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1                                              LCR activities have been discovered in numerous T cell l
2                                              LCR decreased with decreasing dose for all reconstructio
3                                              LCR was attempted in 36,228 patients (42.2%), with 5751
4                                              LCRs activate an inward Na(+)-Ca(2+) exchange current (I
5                                              LCRs at higher Pup exhibit larger amplitudes and faster
6 kb (chr 8) and approximately 287-kb (chr 12) LCR clusters.
7                       40 male (20 HCR and 20 LCR) and 40 female (20 HCR and 20 LCR) rats were randoml
8 HCR and 20 LCR) and 40 female (20 HCR and 20 LCR) rats were randomly assigned to 3 weeks of activity
9                            The Chromosome 22 LCRs (LCR22s) mediate nonallelic homologous recombinatio
10 re: HCR (4726 +/- 3220), SD (2293 +/- 3461), LCR (672 +/- 323).
11                                 In addition, LCRs have been repeatedly identified in very ancient, an
12 ta indicate that establishing full TCR-alpha LCR activity requires critical molecular events occurrin
13    High-level, copy number-related TCR-alpha LCR-linked reporter gene expression levels are cell type
14 eport that de novo introduction of TCR-alpha LCR-linked transgenes into existing T cell lines yields
15   Functional homology to the mammalian alpha-LCR MCS-R2 region was confirmed by robust and specific r
16  that this complex occupies and activates an LCR that regulates the BCL6 proto-oncogene and is unique
17 ts on transcriptional bursting, we forced an LCR-beta-globin promoter chromatin loop.
18  pathway by which long-range looping from an LCR impacts on local chromatin architecture that is link
19 the C terminus was sufficient to generate an LCR(-) phenotype, with variant LcrV capping type III nee
20 trol region (LCR) may function as part of an LCR holocomplex within a larger active chromatin hub (AC
21 ivity depends on the LCR, consistent with an LCR-promoter looping mechanism.
22 topathologic evaluation, HPV L1, E2, E6, and LCR regions were amplified, and phylogenetic analysis of
23 equency between the (G)gamma-globin gene and LCR.
24  gene as well as in the beta-globin gene and LCR.
25 formation between the gamma-globin genes and LCR, which is a critical step for the transcription of t
26                                      HCR and LCR rats were fed a chow or HFD for 3 days and received
27 d hepatomegaly and steatosis in both HCR and LCR rats, while producing greater cholesterol ester accu
28 elay between AP-induced Ca(2+) transient and LCR appearance, defines the time of late diastolic depol
29 sites analyzed are important for appropriate LCR function, some sites are more important than others
30 ding proteins and transcription complexes at LCR HS2 and the adult betamajor-globin gene promoter but
31                     When feasible, attempted LCR had better outcomes than open colectomy in the immed
32 a corticosterone levels were similar between LCR and HCR, and these populations had similar behaviora
33 bbed I(spark)), we explored the link between LCRs and I(spark) in our model.
34 ed (OVX) rats bred for low-running capacity (LCR), a model that has been previously shown to mimic hu
35 cient form of LDB1 in LDB1 knock down cells: LCR/beta-globin proximity was restored without mediator
36 under the regulation of a well characterized LCR containing four DNase I hypersensitive sites (HSs).
37 uences, with all of them broadly considering LCRs as regions with fewer amino acid types compared to
38 mpared to sham-operated (SHM) intact control LCR rats.
39 letions mirror their cytosolic counterparts, LCRs, and occur following SR Ca(2+) refilling.
40 d on unique evolutionary patterns, we create LCR mutations, which systematically tune its biophysical
41 pread belief based on older and sparse data, LCRs actually have a significant, persistent and highly
42 o drive the function of a cell-type-defining LCR.
43 r, more synchronized, and stronger diastolic LCR signal activating an earlier and larger inward NCX c
44 erent state-of-the-art tools for discovering LCRs and provides functional annotations such as domain
45  cells in which two developmentally distinct LCR-regulated globin genes are cotranscribed in cis, bur
46                       Four novel adjacent DP-LCR-flanked and NAHR-prone regions, involving 2q12.2q13,
47               The computationally defined DP-LCRs were cross-referenced with our chromosomal microarr
48                       Several features of DP-LCRs, including length, distance between NAHR substrate
49 tly oriented paralogous low-copy repeats (DP-LCRs) in the most recent version of the human haploid re
50                                       During LCR, the AuNPs were ligated together, resulting in a dis
51  human papillomavirus (HPV) DNA and HPV E5a, LCR and/or full-length genomic variants.
