ライフサイエンスコーパス: dwarfism

1 tic form of short-limbed skeletal dysplasia (dwarfism).

2 and mutations in this gene result in severe dwarfism.

3 promotes the ERAD of bri1-9 and enhances its dwarfism.

4 nical H4K20me2 mark, via ORC1, in primordial dwarfism.

5 der resulting in severe skeletal defects and dwarfism.

6 es, sensorineural hearing loss and cachectic dwarfism.

7 chondroplasia, the most common form of human dwarfism.

8 the size of vegetative organs, resulting in dwarfism.

9 chondroplasia, the most common form of human dwarfism.

10 d by metaphyseal chondrodysplasia and severe dwarfism.

11 by 9 weeks of age they have mild short-limb dwarfism.

12 ertrophy, ossification of growth plates, and dwarfism.

13 PV/+) mice display the striking phenotype of dwarfism.

14 r identifying the defects that contribute to dwarfism.

15 chondroplasia, the most common form of human dwarfism.

16 oid accumulation, reduced lignin content and dwarfism.

17 han control littermates and develop a severe dwarfism.

18 to organogenesis, resulting in proportional dwarfism.

19 resulting in disorganized growth plates and dwarfism.

20 also cause glycogen or fat accumulation and dwarfism.

21 owth, causing several genetic forms of human dwarfism.

22 nging from developmental lethality to severe dwarfism.

23 n display cell elongation defects and severe dwarfism.

24 the basis for several genetic forms of human dwarfism.

25 ology of cotyledons, leaves and flowers; and dwarfism.

26 enes result in a similar achondroplasia-like dwarfism.

27 of syndromic craniosynostosis and short limb dwarfism.

28 hesis of bioactive brassinosteroids, causing dwarfism.

29 g enzyme CONSTITUTIVE PHOTOMORPHOGENESIS AND DWARFISM.

30 opment that underlies the development of 3-M dwarfism.

31 appears to be epistatic to Snell and Jackson dwarfism.

32 tions identified previously in thanatophoric dwarfism.

33 Mutations in this locus result in dwarfism.

34 use of GH secretagogues for the treatment of dwarfism.

35 tations in 29 individuals with microcephalic dwarfism.

36 at mutations that inhibit this process cause dwarfism.

37 e, in patients with microcephalic primordial dwarfism.

38 growth, and missense mutations in GC-B cause dwarfism.

39 ms with hypsarrhythmia, and dysproportionate dwarfism.

40 an disease characterized by microcephaly and dwarfism.

41 utant protein known to cause human pituitary dwarfism.

42 that is mutated in microcephalic primordial dwarfism.

43 ce loss of VHL in chondrocytes causes severe dwarfism.

44 or microcephalic osteodysplastic primordial dwarfism 1, and a hereditary intestinal polyposis condit

45 ad circumference 12 s.d. below the mean) and dwarfism (5 s.d. below the mean).

46 These mutations cause microcephalic dwarfism, a hypocellular disorder of extreme global grow

47 postnatal growth retardation, proportionate dwarfism, absence of the GHR and GH binding protein, gre

48 the most common genetic form of short-limbed dwarfism, achondroplasia (ACH), as well as neonatal leth

49 s, including the most common genetic form of dwarfism, achondroplasia (ACH).

50 ysplasias, including the most common form of dwarfism, achondroplasia.

51 m in mice, resulting in cardiac hypertrophy, dwarfism, alopecia, and prenatal mortality.

52 Kcne2-deficient mice had hypothyroidism, dwarfism, alopecia, goiter and cardiac abnormalities inc

53 Dwarfism also tends to occur where an important predator

54 rted question markJusl. Mill.) shows extreme dwarfism, altered leaf morphology, de-etiolation, and re

55 heritable form of murine pituitary-dependent dwarfism (Ames dwarf, df) has been positionally cloned,

56 anterior pituitary hypoplasia, hypopituitary dwarfism and a complete loss of mature lactotropes.

57 ondrodysplasia characterized by short-limbed dwarfism and a delay in endochondral ossification.

58 features of the disease include proportional dwarfism and a predisposition to develop a wide variety

59 in individuals with microcephalic primordial dwarfism and additional congenital anomalies, including

60 of biological pathways underlying primordial dwarfism and adds to a growing list of human diseases li

61 nt paralogs; their absence results in severe dwarfism and almost complete loss of fertility.

