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1 dia, genitourinary malformations, and mental retardation).
2 , lipodystrophy, hepatosteatosis, and growth retardation.
3  of the 5 patients also had postnatal growth retardation.
4 us human disorders, such as perinatal growth retardation.
5 udley syndrome, characterized by psychomotor retardation.
6 phism, cardiac defects, and postnatal growth retardation.
7  symptoms of reduced motivation and/or motor retardation.
8 e related to symptoms of anhedonia and motor retardation.
9  lead to important, sometimes lethal, growth retardation.
10 to cerebral palsy, hydrocephalus, and mental retardation.
11 esented with epilepsy and severe psychomotor retardation.
12 zed for generalized seizures and psychomotor retardation.
13 umulation in rcy1Delta cells leads to growth retardation.
14 ch manifests as joint deformities and growth retardation.
15 a, hypotonia, oculomotor apraxia, and mental retardation.
16 alth effects, including cretinism and growth retardation.
17 ing animals exhibiting a lifelong 20% growth retardation.
18 ult in Phenylketonuria, a progressive mental retardation.
19 etinal dysplasia, microcephaly and/or mental retardation.
20 bination PIT showed significant tumor growth retardation.
21 impairment, including ataxia and psychomotor retardation.
22 he mutation causes dominant postnatal growth retardation.
23 ylase associated with human syndromic mental retardation.
24                Silencing of fragile X mental retardation 1 (FMR1) gene and loss of fragile X mental r
25 ansion in the 5'-UTR of the fragile X mental retardation 1 (FMR1) gene is known as a premutation.
26 es disrupted by loss of the Fragile X Mental Retardation 1 (Fmr1) gene.
27 (55-200 CGG repeats) of the fragile X mental retardation 1 (FMR1) gene.
28  (PNs) in the cerebellum of Fragile X Mental Retardation 1 (Fmr1) knockout (KO) mice, a model of Frag
29 l tissue from wide type and fragile X mental retardation 1 (Fmr1) knockout mice, we show that variabl
30 dritic spine defects of the Fragile X Mental Retardation 1 gene KO neurons.
31       Finally, upregulating fragile X mental retardation 1 protein (Fmr1, also called FMRP) acts inde
32 analysis converged on FMR1 (Fragile X Mental Retardation 1), an important negative regulator of APP t
33 complex subunit cytoplasmic fragile X mental retardation 1-interacting protein 1 (Cyfip1).
34  silencing of the X-linked, fragile-X mental retardation-1 (FMR1) gene.
35 rotein-like 2 (Cntnap2)(5), fragile X mental retardation-1 (Fmr1)(6) or Sh3 and multiple ankyrin repe
36 mpairment might have resulted in less growth retardation after pediatric kidney transplantation (KT)
37 on of ANAC017 in Arabidopsis leads to growth retardation, altered leaf development with decreased cel
38 ith pathogenic BCS1L variants include growth retardation, aminoaciduria, cholestasis, iron overload,
39 eads to increased R-loop levels, cell growth retardation and accumulation of gammaH2AX, a marker for
40  in the most common inherited form of mental retardation and autism, fragile X syndrome (FXS).
41 inked hypophosphatemia (XLH) leads to growth retardation and bone deformities, which are not fully av
42 cterized by severe pre- and postnatal growth retardation and by mutually exclusive mutations in three
43   Given that Cullin4B mutations cause mental retardation and cerebral malformation, similar regulator
44 N cause infantile hypotonia with psychomotor retardation and characteristic facies (IHPRF).
45 (CMV) infection is a leading cause of mental retardation and deafness in newborns.
46 l CMV infection is a leading cause of mental retardation and deafness in newborns.
47                         We showed that local retardation and degree of polarization provide a robust
48 tch dysregulation are associated with mental retardation and dementia are poorly understood.
49 erm delivery, low birth weight, fetal growth retardation and developmental defects.
50 oxidative stress can ultimately cause growth retardation and developmental defects.
51 f NAA50 expression resulted in severe growth retardation and infertility in two Arabidopsis transfer
52 neurological disorder associated with mental retardation and intractable epilepsy, and Miller-Dieker
53 ven vascular storm included placental growth retardation and intrauterine growth restriction, evidenc
54 luding methylmalonic acidemia, severe growth retardation and lethality.
55                           Conversely, ageing retardation and lifespan extension were achieved in mid-
56  sensitive to salinity stress causing growth retardation and loss in productivity.