52                          Interestingly, each LCR mutation showed contrasting effects on cytokine expr
53 tinguishes itself from other electrochemical LCR detection schemes by integrating a peroxidase-mimick
54 ese HSs had been deleted from the endogenous LCR, and the effect on Th2 cytokine expression was asses
55 ents revealed that the beta-globin enhancer (LCR) predominantly augments transcriptional burst fracti
56 n of numerically simulated LCRs and examined LCR regulation by SR Ca pumping rate (Pup) that provides
57 ly disfavored, suggesting mutually exclusive LCR-gene contacts.
58 web-based tool which allows users to explore LCRs in protein sequences with additional functional ann
59              Importantly, WD-fed low-fitness LCR rats displayed greater inflammatory cell infiltratio
60 oriented paralogous subunits of the flanking LCR clusters, demonstrating non-allelic homologous recom
61                                         FMRP(LCR) posttranslational modifications by phosphorylation
62 low-complexity disordered region (i.e., FMRP(LCR)).
63  between the 2 trial groups were as follows: LCR patients were older at randomization, and their path
64 ition between the beta-type globin genes for LCR contacts and suggest that LCR-promoter loops are for
65 ce-dependent competition between L and M for LCR.
66 tant LDB1 to the beta-globin promoter forced LCR loop formation in the absence of mediator or cohesin
67 sulin sensitivity in glycolytic muscles from LCR rats.
68                                     Further, LCR rats had greater WD-induced decreases in complete FA
69                                 Furthermore, LCR as a target amplification step resulted in a 6000-fo
70  of all key features of mouse TCR-alpha gene LCR function in T cells derived in vitro from mouse embr
71 the locus and facilitates fetal gamma-globin/LCR looping and gamma-globin transcription.
72 on and function in antagonizing gamma-globin/LCR looping.
73 y regulated locus, we have targeted the hCD2-LCR as a single copy into the endogenous mouse CD8 gene
74 t differ in the integration site of the hCD2-LCR within the mCD8 gene complex were generated, and the
75                                         HCR, LCR, and SD rats were grouped by strain and randomly ass
76 ow-capacity for running on a treadmill (HCR; LCR) also differ in wheel-running behavior, but whether
77 of HSII, expanding the role of POU1F1 in hGH LCR activity, and provide insight on the molecular evolu
78 e that a major function of the placental hGH LCR is to insulate the transgene locus from site-of-inte
79            Here, we demonstrate that the hGH LCR 'loops' over a distance of 28 kb in primary placenta
80  HSII as a nonredundant component of the hGH LCR essential for establishment of robust levels of hGH-
81                                      The hGH LCR mediates a domain of histone acetylation targeted to
82 U1F1 binding to cognate sites within the hGH-LCR and hGH1 promoter, but not to sites within the PRL p
83 ses binding affinity to sites within the hGH-LCR.
84 that contribute to the repression of the HPV LCR.
85 oped a neural network web server to identify LCRs and accurately predict whether they can bind nuclei
86  RNA polymerase II (Pol II) with immobilized LCR templates, USF and NF-E2 together regulate the assoc
87 ng greater cholesterol ester accumulation in LCR compared to HCR rats.
88 mportantly, HSP72 induction was decreased in LCR rats after only 3 days of eating the HFD.
89 es were used to interpret the differences in LCR relative to FBP images acquired at 16 mGy.
90 e that a stable MARE-associated footprint in LCR HS2 is important for the recruitment of transcriptio
91               Sufficiency of HSI and HSII in LCR activity was explored by establishing two additional
92 o separate the roles of LDB1 and mediator in LCR looping, we expressed a looping-competent but transc
93 g EPM and restraint that was not observed in LCR animals.
94  other transcription factor binding sites in LCR HS2 or in the adult beta-globin gene promoter region
95 h-sucrose diet produced greater steatosis in LCR and high capacity runner (HCR) rats.
96                            The transition in LCR characteristics was steeply nonlinear over a narrow
97                             The variation in LCR period and size with I(spark) is sufficient to accou
98 into existing T cell lines yields incomplete LCR activity.
99 ng those of fetal cells, including increased LCR-gamma-globin contacts.
100 chromosome synapsis increases with increased LCR length, and that ectopic synapsis is a necessary pre
101  To determine the contribution of individual LCR DNaseI hypersensitive sites (HSs) to transcription a
102                       Previously, we induced LCR-promoter looping by tethering the self-association d
103 50%, both IR techniques resulted in inferior LCR at both strength settings.