62 bri1 brl1 brl3 triple mutants enhance bri1 dwarfism and also exhibit abnormal vascular differentiat

63 family affected by microcephalic primordial dwarfism and biallelic mutation of RTTN was identified.

64 The alopecia, dwarfism and cardiac abnormalities were alleviated by tr

65 ects including neurodevelopmental disorders, dwarfism and cardiac arrhythmia.

66 osvoz1 osvoz2 double mutant exhibits strong dwarfism and cell death, and silencing of both genes via

67 t screening and future treatment of combined dwarfism and chondrodysplasia.

68 nction mutant allele chs3-2D exhibits severe dwarfism and constitutively activated defense responses,

69 pidermal fluorescence4-3 (ref4-3) results in dwarfism and constitutively repressed phenylpropanoid ac

70 Pat1 mutants exhibit dwarfism and de-repressed immunity dependent on the immu

71 th Dermo1-cre resulted in mice with skeletal dwarfism and decreased bone density.

72 served in Ddr2-deficient mice, which exhibit dwarfism and defective bone formation in the axial, appe

73 Here we report that the heterozygotes show dwarfism and develop spinal misalignment with age.

74 -CREB transgenic mice exhibited short-limbed dwarfism and died minutes after birth, apparently due to

75 e several skeletal disorders associated with dwarfism and early bone fusion.

76 t displayed a pleiotropic phenotype, extreme dwarfism and early flowering, which disclosed synergisti

77 al dysplasia (MED), is characterized by mild dwarfism and early-onset osteoarthritis and can result f

78 ias that result in mild to severe short-limb dwarfism and early-onset osteoarthrosis.

79 in DONSON as a common cause of microcephalic dwarfism and established DONSON as a critical replicatio

80 (pwe) that exhibits severe disproportionate dwarfism and female infertility.

81 27(Kip1) in mice give opposite phenotypes of dwarfism and gigantism.

82 ases, shows pleiotropic phenotypes including dwarfism and hypersensitivity to osmotic/salt stress.

83 NMT3 induces severe PC deficiency leading to dwarfism and impaired development.

84 droplasia (ACH) is the most frequent form of dwarfism and is caused by gain-of-function mutations in

85 ndrocyte functions, resulting in progressive dwarfism and kyphosis in mice.

86 but some survived and developed progressive dwarfism and lordosis of the cervical spine.

87 ther single mutant, which include pronounced dwarfism and lung abnormalities.

88 use mutant, chagun, that is affected by both dwarfism and male infertility.

89 compromised in Mia3-null embryos, leading to dwarfism and neonatal lethality.

90 Both dwarfism and NIDDM are most likely due to the loss of ex

91 t a phenotype reminiscent of both Laron-type dwarfism and non-insulin-dependent diabetes mellitus (NI

92 ssed nasal bridge, as well as the rhizomelic dwarfism and nonossifying bone lesions that are characte

93 able deficiencies of aggrecan exhibit severe dwarfism and premature death, demonstrating the essentia

94 es in growth rates and morphology, including dwarfism and reduced apical dominance.

95 nd typical GA deficiency phenotypes, such as dwarfism and reduced fertility.

96 A, transgenic plants exhibited phenotypes of dwarfism and reduced organ size.

97 hanism for the pathogenesis of microcephalic dwarfism and show a surprising but important development

98 ransgenic DKO mice were completely free from dwarfism and spinal defects.

99 asone to these plants greatly alleviates the dwarfism and sterility and substantially reverses the bi

100 e plant types with defects including extreme dwarfism and sterility, leading to poor yield potential.

101 Inactivation of CDKF;1 causes extreme dwarfism and sterility.

102 imate 3'-hydroxylase (C3'H), exhibits severe dwarfism and sterility.

103 espondingly smaller, indicating proportional dwarfism and suggesting a systemic cause for the overall

104 affected by severe microcephalic primordial dwarfism and tested negative on clinical exome sequencin

105 ion in the KAKTUS (KAK) gene that suppressed dwarfism and the collapsed xylem character, the cause of

106 vo has implications for future research into dwarfism and, particularly, growth and development of th

107 d sulfate for sulfation reactions results in dwarfism, and a complete loss of activated sulfate synth

108 inergic tone, anterior pituitary hypoplasia, dwarfism, and an inability to lactate.

109 using several diseases such as microcephaly, dwarfism, and cancer.