57 ed with normal skin with heterogeneous local retardation and low degree of polarization, HTS was char
58 cursor cells (OPC) in mice results in growth retardation and markedly decreased bone mass with impair
59 ml CA-4 treatments resulted in developmental retardation and morphological malformation, and led to p
60 H supplementation was able to correct growth retardation and muscle weakness.
61 nflammatory phenotype associated with growth retardation and paw swelling.
62  disorder characterized by severe neuromotor retardation and progressive loss of vision, leading to b
63                                    Using gel-retardation and RNA/DNA competition assays, we found tha
64 , and correlated with the severity of growth retardation and the in vitro cellular phenotype.
65  the most prevalent form of inherited mental retardation and the primary monogenetic cause of autism.
66 logical disorders, including X-linked mental retardation and tumorigenesis.
67 elopment (collectively abbreviated as mental retardation and/or disorders of psychological developmen
68 se of the heart and the renal tract), growth retardation, and a recognizable facial gestalt (interrup
69 rial biosynthesis and clearance, cell growth retardation, and cellular senescence of DC fibroblasts.
70 xclusion criteria included amblyopia, mental retardation, and concomitant ocular disease that limited
71  two siblings with congenital ataxia, mental retardation, and developmental delay.
72 rological disorder cerebellar ataxia, mental retardation, and disequilibrium (CAMRQ) syndrome, strong
73 rological disorder cerebellar ataxia, mental retardation, and disequilibrium (CAMRQ) syndrome.
74 eviously linked to cerebellar ataxia, mental retardation, and disequilibrium syndrome 2, cause severe
75 sk of status dystonicus, intrauterine growth retardation, and endocrinopathies.
76 ional symptoms, such as anergia, psychomotor retardation, and fatigue.
77 orm of mild syndromic ID with ptosis, growth retardation, and hypotonia, and we identified an inherit
78 isorders are macrocephaly, absence of growth retardation, and more variability in the degree of intel
79 d our understanding of diet-dependent growth retardation, and offers a potential mechanism to treat o
80 seizures, one subject exhibiting mild mental retardation, and one subject exhibiting retinitis pigmen
81 aphy background, developmental regression or retardation, and onset before 1 year of age.
82 l response, poor treatment adherence, growth retardation, and presentation in advanced phases).
83 ess, onychodystrophy, osteodystrophy, mental retardation, and seizures), a condition that includes se
84 dly amenable to experimental acceleration or retardation, and serves as a constitutional component fo
85 tion, results in increased apoptosis, growth retardation, and, ultimately, embryonic death.
86 re promising candidates for integrated phase retardation applications due to their large optical bire
87 ystals are inherently inadequate for optical retardation applications since the supported polaritonic
88 range of values reported for hydration water retardation as a logical consequence of the different le
89                        Using gel banding and retardation as a read-out for protein adsorption, we opt
90 reated promptly in infancy, can cause mental retardation, as the TH decrease results in improper deve
91 with bulkier thiolates causing dramatic rate retardations, as well as (2) the thermodynamics of the s
92 ng factors, in vitro transcriptional and gel retardation assays revealed that the RpoN-recognized P2
93         Only a few genetic studies of growth retardation associated with the KBD have been carried ou
94  are specifically linked to epilepsy, mental retardation, autism, schizophrenia and neuro-degeneratio
95     The RNA-binding protein fragile-X mental retardation autosomal 1 (FXR1) is upregulated in head an
96  expression levels of FXR1 (fragile X mental retardation autosomal homolog 1), an RNA-binding protein
97                             Fragile-X mental retardation autosomal homologue-1 (FXR1) is a muscle-enr
98  display partial embryonic lethality, growth retardation, brain disorders, and maternal effect lethal
99 s, all of whom displayed intrauterine growth retardation, chronic neutropenia, and NK cell deficiency
100 derlies intra-uterine (and postnatal) growth retardation, chronic neutropenia, and NK cell deficiency
101 d to calculate first-order removal rates and retardation coefficients via a one-dimensional reactive
102 ionizing radiation, microcephaly, and growth retardation comparable to mutations in LIG4 and XRCC4, w
103 ne-treated groups showing significant myopic retardation compared to the control group.
104  pH, but exhibit increased mortality, growth retardation, corneal edema, and tooth enamel defects.
