コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 ucial in apoptosis and growth control during normal development.
2 rs, drug resistance in fungal infection, and normal development.
3 e importance of this localization pattern in normal development.
4 nt defective in both vacuole trafficking and normal development.
5 occurs when protein production peaks during normal development.
6 nts of GlcCer in excess of that required for normal development.
7 t developmental stages, suggesting a role in normal development.
8 tic physiological functions during and after normal development.
9 retrotransposon expression is essential for normal development.
10 sympathetic neuroblast proliferation during normal development.
11 of sporadic carcinogenesis and often inform normal development.
12 taining microtubule and genome integrity and normal development.
13 e severe neurodegeneration after a period of normal development.
14 ve SMN knockdown follows variable periods of normal development.
15 scale complex chromosomal errors that impede normal development.
16 h hypnozoites persist and activate to resume normal development.
17 helial-mesenchymal interactions required for normal development.
18 the regulation of non-apoptotic genes during normal development.
19 somatic support cells and depend on them for normal development.
20 TICs), whereas it is largely dispensable for normal development.
21 e somatic-embryo dormancy and promoted their normal development.
22 ing and the acquisition of new cell fates in normal development.
23 yo absolutely requires Hif1alpha to continue normal development.
24 the source of parasympathetic neurons during normal development.
25 conserved morphogens that are essential for normal development.
26 s, which appear after a period of apparently normal development.
27 e challenged by limited understanding of its normal development.
28 roved; currently, she is well and is showing normal development.
29 and in the mouse embryo--without perturbing normal development.
30 alian cellular identity and is essential for normal development.
31 The Hedgehog (Hh) pathway is critical in normal development.
32 and loss of genomic imprinting, compromising normal development.
33 plane roughly orthogonal to that seen during normal development.
34 ability of eggs and oocytes is essential for normal development.
35 coding lncRNAs may affect gene expression in normal development.
36 rn neurons to escape Notch activation during normal development.
37 st-transcriptional regulators is crucial for normal development.
38 pattern of selection different from that of normal development.
39 tic activities of TET1 that is essential for normal development.
40 echanisms to regulate heme metabolism during normal development.
41 te numerous cellular functions essential for normal development.
42 eserve the progenitor state and/or interrupt normal development.
43 any of the experiences that are required for normal development.
44 ld help to identify critical checkpoints for normal development.
45 ne motility and must be restrained to ensure normal development.
46 fferentiation pathways and are essential for normal development.
47 is key for cell-cycle control and needed for normal development.
48 apoptosis, all of which are also critical to normal development.
49 g cellular homeostasis and remodeling during normal development.
50 r identifying local gene interactions during normal development.
51 contributions of TGFbeta family signaling to normal development, adult homeostasis and disease, and a
52 ism resembling some of the broad features of normal development, an initial overproduction of functio
55 d that the trajectory of gyrification during normal development and aging was not linear and could be
56 sensitive to intracortical myelin content in normal development and aging, relates to cognitive funct
57 an increase in sox9b expression during both normal development and AHR2 activation, which suggests r
58 ular polyploidy plays important roles during normal development and also contributes to human disease
60 e control of gene expression programs during normal development and are disrupted in specific disease
61 ycomb repressive complexes (PRCs) are key to normal development and are frequently deregulated in hum
62 ) superfamily members play critical roles in normal development and become disrupted in human disease
65 Alternative splicing has critical roles in normal development and can promote growth and survival i
66 ome that are relevant for understanding both normal development and cancer and may be of use as epige
74 he Hedgehog (Hh) signaling pathway regulates normal development and cell proliferation in metazoan or
75 ifications control fate determination during normal development and dedifferentiation during disease.
76 Messenger RNA expression is important in normal development and differentiation, as well as in ma
78 s whereby periconceptional folate influences normal development and disease are poorly understood: ep
84 his fine-tuning mechanism is critical during normal development and diseases, particularly in relatio
86 MYC genes have both essential roles during normal development and exert oncogenic functions during
88 nderstanding of the functions of IMPs during normal development and focuses on a series of recent obs
89 t give rise to the wing-imaginal disc during normal development and following compensatory growth cau
90 require high levels of SMN protein for their normal development and function in vivo, with reduced le
91 ion of the actin cytoskeleton is crucial for normal development and function of the immune system, as
92 lum kinase (PERK) (EIF2AK3) is essential for normal development and function of the insulin-secreting
93 atus of MeCP2 in neurons is critical for the normal development and function of the mammalian brain.