110 forms of OSD exhibit vitreous dysplasia and dwarfism, and could serve as an animal model for the dis

111 iofacial dysmorphism, arthritis, osteopenia, dwarfism, and fibrosis of soft tissues due to ablation o

112 nathia, rhizomelic shortening, microcephalic dwarfism, and mild developmental delay due to loss-of-fu

113 genes in mice leads to behavioral problems, dwarfism, and multiple other phenotypes including increa

114 -Gorlin syndrome (MGS), a form of primordial dwarfism, and ORC1 depletion in zebrafish results in an

115 expression in mice is known to cause severe dwarfism, and targeted deletion of STC2 causes increased

116 led to developmental abnormalities including dwarfism, anophthalmia, and 80% embryonic lethality.

117 These benefits of male dwarfism apply well to Osedax (Annelida: Siboglinidae),

118 nd ecological implications of a loss of male dwarfism are discussed.

119 Little is known, however, about the basis of dwarfism as a common element in these diverse signaling

120 NH3 knockdown in Arabidopsis thaliana caused dwarfism as the result of a reduced number of mitotic di

121 Overactive defense signaling can result in dwarfism as well as developmental defects.

122 Mice lacking SAFB1 exhibited dwarfism, as a result of in utero growth retardation, an

123 hondrodysplasia, a rare form of short-limbed dwarfism associated with hypercalcemia and normal or low

124 Overexpression of XND1 resulted in extreme dwarfism associated with the absence of xylem vessels an

125 rovides a potential mechanism for primordial dwarfism associated with this lesion, since reduced m(7)

126 n humans, has now been shown to cause severe dwarfism but not neonatal death.

127 growth deficiency (microcephalic primordial dwarfism), but the genetic heterogeneity is probably mor

128 Npr2) gene cause a rare form of short-limbed dwarfism, but its physiological effects have not been we

129 ses enhanced main shoot dominance and tiller dwarfism by an unknown mechanism.

130 This induced dominant dwarfism by local feedback inhibition of GRF.

131 uggesting that the mutated amino acid causes dwarfism by preventing an interaction needed for its deg

132 in Rht-B1 and Rht-D1 confer "GA-insensitive" dwarfism by producing DELLA proteins that do not bind th

133 es Rht-B1b and Rht-D1b are thought to confer dwarfism by producing more active forms of these growth

134 extending conditions, including Prop1(df/df) dwarfism, calorie restriction or dietary rapamycin.

135 ery large decreases (such as extreme insular dwarfism) can happen at more than 10 times the rate of i

136 sent PRKG2 R678X as a causative mutation for dwarfism cattle.

137 lar to achondroplasia, the most common human dwarfism, caused by activating mutations in FGFR3.

138 ng abnormalities resembling atelectasis, and dwarfism characterized by aberrant cartilage morphology.

139 that a double knockout of ALA4/5 results in dwarfism, characterized by reduced growth in rosettes (6

140 ablation in the same cell population caused dwarfism, chondrodysplasia and exostoses.

141 of a constitutive stress response, including dwarfism, closed stomata, and anthocyanin accumulation,

142 recessive disease that results in primordial dwarfism, cognitive deficiencies, and increased sensitiv

143 The iput1 mutants show severe dwarfism, compromised pollen tube guidance, and constitu

144 We show that the severe dwarfism conferred by Rht-B1c is caused by an intragenic

145 Those include dwarfism, constitutive ERK1/2 activation, strongly reduc

146 rant, dominant postnatal lethality, skeletal dwarfism, coronal craniosynostosis and hearing loss; phe

147 Dwarfism correlates with shorter, less mineralized and f

148 Dwarfism could be rescued by the application of brassino

149 s in mammals and suggest that the process of dwarfism could in principle explain small brain size, a

150 bidopsis constitutive photomorphogenesis and dwarfism (cpd) mutant.

151 (det2), constitutive photomorphogenesis and dwarfism (cpd), brassinosteroid insensitive1 (bri1), and

152 nd specific developmental defects, including dwarfism, craniofacial abnormalities and brachymesophala

153 inherited human disease syndromes, including dwarfism, craniosynostosis, heritable cancer susceptibil

154 opic developmental defects, including severe dwarfism, dark green leaves, reduced apical dominance, a

155 The phenotype of TgHMW mice included dwarfism, decreased bone mineral density (BMD), osteomal

156 uding abnormal seedling and leaf phenotypes, dwarfism, delayed flowering and no apical dominance, sug

157 ng of OsGRF3, OsGRF4, and OsGRF5 resulted in dwarfism, delayed growth and inflorescence formation, an

158 e results in a pleiotropic phenotype showing dwarfism, delayed puberty, reduced female reproductive f

159 -terminus linked to Meier-Gorlin syndrome, a dwarfism disorder, impedes proper recruitment of Orc6 in

160 yndrome (ATR-SS), a microcephalic primordial dwarfism disorder.

