to a strong reduction in the stea

169 aternal smoke exposure results in fetal lung growth retardation due to dysregulation in various signa

170 useful therapeutic approach to intrauterine growth retardation due to placental vascular hypofunctio

171 These mice exhibited growth retardation due to reduced intestinal length as w

172 sirtuin 6 (Sirt6) in mice leads to postnatal growth retardation due to somatotropic attenuation throu

173 for a slightly elevated risk of intrauterine growth retardation during the second and third trimester

174 pofacial (CSCF) syndrome is characterized by growth retardation, dysmorphic facial features, brachyda

175 disorders including male infertility, early growth retardation, excessive weight gain in adulthood,

176 l expression during embryogenesis results in growth retardation, eye malformations, multiorgan pathol

177 rized by ID, ASD, microcephaly, intrauterine growth retardation, febrile seizures in infancy, impaire

178 ernal cobalamin may be associated with fetal growth retardation, fetal insulin resistance, and excess

179 printing of Gsalpha, resulting in preweaning growth retardation followed by catch-up growth.

180 on of Mettl14 leads to conspicuous embryonic growth retardation from embryonic d 6.5, mainly as a res

181 the tgd1-1 mutant background causes serious growth retardation, gametophytic defects and premature c

182 ar coloboma, heart defects, choanal atresia, growth retardation, genital abnormalities, and ear abnor

183 for 53BP1 modestly exacerbates phenotypes of growth retardation, genomic instability, and organismal

184 able degrees of neurodevelopmental delay and growth retardation harboring one of 13 heterozygous vari

185 larly speech delay), microcephaly, postnatal growth retardation, heart defects, and hand, foot, and l

186 ch is characterized in part by hypoglycemia, growth retardation, hypertriglyceridemia, hypercholester

187 hyperthermia, hypogonadotropic hypogonadism, growth retardation, hypoglycemia, myopathy, dilated card

188 f physical and neurologic anomalies, such as growth retardation; hypoplastic jaws crowded with multip

189 ouble-knockout (Smad1/5(dKO)) mice displayed growth retardation, hypothyroidism and defective follicu

190 at the age of 5 weeks, HGPS mutant mice show growth retardation, imbalanced gait and spontaneous frac

191 neck cancers, whereas BS is characterized by growth retardation, immunodeficiency, and a wide spectru

192 cell cycle arrest at the G1 phase and causes growth retardation in a panel of prostate cancer cells.

193 These defects result in severe growth retardation in a proportion of Tgif null embryos

194 ns are associated with diabetes mellitus and growth retardation in both rodents and humans.

195 Treatment with the TF:FVIIa inhibitor led to growth retardation in breast tumor models.

196 l as look at evidence for this phenomenon in growth retardation in certain groups of these individual

197 years, coinciding with the period of linear growth retardation in deprived children.

198 related to an increased risk of intrauterine growth retardation in four regions of a Maryland county

199 the fetal ovine pancreatic islets, and that growth retardation in hypothyroid fetal sheep is associa

200 cantly increased p53 protein levels and cell growth retardation in multiple cell lines.

201 n some animals and axial skeletal defects or growth retardation in others.

202 Growth retardation in recombinant PEDV carrying uncleava

203 utants, suggesting that ABA is implicated in growth retardation in such nutritional stress.

204 xic milk" causes inflammation, alopecia, and growth retardation in the nursing neonates.

205 Growth retardation in utero leading to small-for-gestati

206 PEDVAVCT12 harboring uncleavable N displayed growth retardation in Vero E6-APN cells compared to the

207 more, P. yoelii Deltamif parasites exhibited growth retardation in vivo.

208 ed that miR-494 induces a significant cancer growth retardation in vivo.

209 els resulted in reduced cell division rates, growth retardation, increased G:F actin ratios and letha

210 atic individuals were at risk of progressive growth retardation independent from the underlying disea

211 e characterized by severe pre- and postnatal growth retardation, indicating that CUL7 is closely asso

212 We conclude that intrauterine growth retardation induced by uteroplacental insufficien

213 lated individuals with severe prenatal-onset growth retardation, intellectual disability, and muscula

214 Growth retardation is a major adverse long-term outcome

215 x plants have more starch compared to wt and growth retardation is partially rescued by sucrose.