104 25%-50% dose reductions resulted in inferior LCR for vendors 1 and 2 for FBP and 25% dose reductions
105 in the eventual inactivation of the inserted LCR, probably as a result of multiple rounds of replicat
106 -globin gene (beta(m)), coupled to an intact LCR, a 5'HS3 complete deletion (5'DeltaHS3) or a 5'HS3 c
107 length and inversely influenced by the inter-LCR distance.
108 nalyses and identified 1143 interchromosomal LCR substrate pairs, >5 kb in size and sharing >94% sequ
109 he potential involvement of interchromosomal LCRs in recurrent chromosomal translocation formation, w
110 eas the distance between the cluster and its LCR impacts the level of placental expression.
111 ndel, or amino acid change in the E5a-E5b-L1-LCR fragment and were sequenced in full.
112             Initially, a 2,800-bp E5a-E5b-L1-LCR fragment was sequenced from 492/530 (92.8%) HPV6-pos
113          Background Ca (in locations lacking LCRs) quickly decays to resting Ca levels (<100 nM) at h
114 ion is facilitated at higher Pup by a larger LCR amplitude, whereas at low Pup by higher background C
115 crV produced variants with wild-type LCR(+), LCR(-), or dominant negative LCR(-) phenotypes, thereby
116 We discuss emerging evidence that prion-like LCRs are not, as commonly thought, autonomous aggregatio
117  recent findings, we propose that prion-like LCRs have evolved to regulate protein phase behavior and
118 ace-bound capture probes, the DNAzyme-linked LCR products induce electrocatalytic responses that are
119 in short-term surrogate oncological markers, LCR was not inferior to OCR in direct measures of surviv
120        In fact, regardless of the mechanism, LCRs can mediate or stimulate rearrangements, inciting g
121 sposase-based integration machinery, a micro-LCR-driven gamma-globin gene, and an MGMT(P140K) system
122 nd methylation throughout the minichromosome LCR/hGH-N domain.
123 ld-type LCR(+), LCR(-), or dominant negative LCR(-) phenotypes, thereby allowing us to identify discr
124 ls in potato tuber would require ANR but not LCR and that an epimerization process is involved.
125  wholly supports all the critical aspects of LCR activity.
126 tly shifted the cecal microbial community of LCR rats, resulting in a lower Firmicutes:Bacteroidetes
127 bal waves), LCR rhythmicity, and decrease of LCR period that parallels the changes observed experimen
128 in promoters as well as de novo formation of LCR/gamma-globin contacts.
129 d mediator occupancy and resulted in loss of LCR/beta-globin proximity.
130 tence of powerful compensatory mechanisms of LCR regulation via a complex local cross-talk of Ca pump
131 ese data support a site specificity model of LCR HS-globin gene interaction.
132 rythroleukemia cells, but phosphorylation of LCR-associated Pol II at serine 5 of the C-terminal doma
133  facilitate the investigation of the role of LCR variation as a driver of 22q11 rearrangements and th
134 tissue inflammation, and aortic stiffness of LCR rats.
135 le, and more rapid approach for the study of LCR activity in T cells, and its translation to therapeu
136 was a trend toward increasing utilization of LCR from 37.5% in 2008 to 44.1% in 2011.
137 here is a trend of increasing utilization of LCR, with acceptable conversion rates, across hospitals
138 d easily accessible tool for the analysis of LCRs with additional information included to aid the int
139 one cannot capture all structural aspects of LCRs and recommend the combined usage of a variety of pr
140 d exchange of data describing all aspects of LCRs.
141  on the definition of sequence complexity of LCRs and their connection with structure.
142 connection between structure and function of LCRs.