105                      Significant cell growth retardation could be observed for pathogenic bacteria (e
106 ), craniometaphyseal dysplasia (CMD), mental retardation, deafness and ankylosis syndrome (MRDA).
107 hat loss of Ube3b in mice resulted in growth retardation, decreased grip strength, and loss of vocali
108 ckout of p21 can partially rescue the growth retardation defect of Ola1(-/-) embryos but fails to res
109  reductively retarded at Hanford site with a retardation degree dependent on reactive Fe(II) content
110 e overexpression are thought to cause mental retardation, dementia and seizure in this disorder.
111 xhibit a similar pattern of Fe(II) oxidation retardation derived from elevated silicate concentration
112 e with a syndromic disorder marked by growth retardation, diabetes, premature death, and severe lymph
113 s observed in ACH patients, including growth retardation, disproportionate shortening of the limbs, r
114                                Severe growth retardation, distorted branches and up-curled leaves wer
115 pmental delay/intellectual disability/mental retardation, Down syndrome, cerebral palsy, autism spect
116      The ABI3p:OXA2a plants displayed growth retardation due to a reduction in the steady-state abund
117 -complemented plants displayed severe growth retardation due to a strong reduction in the steady-stat
118  smoke exposure results in fetal lung growth retardation due to dysregulation in various signaling pa
119  therapeutic approach to intrauterine growth retardation due to placental vascular hypofunction.
120 l (CSCF) syndrome is characterized by growth retardation, dysmorphic facial features, brachydactyly w
121 a rare Mendelian phenotype comprising severe retardation, early onset epileptic seizures, optic nerve
122 ability and luminous efficiency based on its retardation effect in reorientation.
123 EEG response, however, when tilted such that retardation effects are operative, the sEEG signal emerg
124 l response of metal nanoparticles, including retardation effects, without the requirement of large co
125 ipid nanostructures possessed superior tumor retardation effects.
126 rientations are also investigated to explore retardation effects.
127                      MEDNIK syndrome (mental retardation, enteropathy, deafness, peripheral neuropath
128 ers including male infertility, early growth retardation, excessive weight gain in adulthood, heterot
129 easurement of Orbitrap and comparison of the retardation factors with standards.
130 y ID, ASD, microcephaly, intrauterine growth retardation, febrile seizures in infancy, impaired speec
131 obalamin may be associated with fetal growth retardation, fetal insulin resistance, and excess adipos
132 f 55-200 CGG repeats in the Fragile X mental retardation (FMR1) gene.
133 ettl14 leads to conspicuous embryonic growth retardation from embryonic d 6.5, mainly as a result of
134 ions of flow field profiles and hydrodynamic retardation functions.
135 grees of neurodevelopmental delay and growth retardation harboring one of 13 heterozygous variants in
136 lt in permanent neurological defects, mental retardation, hearing loss, visual impairment, and pregna
137  a regulatory loop with the fragile X mental retardation homologue FXR1 and regulates dopamine D2 rec
138 cal and neurologic anomalies, such as growth retardation; hypoplastic jaws crowded with multiple supe
139 nockout (Smad1/5(dKO)) mice displayed growth retardation, hypothyroidism and defective follicular arc
140 sorder that leads to brain damage and mental retardation if untreated.
141 cle arrest at the G1 phase and causes growth retardation in a panel of prostate cancer cells.
142 velength and maintain the quarter-wave phase retardation in broadband, while the turbine blades consi
143 ransporter 8 (MCT8) cause severe psychomotor retardation in children.
144 ssive disorder that results in severe mental retardation in early adulthood.
145 19) cause female-limited epilepsy and mental retardation in humans.
146 ecular pathomechanism of epilepsy and mental retardation in humans.
147 b locus associate with depression and mental retardation in humans.
148 tal ovine pancreatic islets, and that growth retardation in hypothyroid fetal sheep is associated wit
149                                       Growth retardation in recombinant PEDV carrying uncleavable N s
150 urrently in countries such as Brazil) due to retardation in solute flow associated with the fine root
151  suggesting that ABA is implicated in growth retardation in such nutritional stress.