216 lacental insufficiency leads to intrauterine growth retardation (IUGR) and adult onset insulin resist

217 o 90 days of gestation leads to intrauterine growth retardation (IUGR) and increased prepubertal grow

218 Intrauterine growth retardation (IUGR) has been linked to the onset o

219 s this, we developed a model of intrauterine growth retardation (IUGR) in the rat that leads to diabe

220 Six2-KL(-/-) mice exhibited severe growth retardation, kyphosis, and premature death, close

221 d many phenotypes of H2AX-/- mice, including growth retardation, male infertility, immune defects, ch

222 ependent lethality, severe developmental and growth retardation, marked bradycardia and pericardial e

223 ) is a malformation syndrome associated with growth retardation, mental retardation, and immunodefici

224 a stark phenotype characterized by postnatal growth retardation, metabolic dysfunction, and lethality

225 iation (IR) and are variably associated with growth retardation, microcephaly, and neurodevelopmental

226 evelopmental delay, intellectual disability, growth retardation, microcephaly, and variable craniofac

227 ur individuals share several major features (growth retardation, microcephaly, digital abnormalities,

228 RAD21 have been identified in children with growth retardation, minor skeletal anomalies and facial

229 athy." Children with RAD21 mutations display growth retardation, minor skeletal anomalies, and facial

230 e to inadequate sun exposure and resulted in growth retardation, muscle weakness, skeletal deformitie

231 exhibited a wide range of defects, including growth retardation, neurodegeneration, muscular atrophy,

232 ohol exposure causes craniofacial anomalies, growth retardation, neurological abnormalities, cognitiv

233 We hypothesize that the embryonic growth retardation observed in Cited2 null embryos is du

234 , which explains the perinatal lethality and growth retardation observed in MEX3C-deficient mice.

235 is, insulin resistance, severe diabetes, and growth retardation observed in mice carrying N-ethyl-N-n

236 PSI photo damage, thus explaining the marked growth retardation observed in these conditions.

237 mma (or RARbeta and RARgamma) exhibit severe growth retardation obvious by about 3 weeks postnatally.

238 We proceed to show that growth retardation occurs through the induction of trans

239 disease characterized by metabolic acidosis, growth retardation, ocular abnormalities, and often dent

240 The growth retardation of CMS relative to the wild type was

241 a catalytically inactive MetAP2 resulted in growth retardation of HT1080 tumor cells, suggesting a d

242 t ORC1-H4K20me2-binding mutants, rescues the growth retardation of orc1 morphants.

243 ion of ROP results in repression of AOXI and growth retardation of P. pastoris cultured in YPM medium

244 In addition, KDM5C knockdown resulted in growth retardation of prostate cancer cells in vitro and

245 contrast, the magnitude of the toxin-induced growth retardation of target cells only weakly impacts t

246 Thus, while the growth retardation of the cPGES/p23(-/-) pups and decrea

247 y gene underlying both joint destruction and growth retardation of the KBD.

248 embrane domain of LRP4 (LRP4 ECD) results in growth retardation of the NMJ, and these defects are mar

249 The severe growth retardation of vte6 mutants was partially rescued

250 status of the neonate without indications of growth retardation or impaired neurologic function at bi

251 al anemia accompanied by either intrauterine growth retardation or neutropenia.

252 erized by neuropathology, immune deficiency, growth retardation or predisposition to cancer.