143 es of plasmodial proteins, the occurrence of LCRs cannot be associated with any specific metabolic pa
144  tiled CRISPRi screening indicates that only LCR segments heavily bound by this ternary complex are e
145  to 24 bp within interchromosomal paralogous LCRs of approximately 130 kb in length and 94.7% DNA seq
146     We observed persisting, roughly periodic LCRs in depolarized rabbit sinoatrial node cells (SANCs)
147  of Radiology (ACR) CT accreditation phantom LCR section at volume CT dose indexes of 8, 12, and 16 m
148 ping, via specific deletion of the placental LCR components, triggers a dramatic disruption of the hC
149 rythroblasts increases gamma-globin promoter-LCR contacts, stimulating transcription to approximately
150                             While at low Pup LCRs show smaller amplitudes, their larger durations and
151 ranscription or silencing through long-range LCR interactions involving an intergenic site of noncodi
152 of the product of a ligation chain reaction (LCR) and the use of gold nanoparticles (AuNPs) as signal
153 r, we developed the ligation chain reaction (LCR) assay on the Fiber Optic Surface Plasmon Resonance
154 achieved by using the ligase chain reaction (LCR) to recognize and amplify a C to T base change at a
155 on reaction (LDR) and ligase chain reaction (LCR), respectively.
156 able colon cancer were randomized to receive LCR or OCR.
157 Transcripts of leucoanthocyanidin reductase (LCR), which generates catechin, could not be detected.
158 etween the beta-globin locus control region (LCR) and active globin genes, and although TAL1 is one o
159 n erythroid cells, the locus control region (LCR) and beta-globin promoter form a chromatin loop that
160 etween the beta-globin locus control region (LCR) and gene in adult mouse erythroid cells, but whethe
161 ke (Nipbl) bind to the locus control region (LCR) at the CTCF insulator and distal enhancer regions a
162 nd E4) and a non-coding long control region (LCR) between L1 and E6.
163  regulated by a distal locus control region (LCR) composed of five deoxyribonuclease I hypersensitive
164 n erythroid cells, the locus control region (LCR) contacts beta-type globin genes in a developmental
165 e binding of Pol II at locus control region (LCR) element HS2, suggesting that Pol II is transferred
166 ion is controlled by a locus control region (LCR) embedded within this locus.
167                        Locus control region (LCR) functions define cellular identity and have critica
168 tion element (MARE) in locus control region (LCR) hypersensitive site 2 (HS2) reveals a remarkably hi
169 eviously described TH2 locus control region (LCR) in the mouse.
170        The beta-globin locus control region (LCR) is necessary for high-level beta-globin gene transc
171  that the L/M enhancer locus control region (LCR) loops with either the L or M promoter in a near 3:1
172  the human beta-globin locus control region (LCR) may function as part of an LCR holocomplex within a
173                     The long control region (LCR) of human papillomavirus (HPV) regulates early gene
174 udy the influence of a locus control region (LCR) on the expression of a highly characterized, develo
175 protein can silence the long control region (LCR) promoter that controls viral E6 and E7 oncogene exp
176 repression of the viral long control region (LCR) promoter.
177 ing of the beta-globin locus control region (LCR) to the active beta-globin promoter.
178 re that juxtaposes the locus control region (LCR) with downstream globin genes.
179 obin locus, called the locus control region (LCR), dynamically interacts with the developmental stage
180 11A binds the upstream locus control region (LCR), epsilon-globin, and the intergenic regions between
181 egulatory element, the locus control region (LCR), was revealed by analyzing DNase I hypersensitive s
182 gulated by the distant locus control region (LCR), which is brought into direct gene contact by the L
183  regulated by a distal locus control region (LCR), which is required in cis for the proper expression
184 ich are members of the locus control region (LCR)-associated remodeling complex (LARC).
185 is by a multicomponent locus control region (LCR).
186 trol of a reduced-size locus-control region (LCR).
187 moter, enhancer, and a locus control region (LCR).
188 components of a remote locus control region (LCR).
189 in to establishment of locus control region (LCR)/beta-globin proximity.
190 nes from the enhancer (locus control region [LCR]).
191 rgue that prion-like low-complexity regions (LCRs) are key regulators of protein solubility and foldi
192 d functional role of Low Complexity Regions (LCRs) in more than 1500 prokaryotic and phage proteomes.
193                      Low complexity regions (LCRs) in protein sequences are characterized by a less d
194 iple definitions for low complexity regions (LCRs) in protein sequences, with all of them broadly con
195 iple definitions for low complexity regions (LCRs) in protein sequences.
196 eats associated with low complexity regions (LCRs) in proteins of the malarial parasite Plasmodium fa
197 proteins depend upon low-complexity regions (LCRs) or RNA for phase separation, whereas Pab1's LCR is
198                       Locus control regions (LCRs) are cis-acting gene regulatory elements with the u
199                       Locus control regions (LCRs) comprise sets of DNA elements capable of establish
200 al (HSIII, IV, and V) locus control regions (LCRs).