152                                              Retardation in the degraded chain is given by a simple s
153 , knocking out EVI and MDS/EVI causes severe retardation in the growth and development of the tadpole
154 T12 harboring uncleavable N displayed growth retardation in Vero E6-APN cells compared to the wild-ty
155 dividuals were at risk of progressive growth retardation independent from the underlying disease and
156 ndividuals with severe prenatal-onset growth retardation, intellectual disability, and muscular hypot
157 g to directly measure the birefringent phase retardation introduced by metasurface wave plates with a
158 edium whereas inside neuronal dendrites this retardation is 70%.
159                                       Growth retardation is a major adverse long-term outcome among B
160 ral cortex, an important target since mental retardation is an important component of many of the hum
161 mulations of model peptides suggest that the retardation is due to an underlying general physicochemi
162 ater dynamics, whereas protein-induced water retardation is weaker and dominates only at distances be
163 S), the most common form of inherited mental retardation, is caused by silencing of the FMR1 gene.
164 systemic neuromuscular phenotype with mental retardation, leading to premature death at age 36 years
165 ental delay, intellectual disability, growth retardation, microcephaly, and variable craniofacial dys
166 posure causes craniofacial anomalies, growth retardation, neurological abnormalities, cognitive impai
167 ulin resistance, severe diabetes, and growth retardation observed in mice carrying N-ethyl-N-nitrosou
168 to damage, thus explaining the marked growth retardation observed in these conditions.
169                 With mutation and selection, retardation occurs only when S, the product of twice the
170               We proceed to show that growth retardation occurs through the induction of transcriptio
171  characterized by metabolic acidosis, growth retardation, ocular abnormalities, and often dental abno
172 ad, which could be principally attributed to retardation of amylopectin retrogradation in the presenc
173 o mechanisms of glass formation: (i) kinetic retardation of atom rearrangement or structural relaxati
174 ons of 3D-spheroid size and shape as well as retardation of cell cycle and induction of apoptosis hav
175                                              Retardation of diclofenac was reflected in additional (1
176 mechanisms of resistance within a biofilm is retardation of drug diffusion due to poor penetration ac
177 ength of interaction), which originates from retardation of electromagnetic waves at the distances co
178 rom light-induced damage despite significant retardation of FTY720 phosphorylation in Sphk2 KO mice.
179                    Weak coupling resulted in retardation of growth and differentiation.
180 ar catabolic routes were supported by severe retardation of growth of the DeltandbC mutant under ligh
181 rticipants; however, improvement in GA area, retardation of growth, or visual acuity were not demonst
182  eye, Heart defects, Atresia of the choanae, Retardation of growth/development, Genital abnormalities
183                This phenotype was due to the retardation of LRP emergence.
184 rsible sorption processes led to substantial retardation of many TrOCs along the investigated hyporhe
185 ex3 prostates, there was an ERbeta-dependent retardation of migration of activator protein-1 response
186 ss, indicated by increased origin firing and retardation of replication fork progression.
187 ly impairing CUL4, DDB1 or DET1 results in a retardation of SlGLK2 degradation by the 26S proteasome.
188 t, the magnitude of the toxin-induced growth retardation of target cells only weakly impacts the comp
189 underlying both joint destruction and growth retardation of the KBD.
190 tral locus (associative overdominance) and a retardation of the rate of loss of variability by geneti
191                                 We show that retardation of water motions near phospholipid bilayers
192 lyphenols may present a dietary route to the retardation or amelioration of neurodegenerative-related
193 en a diagnosis of mild or unspecified mental retardation or disorders of psychological and motor deve
194 rolled dimerization, which results in either retardation or enhancement of the transport of a reporte
195 ia accompanied by either intrauterine growth retardation or neutropenia.
196 f neurologic diseases associated with mental retardation or/and dementia.
197 ase content/activity, and displayed a growth retardation phenotype similar to that of the ndufs4 muta
198 me proteins cause microcephaly and/or growth retardation, phenotypes that are strongly linked to cent
199  brain development, the ZIKV-mediated growth retardation potentially contributes to the neurodevelopm
200 ancy are associated with intrauterine growth retardation, preterm birth, and fetal demise through mec
201 ted the RNA-binding protein fragile X mental retardation protein (encoded by Fmr1), which constrains
202 -dependent interaction with fragile X mental retardation protein (FMRP) and bind to one another's mRN
203 associated with the loss of fragile X mental retardation protein (FMRP) and haploinsufficiency of syn
204 lity was reduced by loss of fragile X mental retardation protein (FMRP) and that FMRP acts on BK chan
205  binding proteins including Fragile X mental retardation protein (FMRP) and the related protein FXR2P
206 ncoding the mRNA targets of fragile X mental retardation protein (FMRP) are enriched for genetic asso
207                             Fragile X mental retardation protein (FMRP) binds to and regulates the tr
208 n 1 (FMR1) gene and loss of fragile X mental retardation protein (FMRP) cause fragile X syndrome (FXS
209                 The loss of fragile X mental retardation protein (FMRP) causes fragile X syndrome (FX
210                     Loss of fragile X mental retardation protein (FMRP) causes fragile X syndrome (FX
211 how the loss of function of fragile X mental retardation protein (FMRP) causes fragile X syndrome (FX
212 of the gene (Fmr1) encoding Fragile X mental retardation protein (FMRP) causes increased mRNA transla
213 f the Fmr1 gene and loss of fragile X mental retardation protein (FMRP) expression.
