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 n important trypanosomatid clade relevant to human disease.
2 ng - whose disrupted expression is linked to human disease.
3 ntify alternative animal models that reflect human disease.
4 on of these findings to our understanding of human disease.
5 and strategies for establishing causation in human disease.
6 pathophysiology and therapeutic response in human disease.
7 viding a foundation to explore their role in human disease.
8 s to animal systems and even to diagnosis of human disease.
9 tions for understanding sexual dimorphism in human disease.
10 and is frequently mutated in the context of human disease.
11 little efficacy in various animal models of human disease.
12 of C. elegans and to connect the results to human disease.
13 ntial to provide improved cellular models of human disease.
14 liary protein that underlies development and human disease.
15 g that our findings in mice are relevant for human disease.
16 ariation leads to phenotypic differences and human disease.
17 al microbes are recognized for their role in human disease.
18 gnaling and may open therapeutic avenues for human disease.
19 confirming their differential expression in human disease.
20 critical roles for Stac3 in EC coupling and human disease.
21 fibrosis and cirrhosis characteristic of the human disease.
22 uito-borne arboviruses are a major source of human disease.
23 other divergent ebolaviruses associated with human disease.
24 histological and molecular similarities with human disease.
25 etion of p19/Arf is detected, recapitulating human disease.
26 st-microbiome interactions and their role in human disease.
27 remain a potentially important reservoir for human disease.
28 ions and therapeutic approaches for treating human disease.
29 ignalling, which, like GATOR1, is mutated in human disease.
30 te of the lack of successful applications to human disease.
31 e advantages in the fly system when modeling human disease.
32 sion variability, with a potential impact on human disease.
33 t should be considered in genomic studies of human disease.
34 mice can potentially improve mouse models of human disease.
35 ng pAkt and CD47, which were also induced in human disease.
36 signaling pathway genes are responsible for human disease.
37 experimental findings into understanding the human disease.
38 eing realized as an important contributor to human disease.
39 ms the usefulness of taiep as a model of the human disease.
40 s was the preferred pathway of disruption in human disease.
41 ile proteins, mimicking the hallmarks of the human disease.
42 ariants in repetitive DNAs may contribute to human disease.
43 as been instrumental in the understanding of human disease.
44 ve-strand RNA viruses that cause significant human disease.
45 assemblies implicated in gene regulation and human disease.
46 ences genome organization and contributes to human disease.
47 gical control of insect pests and vectors of human disease.
48 in cats for applicability to both feline and human disease.
49 sembly, function, evolution, and its role in human disease.
50 in tissues, or whether this plays a role in human disease.
51 tant tool for understanding the aetiology of human disease.
52 nction and neurodegeneration associated with human disease.
53 large-scale discovery of de novo variants in human disease.
54 is implicated in bacterial pathogenesis and human disease.
55 mal models do not reflect the biology of the human disease.
56 ts, implying that this mechanism also drives human disease.
57 drawing on observations in mouse models and human disease.
58 d be harnessed to minimize hypoxic damage in human disease.
59 hanism of glutamate transport dysfunction in human disease.
60 ical, diagnostic, and therapeutic aspects of human disease.
61 genome and to increase the understanding of human disease.
62 of NAFLD that closely mimics most aspects of human disease.
63 tial to identify Ag-activated lymphocytes in human disease.
64 RNAs (lncRNAs) play important roles in many human diseases.
65 ynamic regulation of PI(3,5)P2 are linked to human diseases.
66 dysregulation underlies a number of complex human diseases.
67 approaches to gain a better understanding of human diseases.
68 and its pathophysiological implications for human diseases.
69 osition are associated with many intractable human diseases.
70 nucleases have been implicated in hereditary human diseases.
71 this phenomenon, which is linked to diverse human diseases.
72 genes has limited molecular understanding of human diseases.
73 tive information, and their relationships to human diseases.
74 sative agents of some of the most widespread human diseases.
75 atalytic activity is associated with several human diseases.
76 ization of the abnormalities associated with human diseases.
77 cesses and play an essential role in various human diseases.
78 ence in correlating biological pathways with human diseases.
79 s to minimize mosquito-borne transmission of human diseases.
80 erapeutic possibilities for the treatment of human diseases.
81 s, and NF-kappaB activity is altered in many human diseases.
82 , preclinical animal models for the study of human diseases.
83 sfunction is associated with a wide range of human diseases.
84 athogenic Yersinia bacteria cause a range of human diseases.
85 Similar chromatin regulation occurred in human diseases.
86 nerate genetically modified animal models of human diseases.
87 or developing monoclonal antibodies to treat human diseases.
88 ew drugs against the VCP/p97/ERAD pathway in human diseases.
89 ghout the body and are implicated in several human diseases.
90 microbiome have been implicated in multiple human diseases.
91 in myriad biological processes and numerous human diseases.
92 n is thus important for studying biology and human diseases.