161 Dwarfism disproportionately affects long bones and is ch

162 s homozygous Amish EVC mutations causing EvC dwarfism do so by disrupting sonic hedgehog (Shh) signal

163 chlorosis, increased light sensitivity, and dwarfism due to decreased levels of chlorophylls, carote

164 subsequent depletion of cilia and post-natal dwarfism due to premature loss of the growth plate likel

165 been identified for microcephalic primordial dwarfism, encoding proteins involved in fundamental cell

166 we characterized 2 patients with primordial dwarfism, extreme insulin resistance, and gonadal failur

167 Male dwarfism has evolved multiple times in a range of animal

168 tion of Prop1, the gene responsible for Ames dwarfism, has been localized within the contig.

169 Several genetic forms of human dwarfism have been linked to activating mutations in FGF

170 lar defects in mouse models of overgrowth or dwarfism helps to identify the key genes and pathways th

171 ese results, smr1-1 partially suppressed the dwarfism, high SA levels, and cell death phenotypes in a

172 me, microcephalic osteodysplastic primordial dwarfism I [MOPD] types I and II, and Meier-Gorlin syndr

173 rare human genetic disorder characterized by dwarfism, immunodeficiency, genomic instability and canc

174 e (BS) is a genetic disorder associated with dwarfism, immunodeficiency, reduced fertility, and an el

175 pedigree to identify the mutation underlying dwarfism in American Angus cattle.

176 function mutations in AtIWS1 lead to overall dwarfism in Arabidopsis, reduced BR response, genome-wid

177 n understanding the etiology of proportional dwarfism in BS.

178 Similarly, primordial dwarfism in domesticated animals is linked to positive s

179 plasia is the most common form of short limb dwarfism in human beings, affecting more than 250,000 in

180 chondroplasia (ACH), the most common genetic dwarfism in human, is caused by a gain-of function mutat

181 s comprises the most common genetic forms of dwarfism in humans and includes achondroplasia, hypochon

182 plasia is the most prevalent genetic form of dwarfism in humans and is caused by activating mutations

183 Achondroplasia, the most common form of dwarfism in humans, results from a G380R mutation in FGF

184 last growth factor receptor 3 (FGFR3), cause dwarfism in humans.

185 ondroplasia, the most common genetic form of dwarfism in humans.

186 Activating mutations of its c isoform cause dwarfism in humans; somatic mutations can drive oncogeni

187 rtebrates from gigantism in small species to dwarfism in large species.

188 role is further supported by the presence of dwarfism in mice overexpressing STC1.

189 CMG assembly and recapitulates microcephalic dwarfism in mice.

190 utations in RNU4ATAC is linked to primordial dwarfism in microcephalic osteodysplastic primordial dwa

191 endochondral bones was evident, resulting in dwarfism in mutant mice.

192 Here, we show that this dwarfism in pea (Pisum sativum) is not attributable to t

193 r bone growth and the resulting short-limbed dwarfism in the mutant mice.

194 cylic acid is unlikely to be responsible for dwarfism in this mutant.

195 an intraspecific 'late ontogenetic' model of dwarfism in which brain size scales to body size with an

196 with an apparently novel form of primordial dwarfism in which severe growth deficiency is accompanie

197 are associated with decreased body weights (dwarfism), increased longevity, increased resistance to

198 exhibit specific endocrine phenotypes, i.e. dwarfism, infertility, and diabetes.

199 Besides skeletal dwarfism, internal organs are correspondingly smaller, i

200 Primordial dwarfism is a group of human single-gene disorders with

201 Primordial dwarfism is a state of extreme prenatal and postnatal gr

202 3-M primordial dwarfism is an inherited disease characterized by severe

203 Dwarfism is associated with reduced abundance of a small

204 The mechanism underlying 3-M dwarfism is not clear.

205 es evidence that lignin-modification-induced dwarfism is not merely due to compromised water transpor

206 these techniques for stature lengthening in dwarfism is somewhat less widespread.

207 ondroplasia, the most common genetic form of dwarfism, is an autosomal dominant disorder whose underl

208 chondroplasia (ACH), the most common form of dwarfism, is an inherited autosomal-dominant chondrodysp

209 lasia, the most common genetic form of human dwarfism, is caused by a similar transmembrane domain mu

210 ondroplasia, the most common genetic form of dwarfism, is caused by mutations in FGFR3.