214 CE STATEMENT The absence of Fragile X Mental Retardation Protein (FMRP) from birth results in develop
215             How the loss of fragile X mental retardation protein (FMRP) in different brain cell types
216 aused by the absence of the Fragile X Mental Retardation Protein (FMRP) in neurons.
217 used by a deficiency of the fragile X mental retardation protein (FMRP) in neurons.
218                             Fragile X mental retardation protein (FMRP) is a multifunctional RNA-bind
219                             Fragile X Mental Retardation Protein (FMRP) is a regulatory RNA binding p
220                         The Fragile X Mental Retardation Protein (FMRP) is an RNA binding protein tha
221                             Fragile X mental retardation protein (FMRP) is an RNA-binding protein abu
222                             Fragile X mental retardation protein (FMRP) is thought to regulate neuron
223 esis resulting from loss of fragile X mental retardation protein (FMRP) is thought to underlie cognit
224                             Fragile X mental retardation protein (FMRP) is well-studied, as its loss
225  X syndrome, the absence of fragile X mental retardation protein (FMRP) leads to defects in plasticit
226                             Fragile X mental retardation protein (FMRP) loss causes Fragile X syndrom
227  that the effect of loss of fragile X mental retardation protein (FMRP) on these pathways is brain re
228 062) and for targets of the fragile X mental retardation protein (FMRP) pathway (10 observed vs. 4.4
229 ceptor signaling though the fragile X mental retardation protein (FMRP) pathway may underlie synaptic
230                         The fragile X mental retardation protein (FMRP) plays an important role in no
231 ndem Agenet domain (TAD) of fragile X mental retardation protein (FMRP) protein is considered to be a
232                             Fragile X mental retardation protein (FMRP) sculpts synaptic refinement i
233                     Whether fragile X mental retardation protein (FMRP) target mRNAs and neuronal act
234                By using the Fragile X Mental Retardation Protein (FMRP), an abundant neuronal granule
235 at results from the loss of fragile X mental retardation protein (FMRP), an mRNA binding protein that
236 XS is caused by the loss of fragile X mental retardation protein (FMRP), an mRNA binding protein, and
237              More recently, fragile X mental retardation protein (FMRP), an RNA-binding protein that
238                             Fragile X mental retardation protein (FMRP), an RNA-binding protein, has
239 use of its interaction with Fragile X mental retardation protein (FMRP), its upregulation in transfor
240 slation and is dependent on fragile X mental retardation protein (FMRP), the protein that is deficien
241                             Fragile X mental retardation protein (FMRP), the protein that is lacking
242 rom the loss of function of fragile X mental retardation protein (FMRP), which represses translation
243 XS is caused by loss of the fragile X mental retardation protein (FMRP), which translationally repres
244 srupts the transcription of Fragile X Mental Retardation Protein (FMRP).
245 ), results from the loss of Fragile X mental retardation protein (FMRP).
246 abrogated expression of the Fragile X Mental Retardation Protein (FMRP).
247 ng translational suppressor Fragile X Mental Retardation Protein (FMRP).
248 thanol treatment, requiring fragile-X mental retardation protein (FMRP).
249 partial or complete loss of fragile X mental retardation protein (FMRP).
250 e process is antagonized by fragile X mental retardation protein (FMRP).
251  of the RNA-binding protein fragile X mental retardation protein (FMRP).
252 ale mice, we tested whether Fragile X Mental Retardation Protein (FMRPO), the protein whose absence c
253  10(-4)) and targets of the Fragile X mental retardation protein (P=0.0018).