93 tools for discovery of novel treatments for human diseases.
94 n findings into novel biological insights of human diseases.
95 itable for studying development and relevant human diseases.
96 ion of lncRNAs could be a prevalent cause in human diseases.
97 tors are the most important drug targets for human diseases.
98 rmaceutical targets involved in a variety of human diseases.
99 ated to activate caspase-1 and implicated in human diseases.
100 n implicated in genomic instability and some human diseases.
101 powerful innate immune system leads to these human diseases.
102 er understanding the molecular mechanisms of human diseases.
103 nt advantages for miRNA-based diagnostics of human diseases.
104 idogenic proteins implicated in a variety of human diseases.
105 events are thought to contribute to several human diseases.
106 ructural changes are associated with several human diseases.
107 data that contain comprehensive knowledge of human diseases.
108 stantially to the understanding of important human diseases.
109 s well as their impact on the development of human diseases.
110 recapitulate the heterogeneity seen in these human diseases.
111 tochondrial structure-function as a cause of human diseases.
112 he onset and progression of a broad range of human diseases.
113 ate the therapeutic relevance of V-ATPase in human diseases.
114 of drug molecules effective against critical human diseases.
115 tion of apoptosis is associated with several human diseases.
116 erstanding their pathophysiological roles in human diseases.
117 loping targeted epigenetic therapies against human diseases.
118 ays and identifying new targets for treating human diseases.
119 ive therapeutic targets for cancer and other human diseases.
120 rgeting SFKs could modulate pDC responses in human diseases.
121 ing of quantitative traits including complex human diseases.
122 nst age-associated changes and a plethora of human diseases.
123 nd highlights their utility for the study of human diseases.
124 y on the fidelity of mimicking facets of the human disease; (2) experimental design and its impact on
125 ecular and phenotypic characteristics of the human disease; (2) to test the hypothesis that SOX2 dere
128 function of HCS and biotin in metabolism and human disease, a putative role for the enzyme in histone
131 employing rhesus rotavirus (RRV), parallels human disease and has been used to elucidate mechanistic
132 ions for understanding mechanisms underlying human disease and protein production in biotechnology.
133 ere length in a mouse model of age-dependent human disease and provide an in vivo model in which to t
135 efective CLL mimicking the high-risk form of human disease and show that Atm-deficient CLL is sensiti
136 rylation (OXPHOS) system is a major cause of human disease and the cellular consequences are highly c
138 posures and gene-environment interactions in human disease and to inform human health risk assessment
139 ish a mouse model of fish allergy resembling human disease and to investigate whether mouse and rabbi
141 ons (indels) have a significant influence in human disease and, in terms of frequency, they are secon
142 ed DNA methylation status is associated with human diseases and cancer; however, the underlying molec
143 of these PTP regulatory mechanisms can cause human diseases and how these diverse regulatory mechanis
147 mic species-specific mechanisms occurring in human diseases and may preclude successful clinical tran
150 o highlight how KLFs have been implicated in human diseases and outline potential avenues for future
153 actor for leishmaniasis in rodent models and human disease, and associated with drug-treatment failur
154 , describe a link between KEOPS function and human disease, and delineate potential pathogenic mechan
155 toire of cGAS and caspase-4 to noninfectious human disease, and identify new potential targets for tr
156 of gene networks as well as their impact on human disease, and provide novel data for the developmen
157 udies where mouse models are used to examine human disease, and where plasma may be interrogated in l
158 alpha-synuclein probably acts as a prion in human diseases, and a deeper understanding of this step
159 inflammation contributes to a wide range of human diseases, and environments in infancy and childhoo
160 ls traverse BM barriers, the roles of BMs in human diseases, and future directions for the field.
161 AKT-TOR signaling pathway is linked to major human diseases, and key components of this pathway are t
164 Escherichia coli that are capable of causing human disease are often classified into pathogenic varia
166 well they have recapitulated aspects of the human disease as well as highlights the biological insig
169 t the SNX9-driven actin comets that arise on human disease-associated oculocerebrorenal syndrome of L
170 d to identify genes and pathways affected by human disease-associated variation, enabling a mechanist
172 oncepts and opinions regarding their role in human diseases beyond IgE-mediated allergic responses an
173 for the treatment of previously intractable human diseases but to exert their effects on cellular RN
174 (CV-A24) was not originally associated with human disease, but in 1970 a pathogenic "variant" (CV-A2
175 vity inhibition is proposed to be a basis of human disease, but the impacts of different levels of pr
176 gonists are used for treatment of a range of human diseases, but they present challenging issues of c
179 therapeutic approaches to prevent and treat human disease caused by highly pathogenic avian influenz
182 response and its potential participation in human diseases caused by unfolded protein response.IRE1a
184 These genes, which are often associated with human diseases, control the L1 life cycle at the transcr
187 nized the ability to associate variants with human diseases, diagnostic rates and development of new
190 of the role of genetic variation in complex human diseases, especially via genome-wide association s
192 diverse realms such as biological function, human diseases, evolution, ecosystems, and agriculture.