253 OR = 2.7, 95% CI: 1.2, 5.7) and intrauterine growth retardation (OR = 3.3, 95% CI: 1.2, 9.4).

254 g neonates suffer from alopecia, anaemia and growth retardation owing to elevated levels of pro-infla

255 tal insufficiency can result in intrauterine growth retardation, perinatal death and spontaneous abor

256 rprisingly, FACC1KO mice manifested skeletal growth retardation phenotype accompanied by decreased ch

257 All Hpse2 mutants have a growth retardation phenotype and die within a month afte

258 We observed a temperature sensitive growth retardation phenotype and specific decrease of he

259 ve oxidase content/activity, and displayed a growth retardation phenotype similar to that of the nduf

260 e exhibited a maternal-specific intrauterine growth retardation phenotype that resulted in a 33% redu

261 A growth retardation phenotype, a reduction in the amount

262 se mice are viable and fertile but display a growth retardation phenotype.

263 liceosome proteins cause microcephaly and/or growth retardation, phenotypes that are strongly linked

264 cient embryos exhibited embryonic lethality, growth retardation, polyhydramnios, cardiac ventricular

265 g early brain development, the ZIKV-mediated growth retardation potentially contributes to the neurod

266 eloid specific Flip-deficient mice exhibited growth retardation, premature death, and splenomegaly wi

267 g pregnancy are associated with intrauterine growth retardation, preterm birth, and fetal demise thro

268 Mis-specification and growth retardation rather than cell death most likely ac

269 RNA interference of delta resulted in growth retardation, reduced ATP synthase amounts, and in

270 /- mice exhibited severe metabolic acidosis, growth retardation, reduced plasma Na+, hyperal-dosteron

271 How mutated SHP2 induces growth retardation remains poorly understood.

272 Fancd2/Mlh1 double-mutant embryos displayed growth retardation resulting in embryonic lethality and

273 ult in the pathological consequences such as growth retardation seen in VGV mice.

274 ia, congenital cataracts, profound postnatal growth retardation, severe intellectual disability, and

275 opy both JATD and SRP type III by exhibiting growth retardation, shortening of the long bones, constr

276 y recapitulates the human pathology, showing growth retardation, skeletal and facial abnormalities, i

277 0-knockout mice died postnatally with severe growth retardation, skeletal defects, and kidney and lun

278 ously unidentified syndrome characterized by growth retardation, spine malformation, facial dysmorphi

279 g csCSF-1, both failed to completely correct growth retardation, suggesting a role for csCSF-1 in the

280 mutated in a mutually exclusive manner in 3M growth retardation syndrome and function in microtubule

281 Silver-Russell syndrome (SRS) is a growth retardation syndrome in which loss of methylation

282 a mutually exclusive manner in 3M and other growth retardation syndromes.

283 ing A(1)ARs (A(1)AR-/-) had much more severe growth retardation than A(1)AR+/+ or +/- embryos.

284 Double mutant animals show a more severe growth retardation than ob/ob mice with similar levels o

285 r perinatal respiratory failure or exhibited growth retardation that was not due to the renal disease

286 d that its up-regulation induces cancer cell growth retardation through multiple targets involved in

287 splays early-onset severe tonic seizures and growth retardation, thus recapitulating the human phenot

288 adulthood, thereby potentially linking fetal growth retardation to cardiovascular disease and diabete

289 antitumor activity, ranging from pronounced growth retardation to complete tumor regression.

290 and the grik1-1 grik2-1 double mutant shows growth retardation under regular growth conditions.

291 s4(fky/fky) mice include temporary fur loss, growth retardation, unsteady gait, and abnormal body pos

292 The cancer-specific growth retardation was mediated by an increased level of

293 luding exencephalia, anophthalmia and severe growth retardation were noted in heterozygous embryos, a

294 ntribute to microcephaly, pre- and postnatal growth retardation, which constitute the core clinical f

295 These mice displayed growth retardation with a significant reduction of body

296 deficiency results in a genetic syndrome of growth retardation with adrenal insufficiency and select

297 Null embryos at 3.5 d.p.c. reveal growth retardation with cells in mitotic disarray manife

298 o thrive within 2 weeks, displaying profound growth retardation with communicating hydrocephalus and

299 e map65-1 map65-2 mutants showed significant growth retardation with no obvious cell swelling, twisti

300 lay, microcephaly, absent speech, hypotonia, growth retardation with prenatal onset, feeding difficul