254    The resulting absence of fragile X mental retardation protein 1 (FMRP) leads to both pre- and post
255 ociated genes such as Fmr1 (fragile X mental retardation protein 1).
256 ein synthesis controlled by fragile X mental retardation protein and on Arc signaling.
257 on-independent role for the fragile X mental retardation protein as a regulator of neural excitabilit
258                  Absence of fragile X mental retardation protein causes fragile X syndrome.
259 tions of cytoplasmic CYFIP1-fragile X mental retardation protein complexes.
260 nhibition by overexpression of the fragile X retardation protein Fmr1.
261 ion-independent function of fragile X mental retardation protein has a major role in regulating ion-c
262 entify a novel role for the fragile-X mental retardation protein in the posttranscriptional regulatio
263                 Loss of the Fragile X mental retardation protein leads to excessive excitatory compar
264  co-localizes with YB-1 and fragile X mental retardation protein on stress granules in response to ar
265  These results suggest that Fragile X Mental Retardation Protein regulates dendritic HCN channels via
266 atory complex that includes fragile X mental retardation protein, DEAD box helicase 5, and the poly(A
267 inding protein 1 (YB-1) and fragile X mental retardation protein, proteins that function in translati
268  study shows that replacing Fragile X Mental Retardation Protein, which is absent in Fragile X syndro
269 mics and interacts with the fragile X mental retardation protein.
270                            But developmental retardation, reduced brood size, altered survival and in
271  to investigate pertechnetate (Tc(VII)O4(-)) retardation, reduction, and rate scaling in three sedime
272               We identified fragile X mental retardation-related protein 1 (FXR1P), a RNA binding pro
273      Here, we show that the fragile X mental retardation-related protein 2 (FXR2P) cooperates with FM
274  % were achieved with remarkably little rate retardation relative to ethylene homopolymerizations.
275 ess, onychodystrophy, osteodystrophy, mental retardation, seizures) to non-syndromic hearing loss.
276 nt neuropathological symptoms such as mental retardation, seizures, and epilepsy.
277 f the first protein content and its absolute retardation signal is equal to that of the second protei
278 d its relevant leverage theory relied on the retardation signal of chip moving reaction boundary elec
279 d that (i) there was a leverage principle of retardation signal within the TDP of two pure proteins,
280 out mice died postnatally with severe growth retardation, skeletal defects, and kidney and lung abnor
281 with wide-ranging symptoms, including mental retardation, speech and language impairment and other ne
282 nidentified syndrome characterized by growth retardation, spine malformation, facial dysmorphisms, an
283 ptic proteins in normal and Fragile X mental retardation syndrome (FXS) model mouse cortex, and revea
284    Silver-Russell syndrome (SRS) is a growth retardation syndrome in which loss of methylation on chr
285 complex containing alpha-thalassaemia/mental retardation syndrome X-linked (ATRX) and death-domain-as
286          Here, we identify alpha-thalassemia retardation syndrome X-linked (ATRX) as a novel physical
287                     Alpha thalassemia/mental retardation syndrome X-linked chromatin remodeler (ATRX)
288 hromatic nearly 90 degrees transmitted phase retardation through the metasurface is precisely charact
289 um of clinical outcomes, ranging from mental retardation to microcephaly, caused by congenital HCMV i
290 (zinc finger, myeloproliferative, and mental retardation-type 3) as a chromatin-interacting protein t
291 e grik1-1 grik2-1 double mutant shows growth retardation under regular growth conditions.
292 ith clinical manifestations including mental retardation, vision impairment, and sensorineural hearin
293 hat shed light on the conditions under which retardation vs. acceleration of loss of variability occu
294 ted with mutism, withdrawal, and psychomotor retardation, which constitute the neurovegetative featur
295  anergia, fatigue, lassitude and psychomotor retardation, which cross multiple pathologies, including
296  was characterized by an initially low local retardation, which increased as collagen fibers remodele
297 crocephaly, absent speech, hypotonia, growth retardation with prenatal onset, feeding difficulties, s
298 rabidopsis thaliana Alpha Thalassemia-mental Retardation X-linked (ATRX) ortholog and show that ATRX
299 activation of ATRX (alpha-thalassemia mental retardation X-linked) represents a defining molecular al
300  deletions of ATRX (Alpha Thalassemia/Mental Retardation, X-linked) that generate in-frame fusion (IF

 
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