193 nsmits a highly contagious, frequently fatal human disease for which there is no specific antiviral t
195 identified by en masse transformation of the human disease genes into a pool of 4653 homozygous diplo
196 sequencing has accelerated the discovery of human disease genes, progress has been largely limited t
202 LCV-1 could provide valuable information for human disease in a natural great ape setting and have po
207 odel for in vivo studies of a broad range of human diseases, in particular for understanding their ge
208 is Wwox effect has important consequences in human disease: in a cohort of cancer patients treated wi
213 athway has been associated with a variety of human diseases including diabetes, neurodegeneration and
214 ential role, is associated with a variety of human diseases including proliferative diabetic retinopa
216 the environment and cause a wide spectrum of human disease, including infections associated with high
217 bally exhibit several characteristics of the human disease, including systemic inflammation and carti
222 UG initiation events contributes to multiple human diseases, including cancer and neurodegeneration,
223 activity have been associated with numerous human diseases, including cancer stem cell survival and
227 chanistic understanding of a wide variety of human diseases, including diabetes mellitus, neurodegene
228 is an essential pathogenic mechanism in many human diseases, including diseases involving tumor growt
229 ed nuclear mechanics is associated with many human diseases, including heart disease, progeria, and c
230 ale mosquitoes transmit numerous devastating human diseases, including malaria, dengue fever, Zika vi
231 ic to cells and is believed to underlie many human diseases, including many neurodegenerative disease
232 R signalling is associated with a variety of human diseases, including metabolic disorders and cancer
233 d significant pathogenicity, causing serious human diseases, including microcephaly and Guillain-Barr
234 drug discovery for the treatment of several human diseases, including multidrug-resistant infections
235 atellite repeats is associated with multiple human diseases, including myotonic dystrophy, Fuchs endo
236 is a promising approach for treating diverse human diseases, including neurodegenerative disorders an
237 DNA repair have been associated with several human diseases, including tissue-fibrosis, neurodegenera
244 y of genetic variants associated with common human diseases map to enhancers, non-coding elements tha
246 his goal, including enhanced orthology data, Human Disease Model Reports, protein domain search and v
252 pe 2 diabetes, metabolic syndrome, and other human diseases modulated by glucocorticoid control.
253 rt for gene expression phenotypes, models of human disease, mutation details at the DNA, RNA and prot
254 mutagenesis experiments and measurements of human disease mutations and show that it outperforms met
256 sion signature including Lgals3 relevant for human disease of TSC1/TSC2 inactivation and mTORC1 hyper
258 el of ALD that recapitulates key features of human disease pathology and which reveals novel features
259 e embryonic fibroblasts (MEFs) resembled the human disease phenotype by showing multiple defects in o
265 A mouse model of fish allergy mimicking human disease regarding IgE epitope recognition and symp
270 class show several protective activities in human disease studies, and the list of potential therape
272 tabolite-sensing GPCRs likely contributes to human diseases such as asthma, food allergies, type 1 an
273 annabinoid-based medications relieve pain in human diseases such as cancer, multiple sclerosis, and f
276 ng of how altered folate availability causes human diseases such as fetal growth restriction, fetal m
277 ing of these channels has been implicated in human diseases such as lysosomal storage disorders, neur
278 portant risk factors that contribute to many human diseases, such as age, gender and prior diagnoses,
279 Misfolded proteins are associated with many human diseases, such as amyloid diseases, cancer, and ne
281 P/p97 have been implicated in a multitude of human diseases, such as neurodegenerative diseases and c
283 egulation of this function results in severe human disease, thereby emphasizing a critical role for N
284 prior studies implicate stem cell defects in human disease, this work shows that niche dysfunction ma
285 ision, which allows novel in vitro models of human disease to be generated-e.g., in pluripotent stem
286 reatment regimens on organotypic cultures of human disease to expedite drug and therapy development.
287 ng mouse models that faithfully recapitulate human disease together with organoid cultures, we have d
288 etic association of molecular, cellular, and human disease traits and experimental validation to demo
289 contribution of MRSA agr type I isolates to human disease, vaccine targeting of AIP1-regulated virul
290 ired Fe-S cluster biogenesis associates with human disease, we determined the importance of FBXL5 for
294 e in vitro results in rats were validated in human disease where myelin-positive hypertrophic astrocy
295 t can serve as a trigger for a wide range of human diseases, which include autoimmune, inflammatory,
296 ein tyrosine phosphorylation causes numerous human diseases, which presents enormous opportunities fo
297 rt of delivering effective cures for complex human diseases with complicated causes, such as cancer,
299 genes as human autoantigens and 1071 related human diseases, with which we constructed a human autoan
300 of FUS expression and that recapitulate the human disease-with progressive loss of motor neurons in
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。