97 n in eIF4E expression, while compatible with normal development and global protein synthesis, signifi
98 in states and genomic stability is vital for normal development and health across a range of organism
101 C. trachomatis require mitochondrial ATP for normal development and hence postulate that they preserv
103 ATX-LPA receptor signaling is essential for normal development and implicated in various (patho)phys
106 gration and differentiation are important in normal development and in demyelinating/remyelinating co
107 mGlu5 receptors play important roles in both normal development and in disorders such as Fragile X sy
110 each cell class to neocortical growth during normal development and in neurodevelopmental disorders h
112 es to epithelial tissue morphogenesis during normal development and in tumor invasiveness and metasta
113 endent cellular reprogramming is integral to normal development and is central to production of induc
114 are cell adhesion junctions required for the normal development and maintenance of mammalian tissues
115 hanism by which epithelial Wnts regulate the normal development and maintenance of pulmonary vasculat
120 rikingly, Hdac1(-/-)Hdac2(+/-) brains showed normal development and no obvious phenotype, whereas Hda
121 alternative splicing, a process important in normal development and often dysregulated in disease.
124 ular localization may impact its function in normal development and pathologic conditions such as NB
125 e multifaceted roles of Wnt signaling in the normal development and pathology of skin, including the
126 e genes, regulated by VHL, are essential for normal development and physiologic adaptation of renin-p
127 Directional cell motility is essential for normal development and physiology, although how motile c
128 dation and recycling pathway is important in normal development and physiology, and defects in this p
131 cluding HIF1alpha, ATF4, and p53, are key to normal development and play critical roles in disease, i
132 ing reinforces Tcf-1 activity to both ensure normal development and prevent thymocyte neoplasia.
133 ine RNA editing, and editing is required for normal development and proper neuronal function of anima
134 ellent tools for dissecting SFK functions in normal development and signaling and to interfere with a
135 The human cerebral cortex depends for its normal development and size on a precisely controlled ba
137 We conclude that HDAC3 is essential for the normal development and suppressive functions of thymic a
138 critical for ciliary functions essential to normal development and survival, most probably as a prev
140 itiated axon wrapping were stabilized during normal development and that initiation did not require a
141 s has advanced our understanding of both the normal development and the pathobiology of ocular neovas
142 ial roles for RNA regulatory networks in the normal development and their implications in a variety o
143 by Wnt proteins is finely balanced to ensure normal development and tissue homeostasis while avoiding
145 defective cells from metazoans occurs during normal development and tissue homeostasis, as well as in
149 The full repertoire of Fancd2 functions in normal development and tumorigenesis remains to be deter
152 behavior of dying cells that is seen both in normal development and under pathological conditions.
155 ng expression patterns of genes required for normal development, and generating small interfering RNA
156 onal regulators identified as key players in normal development, and in identifying conditions that i
157 hology following unexpected cell loss during normal development, and may also be a contributing facto
158 imately 92 microRNA (miRNA) is essential for normal development, and overexpression of certain miRNAs
159 marks on DNA and histones is fundamental to normal development, and perturbations contribute to a va
160 ased exchange is essential for signaling and normal development, and that morphogen distribution and
163 s the utility of genetic characterization of normal development as an integral part of a disease gene
165 the specific articulations that close during normal development as well as in pathological conditions
166 e expression and are essential components of normal development as well as modulators of disease.
167 rs, regulate the transcriptomic landscape in normal development as well in diseases such as cancer.
168 on of a small number of genes is crucial for normal development, as these genes often directly regula
171 cate that the change in NCoR splicing during normal development both helps drive normal adipocyte dif
173 epend on cellular hierarchies reminiscent of normal development but superimposed on underlying geneti
176 ion of adaptive immune responses, regulating normal development, changes the paradigm for studying pl
177 vidence that specific HARs are essential for normal development, consistent with suggestions that the
178 nonroot tissue and are produced both during normal development (crown roots on cereals and nodal roo
182 of environmental stressors as part of their normal development, during which they undergo a dramatic
183 disorder typified by a period of apparently normal development followed by loss of cognitive and psy
184 RTT is characterized by a period of largely normal development followed by regression in language an
185 ients with Rett syndrome exhibit a period of normal development followed by regression of brain funct
186 haracterized by a brief period of apparently normal development followed by the loss of purposeful ha
187 itical for cell-lineage specification during normal development; functions that often become deregula
190 tebrate trunk neural crest cell fates during normal development, highlight the likely primitive skele
191 sion in GATA1s mutant megakaryocytes rescued normal development, implicating this morphogenetic pathw
192 Some cells activated caspase-3 during their normal development in every cell and in every animal wit
193 ylase (NuRD) complex, which is essential for normal development in higher organisms, is one such macr
194 ned spine morphology at the nanoscale during normal development in mice, and tested the hypothesis th
199 are an unexpected source of VEGFA and their normal development is required for alveolar angiogenesis
200 mportance of maternal folate consumption for normal development is well established, yet the molecula
203 L proteins being postulated as essential for normal development, little is known about the specific f
208 f ghrelin during postnatal life impaired the normal development of ARH projections and caused metabol
209 u receptor with specificity for PE supported normal development of B cells, whereas a VLR:Tmu recepto
210 (y442) homozygous mutant zebrafish displayed normal development of blood and lymphatic vasculature.