201 of SR Ca pump and release channels regulates LCRs and Ca transient decay to insure fail-safe pacemake
202 rolled, in part, by local Ca(2)(+) releases (LCRs) from the sarcoplasmic reticulum, which couple to t
203             Intracellular Local Ca releases (LCRs) from sarcoplasmic reticulum (SR) regulate cardiac
204 kb and approximately 215-kb low-copy repeat (LCR) clusters, respectively, by aCGH and SNP array analy
205 ssociated with the flanking low-copy repeat (LCR) length and inversely influenced by the inter-LCR di
206 ombination between distinct low-copy repeat (LCR) substrates.
207  (NAHR), occurring between low-copy repeats (LCRs) >10 kb in size and sharing >97% DNA sequence ident
208                            Low copy repeats (LCRs) are recognized as a significant source of genomic
209 sion polymorphisms between low-copy repeats (LCRs) might predispose chromosomes to meiotic non-alleli
210 c architecture, especially low copy repeats (LCRs) or segmental duplications (SDs).
211  flanked by large, complex low-copy repeats (LCRs) with directly oriented subunits of ~109 kb in size
212 ments mediated by flanking low-copy repeats (LCRs), NF1 intragenic rearrangements vary in size, locat
213 aring laparoscopic-assisted colon resection (LCR) with open colon resection (OCR) for colon cancer.
214 ts undergoing laparoscopic colon resections (LCR).
215 he absence of calcium (low-calcium response [LCR(+)] phenotype) was exploited to isolate dominant neg
216 ed to LMO2, sufficient to completely restore LCR-promoter looping and transcription in LDB1-depleted
217      We introduce laser cavitation rheology (LCR) as a minimally-invasive optical method to character
218         Translation of these asparagine-rich LCRs demands extraordinarily high amounts of asparaginyl
219 m single As exposure (Life time Cancer Risk, LCR>1x10(-4)).
220 performed the L. camara leaf (LCL) and root (LCR) de novo transcriptome analyses.
221 d 513,985 unigenes from leaf (LCL) and root (LCR) respectively.
222 aerobic capacity in the low capacity runner (LCR) rat increases susceptibility to acute and chronic h
223 r low aerobic capacity (low capacity runner; LCR) displayed susceptibility to high fat diet-induced s
224 selectively bred to be low-capacity runners (LCRs) and high-capacity runners (HCRs)-selective breedin
225 nsic aerobic capacity (Low Capacity Runners, LCR), and 3) unselected Sprague-Dawley (SD) rats with or
226 w intrinsic endurance (low capacity runners; LCR).
227  or RNA for phase separation, whereas Pab1's LCR is not required for demixing, and RNA inhibits it.
228 known transcription factors but not the same LCR architecture.
229  This resulted in a progression in simulated LCR size (from sparks to wavelets to global waves), LCR
230 automatic detection of numerically simulated LCRs and examined LCR regulation by SR Ca pumping rate (
231                 The single placenta-specific LCR component, HSIV, is located at -30 kb to the cluster
232                         Moreover, the FO-SPR LCR assay could discriminate single nucleotide polymorph
233   While the methodologies available to study LCRs are already very advanced, we foresee that a more c
234 -LCR, we refer to this lncRNA cluster as TH2-LCR lncRNA.
235       Given its genomic synteny with the TH2-LCR, we refer to this lncRNA cluster as TH2-LCR lncRNA.
236 mals exhibited more anxiotypic behavior than LCR animals on the EPM, and exhibited an increase in pla
237             HCR rats expressed less ENK than LCR rats in the nucleus accumbens among females (p<0.01)
238 r obstacle to study these mechanisms is that LCR exhibit complex Ca release propagation patterns (inc
239 obin genes for LCR contacts and suggest that LCR-promoter loops are formed and released with rapid ki
240               Recent studies have shown that LCRs may co-occur with intrinsically disordered regions,
241                                          The LCR and beta-globin gene establish proximity in these ce
242                                          The LCR is composed of a number of DNase I-hypersensitive si
243                                          The LCR period, a critical determinant of the spontaneous SA
244                                          The LCR period, ie, a delay between AP-induced Ca(2+) transi
245 between the BGL3/gamma-globin region and the LCR is established.
246 ment of SMAR1-HDAC1 repressor complex at the LCR and E6 MAR sequences, thereby decreasing histone ace
247 racted with endogenous Ldb1 complexes at the LCR to form a chromatin loop, causing recruitment and ph
248  were no significant differences between the LCR and OCR groups in 5-year follow-up of overall surviv
249 ed the frequency of interactions between the LCR and the adult beta-globin promoter.