211 chondroplasia, the most common form of human dwarfism, is due to a G380R mutation in the transmembran

212 omal recessively inherited chondrodysplastic dwarfism, is frequent among Old Order Amish of Pennsylva

213 Abnormal growth plate function, resulting in dwarfism, is the consequence of mutations in receptors f

214 acterized by neonatal lethality and profound dwarfism, is the result of FGFR3 mutations, including an

215 ized epi-metaphyseal dysplasia, short-limbed dwarfism, joint laxity and early onset osteoarthritis.

216 l dysplasia, including the neonatally lethal dwarfism known as thanatophoric dysplasia.

217 rred other general growth defects, including dwarfism, late flowering, and smaller seeds.

218 Phenotypes include dwarfism, leaf twisting, disorganized differentiation of

219 Although the microcephaly- and primordial dwarfism-linked centrosomal protein CEP215 has been impl

220 rogeroid phenotypes, such as short lifespan, dwarfism, lipodystrophy, sarcopenia, and low cardiac str

221 The dwarfism locus was fine-mapped to BTA6 between markers A

222 eatures, including short lifespan, cachectic dwarfism, lordokyphosis, cataracts, loss of subcutaneous

223 settes, floral organ defects, low fertility, dwarfism, loss of apical dominance, and altered response

224 rproduction in Arabidopsis thaliana leads to dwarfism, making in planta assessment of SA effects diff

225 lso causes pleiotropic phenotypes, including dwarfism, male sterility and the development of swelling

226 ble way of treating the ER stress-associated dwarfism MCDS.

227 The short-limbed dwarfism metaphyseal chondrodysplasia type Schmid (MCDS)

228 cterized by intrauterine growth retardation, dwarfism, microcephaly and mental retardation.

229 (XP20BE) who had severe symptoms of CS, with dwarfism, microcephaly, retinal degeneration, and mental

230 oth genes via RNA interference also leads to dwarfism, mild cell death, and enhanced resistance to M.

231 and microcephalic osteodysplastic primordial dwarfism (MOPD II), both of which are characterized by g

232 e a common cause of microcephalic primordial dwarfism (MPD), a phenotype characterized by prenatal-on

233 ontribute to the pronounced microcephaly and dwarfism observed in these individuals by altering centr

234 ell division and cell expansion underlie the dwarfism of an Arabidopsis lignin mutant ref8, and repor

235 sitive receptor, indicated by suppression of dwarfism of BR-deficient and BR-perception mutants and b

236 d has been questioned in the special case of dwarfism of mammals on islands.

237 Severe dwarfism of psi2-1 psi3-1 plants results from reduced ce

238 In contrast, the extreme dwarfism of Rht-D1c is due to overexpression of the semi

239 oring the BR sensitivity and suppressing the dwarfism of the bri1-9 mutant.

240 encoding a DNAJ protein, is involved in the dwarfism of the med5 mutants.

241 nd mur10 co-segregated with reduced vigor or dwarfism of the plants.

242 y but did not rescue either the short-limbed dwarfism or decreased chondrocyte proliferation.

243 ecular basis of two patients with primordial dwarfism (PD) in a single family through utilization of

244 g a potential mechanism for microcephaly and dwarfism phenotypes.

245 failure, neurological dysfunction, cachetic dwarfism, photosensitivity, sensorineural hearing loss,

246 ns in the parent organism (e.g., shrubbiness/dwarfism, pleiocotyly, abnormal leaf morphogenesis, dist

247 e disorder characterized by disproportionate dwarfism, polydactyly, and congenital heart disease.

248 ed dramatic developmental defects, including dwarfism, reduced apical dominance, extreme longevity, d

249 These changes were associated with dwarfism, reduced carbon dioxide assimilation, and accel

250 ve phenotypes including delayed germination, dwarfism, reduced fertility, and overaccumulation of the

251 sults in GA-insensitive phenotypes including dwarfism, reduced fertility, delayed flowering, and incr

252 e entire ERECTA family genes led to striking dwarfism, reduced lateral organ size and abnormal flower

253 xhibit strong pleiotropic effects, including dwarfism, reductions in chlorophyll levels, photosynthet

254 icular skeleton lengths, and improvements in dwarfism-related clinical features included flattening o

255 Tcf1-/- mice have type 2 diabetes, dwarfism, renal Fanconi syndrome, hepatic dysfunction an

256 tion complex, cause microcephalic primordial dwarfism resembling Meier-Gorlin syndrome.