211 opriate regulation of ARID3a is critical for normal development of both myeloid and B lineage pathway
212 indicate that CRKL is intimately involved in normal development of both the upper and lower GU tracts
213 ion of Rab43 are viable and fertile and have normal development of cDCs but show a defect for in vivo
214 transcription factors are essential for the normal development of eukaryotes and are the downstream
217 ect biosynthesis of proteins involved in the normal development of gonads and external genitalia.
218 e, we demonstrate that Nfil3 is critical for normal development of gut-associated ILC3s in a cell-int
219 sh results in impaired myelopoiesis, despite normal development of haematopoietic stem cells (HSCs).
220 RID3a, in mouse stem cells was important for normal development of hematopoietic lineages; however, p
222 scription factor Runx3 was essential for the normal development of ILC1 and ILC3 cells but not of ILC
224 caregivers and society in general concerning normal development of infants and the significance of ea
226 d deletion of a peripheral sensor alters the normal development of local and global features of twitc
227 major role in iron detoxification and, thus, normal development of malaria parasites in their mammali
232 ruption by homologous recombination leads to normal development of motile ookinetes that exhibit a se
233 ng transcription factor, is required for the normal development of mouse and human enteroendocrine ce
234 ranscription factor that is important in the normal development of multiple tissues, including both t
236 urrounding somatic cells is critical for the normal development of ovarian follicles, perturbations i
238 f basal epithelial cells and is required for normal development of several epithelial tissues, includ
240 on of the neural crest, which is crucial for normal development of the aortic arch arteries and crani
242 ized that the molecular regulators governing normal development of the breast epithelium may double a
243 provide insight into the role of DSPP in the normal development of the calvaria, alveolar bone, and d
246 ow that both Mafb and Magi2 are required for normal development of the embryonic zebrafish kidney.
249 se data indicate that disc1 is essential for normal development of the hypothalamus and for the corre
251 may cause severe damage to maize, affecting normal development of the plant and decreasing grain yie
253 cells bordering the internal capsule for the normal development of the striatonigral pathway involvin
254 In the companion article we described the normal development of the trigeminal lemniscal pathway i
255 singly, alphavbeta3-deficient mice displayed normal development of the virgin gland with no effect on
257 Notch is required in type II neuroblasts for normal development of their transit amplifying progeny,
260 racellular matrices (ECMs) is crucial to the normal development of tissues and organs and in disease
261 3D extracellular matrices is critical to the normal development of tissues and organs and in disease
262 ions revealed that CD81 was not required for normal development of Treg and MDSC but was essential fo
263 ur data show that CX3CR1 is not required for normal development of V1 responses to visual stimulation
265 tein for multiple splicing 2 (RBPMS2) during normal development of visceral smooth muscle in chicken
267 Understanding the relationships between the normal development of-and the schizophrenia-associated a
269 emonstrate that p300 is not required for the normal development or functioning of adult skeletal musc
271 response to changes in oxygen tension during normal development or pathologic processes is, in part,
272 nderstanding of the epigenetic regulation of normal development, our work will be useful in decipheri
273 sly, or, sequentially, in tumourigenesis and normal development per cell differentiation, indicating
275 olecules that maintain these fates stably as normal development proceeds or how their dysregulation m
277 ll fate maintenance and reprogramming during normal development, regeneration and oncogenic transform
279 contrast to common belief, we find that, in normal development, spine heads become smaller, while th
280 eIF4E is maintained at levels in excess for normal development that are hijacked by cancer cells to
282 Although PTCHD1 is probably critical for normal development, the connection between its deletion
283 eased proliferation, indicating that, during normal development, the growth of the tooth germ is cons
285 oup of genes has been extensively studied in normal development, the second finding suggests importan
287 Collective cell migration is critical for normal development, tissue repair and cancer metastasis.
288 the types of mechanisms that are used during normal development to ensure that division timing and fa
289 ing in severity from epilepsy with otherwise normal development to epileptic encephalopathy resulting
290 ical roles in various processes ranging from normal development to human diseases such as cancer prog
291 remains to be learned about this process in normal development, two recent studies in Cell (Groschel
292 In contrast, Pcbp2-null embryos undergo normal development until midgestation (12.5 to 13.5 days
293 bly, in a self-organized process that mimics normal development, vesicles containing prosensory cells
294 ular trafficking genes affected by AS during normal development (when Celf1 is downregulated) show a
295 tions not only under stress, but also during normal development, when they are expressed in organ-spe
296 gulatory hierarchy of HOX control of LMO2 in normal development, which can be resurrected during leuk
297 iated variant nonketotic hyperglycinemia had normal development with childhood-onset spastic parapleg
298 tubule (MT) motor kinesin-1 is essential for normal development, with key roles in the nervous system
299 hood exposure to some phthalates may perturb normal development, with several studies consistently re
300 orm of directed cell migration important for normal development, wound healing, and cancer metastasis
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。