250 ntial for efficient interactions between the LCR and the beta(maj)-promoter as well as transcription
251  the CTCF insulator elements and between the LCR distal enhancer and the target gene.
252                In adult erythroid cells, the LCR can be redirected from the adult beta- to the fetal
253                  Mechanisms that control the LCR period, however, are still unidentified.
254 ggesting that Pol II is transferred from the LCR to the globin gene promoters.
255                                 However, the LCR rat demonstrated greater susceptibility to increased
256 omoter contains consensus MAR element in the LCR and E6 sequences where SMAR1 binds and reinforces HP
257 ere associated with hepatic steatosis in the LCR including higher liver triglycerides (6.00 +/- 0.71
258 lcoholic fatty liver disease observed in the LCR rats following western diet feeding was associated w
259 Fs tested, 28 activated and 36 inhibited the LCR of HPV-18 by more than 2-fold.
260 roxidase-mimicking DNAzyme sequence into the LCR amplification probes design which in turn, serves as
261 roteins were inactive at alleles lacking the LCR, demonstrating that their activities depend on long-
262 s at the DNase I hypersensitive sites of the LCR could be either depleted or retained depending on th
263 e switching, a change in conformation of the LCR holocomplex, or both.
264 tion and the gene activation function of the LCR in mammalian cells.
265   DNase I-hypersensitive site I (HSI) of the LCR is essential to full developmental activation of the
266  new TFs implicated in the regulation of the LCR of HPV-18 and HPV-16.
267 on at the hGH-N promoter, and looping of the LCR to its target promoter.
268  is dependent not only on the actions of the LCR, but also on the multigene composition of the cluste
269 eved to encompass the regulatory core of the LCR.
270 de insight on the molecular evolution of the LCR.
271 pe-specific hGH-N activation function of the LCR.
272 ith DNaseI hypersensitive site (HS) I of the LCR.
273                 This activity depends on the LCR, consistent with an LCR-promoter looping mechanism.
274 e diagnostic medical physicists reviewed the LCR images in a blinded fashion and graded the visibilit
275 ifted T-90(C) and proportionally shifted the LCR period and spontaneous cycle length (R(2)=0.98).
276                 Recruitment of Pol II to the LCR occurs in undifferentiated murine erythroleukemia ce
277 strated FOXA1 and MYC in vivo binding to the LCR of both HPV types using chromatin immunoprecipitatio
278                           In addition to the LCR, we found robust NLI complex occupancy at a site dow
279 to the globin gene promoters but also to the LCR.
280 pected fluid chromatin dynamics, whereby the LCR can be initially dominant over the endogenous CD8 ge
281 looping of the (G)gamma-globin gene with the LCR was disrupted with decreased occupancy of the comple
282 wnstream promoter region interferes with the LCR-mediated recruitment and activity of Pol II.
283 d MYC have putative binding sites within the LCR sequence, as indicated using the TRANSFAC database.
284                                          The LCRs flanking a contiguous genomic interval encompassing
285                                          The LCRs overlap with Ca transient decay, causing an elevati
286 spite their abundance, the function of these LCRs remains unclear.
287                        The features of these LCRs were reproduced by a numerical model consisting of
288 lected TF expression plasmids in addition to LCR-luciferase vectors of different molecular variants o
289 ehavior in the novel environment compared to LCR animals.
290 laps between different properties related to LCRs, using examples.
291 laps between different properties related to LCRs, using examples.
292 were 27.0 and 18.0, respectively while total LCR values for adult and children were 0.0049 and 0.0032
293 ons of LcrV produced variants with wild-type LCR(+), LCR(-), or dominant negative LCR(-) phenotypes,
294                         Following this view, LCRs can also be defined as regions showing composition
295 e (from sparks to wavelets to global waves), LCR rhythmicity, and decrease of LCR period that paralle
296 eletions of 2 HSs, and deletion of the whole LCR and found all of the HSs had a similar spectrum of a
297 ther the short-term benefits associated with LCR for colon cancer could be achieved safely, without s
298 have been developed to identify regions with LCRs or amino acid bias, but most of them as stand-alone
299 on boundaries for all individuals are within LCRs distal to the DiGeorge/velocardiofacial microdeleti
300                  Motifs within the zebrafish LCR include CACCC, GATA, and NFE2 sites, suggesting func

 
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