257 (GH) insensitivity syndrome] is a hereditary dwarfism resulting from defects in the GH receptor (GHR)

258 Dwarfism results when this process is disrupted, as in t

259 which is non-lethal and presents less severe dwarfism, results almost exclusively from a G380R substi

260 ce resulted in phenotypic changes, including dwarfism, rickets, osteomalacia, hypophosphatemia, incre

261 The proportional dwarfism seen in the human is consistent with the small

262 Homozygous mutants exhibit extreme dwarfism, sexual infantilism and significant perinatal m

263 )) mouse results in a novel form of juvenile dwarfism, suggesting smpd3 is a polygenetic determinant

264 outbreak, in China, of duck beak atrophy and dwarfism syndrome (BADS) was investigated using electron

265 ndrome) is an autosomal recessive primordial dwarfism syndrome characterized by absent or hypoplastic

266 ans, CUL7 was found to be mutated in the 3-M dwarfism syndrome characterized by severe pre- and postn

267 S) is a genetically heterogeneous primordial dwarfism syndrome known to be caused by biallelic loss-o

268 terozygous mutations in SOX9 lead to a human dwarfism syndrome, Campomelic dysplasia.

269 n FGF receptor 3 (FGFR3) cause several human dwarfism syndromes by affecting both chondrocyte prolife

270 mutations cause several craniosynostoses and dwarfism syndromes in humans.

271 rlying cause of several craniosynostoses and dwarfism syndromes in humans.

272 cts the embryonic onset of a neonatal lethal dwarfism, thanatophoric dysplasia type II (TDII).

273 Two particularly severe dwarfisms, thanatophoric dysplasia type II (TDII) and se

274 progressive dysplasia and have short-limbed dwarfism that is consistent in severity with the relevan

275 ernebrae and, in addition, exhibit postnatal dwarfism that is coupled to significantly decreased expr

276 , cause a form of osteodysplastic primordial dwarfism that is sometimes reported to be associated wit

277 igh redundancy was lost, and gid1a exhibited dwarfism that was strongly exacerbated by the loss of an

278 the additional features of disproportionate dwarfism, thoracic dysplasia, and congenital heart disea

279 ssibility that loss of its function produces dwarfism through reduced tolerance of replicative stress

280 hx3 W227ter mice survive, but display marked dwarfism, thyroid disease, and female infertility.

281 the genetic basis for a recessive brachytic dwarfism trait (dw) in peach (Prunus persica) that has l

282 in microcephalic osteodysplastic primordial dwarfism type 1, Roifman syndrome, and Lowry-Wood syndro

283 ith microcephalic osteodysplastic primordial dwarfism type I (MOPD I), a severe developmental disorde

284 CPH) and Majewski osteodysplastic primordial dwarfism type II (MOPDII) are both genetic diseases that

285 Majewski osteodysplastic primordial dwarfism type II (MOPDII) is caused by mutations in the

286 rome and Majewski osteodysplastic primordial dwarfism type II) have implicated fundamental cellular p

287 ski/microcephalic osteodysplastic primordial dwarfism type II, making a detailed understanding of its

288 A crippling dwarfism was first described in the Miniature Poodle in

289 fed a high P(i) diet, BMD was increased, and dwarfism was partially reversed.

290 Historically, dwarfism was the major genetic defect in U.S. beef cattl

291 mise ER retention of bri1-9 and suppress its dwarfism, whereas EBS2 over-expression enhances its dwar

292 Strikingly, these mice show marked dwarfism, which is first detectable around weaning, and

293 h, knockdown of the NSMCE2 ortholog produced dwarfism, which was ameliorated by reexpression of WT, b

294 ons severely limit bone growth, resulting in dwarfism, while inactivating mutations significantly enh

295 rogyria, to include microcephalic primordial dwarfism with a complex brain phenotype involving simpli

296 trophic zone creating a phenotype resembling dwarfism with chondrodysplasia.

297 ouse embryos produces a similar phenotype of dwarfism with decreased chondrocyte proliferation, delay

298 sition 369 (Gly369Cys) in mouse FGFR3 causes dwarfism with features mimicking human achondroplasia.

299 eted deletion of Ihh results in short-limbed dwarfism, with decreased chondrocyte proliferation and e

300 nconspicuous differences in size but develop dwarfism within the first 4 weeks of life.