ライフサイエンスコーパス: explanation for how

1 cells to a duct-like phenotype, providing an explanation for how a characteristically ductal tumor ca

2 These observations provide a possible explanation for how a linear bacterial chromosome can ex

3 The conventional explanation for how a morphogen patterns a tissue holds

4 And, there is now a testable explanation for how a protein can fold so quickly: A pro

5 t model provides an attractive and plausible explanation for how a typical antigen presenting cell, e

6 tabolite-initiated amyloidogenesis offers an explanation for how Abeta aggregation could occur at phy

7 orepressor, HPr-Ser46-P, provide a molecular explanation for how adjunct corepressors G6P and FBP enh

8 Our work provides an explanation for how AIDA-1 dysfunction might contribute

9 This mechanism provides an explanation for how an agonist-bound nuclear receptor ca

10 Still needed is a synthetic explanation for how and why growth rates vary as body si

11 These results offer an explanation for how and why unmethylated microsatellite

12 These results provide a simple evolutionary explanation for how ankyrin-B and ankyrin-G have acquire

13 ights into the function of ATDC and offer an explanation for how ATDC promotes cancer cell proliferat

14 production by cDCs and provides one possible explanation for how bacterial infection might precipitat

15 These findings provide an explanation for how beta-catenin localizes to the nucleu

16 amin A production and provides a mechanistic explanation for how both genetics and diet can affect th

17 a loss of protein motion may also provide an explanation for how calcium-ion-binding affinity is incr

18 of karyokinesis and cytokinesis provides an explanation for how cell cycle flexibility is achieved i

19 degeneration in SCA7 and thus may provide an explanation for how cell-type specificity is achieved in

20 Regulated tip growth provides an attractive explanation for how cells are able to synthesise very lo

21 on-condensation dynamics creates mechanistic explanation for how cells properly respond to variable l

22 neage specification, and suggest mechanistic explanations for how CIC mutations may impact the pathog

23 We believe that our data provide a molecular explanation for how circadian phases, such as wake-sleep

24 n of the coactivator and suggest a molecular explanation for how coactivators increase the transcript

25 This study provides a structural explanation for how CobT can phosphoribosylate most of t

26 hieve distinct cohesin functions provides an explanation for how cohesin mutations can specifically l

27 This regular distribution provides an explanation for how complete chromosome replication can

28 pithelial differentiation, and they offer an explanation for how decreased levels of GLI1 are likely

29 al states of SERCA and provides a structural explanation for how dephosphorylated PLB decreases Ca(2+

30 fense (PATHOS-D) hypothesis provides a novel explanation for how depression can be nonadaptive in the

31 3 function as a PRROS provides a mechanistic explanation for how diastolic Ca(2+) influx specifically

32 is finding is that it provides a mechanistic explanation for how different types (strains) of rhinovi

33 Information theory has offered explanations for how different types of neurons can maxi

34 re of these interactions provide a molecular explanation for how distinct SNX-BAR-decorated tubules a

35 One potential explanation for how divergent circuits have evolved is t

36 ction by pDCs in mice, providing a potential explanation for how DMPA impairs innate antiviral immuni

37 oss promotes tumor progression, providing an explanation for how E-cadherin loss increases metastasis

38 for GMP-PCP-bound Cdc42, provides a possible explanation for how effectors can distinguish between th

39 ream effector of Sema3E-PlexinD1 provides an explanation for how extracellular signals are translated

40 ds to the 36-bp DNA fragment and provides an explanation for how FitB enhances the DNA binding affini

41 lpha/GPR-1/2 signaling pathway, providing an explanation for how Galpha-dependent force is regulated

42 read among neuronal cells and may provide an explanation for how glucocerebrosidase mutations increas

43 ilize range boundaries and provide a general explanation for how groups of widely divergent sizes can

44 They also may provide a refined biochemical explanation for how H3K36me3 loss leads to genomic insta

45 hobic face of the epitope, thus providing an explanation for how HCV isolates bearing mutations at As

46 hromatin proteins and provides a mechanistic explanation for how Hmgb2 regulates gene expression and

47 These observations provide a partial explanation for how homogenization of centromere DNA seq

48 to BCAA catabolism, providing a mechanistic explanation for how increased BCAA catabolic flux can ca

49 calcium entry pathways provided a plausible explanation for how inflammatory [Ca2+]i mediators may d

50 III by the DnaX complex provides a molecular explanation for how initiation complexes form when suppo

51 l via IRS1/PI3K/Akt2 activation, a potential explanation for how insulin is retarding the progression

52 to alter the Ab paratope, thus providing an explanation for how isotype can affect Ab specificity.

53 n the absence of ring stacking, providing an explanation for how it can reset the clock.

54 eviously appreciated and provide a molecular explanation for how it moves actin at fast speeds.

55 ular organisms, we hope to uncover proximate explanations for "how" it causes disease in humans.

56 al constraints but also provide a mechanical explanation for how large-scale interactions through cel

57 igomerize syt II offers a possible molecular explanation for how lead interferes with calcium-evoked

58 Together these results provide a plausible explanation for how male and female moths, and maybe oth

59 ovel hypothesis provides the first plausible explanation for how marine animals can navigate to natal

60 ion, the mechanism proposed here provides an explanation for how MDA5 uses filament assembly and disa

61 t on magnesium affinity provides a plausible explanation for how mechanical strain can alter this act

62 This nucleation mechanism provides one explanation for how mercury may be immobilized, and even

63 In addition, we provide a mechanistic explanation for how mesangial cells in primary culture a

64 tion and this mechanism provides a plausible explanation for how metal binding controls the DtxR repr

65 ia throughout the mouse lifespan provides an explanation for how microglial priming early in life can

66 We provide a possible physiological explanation for how microgravity can cause symptoms simi

67 These results provide an explanation for how mitotic HSF2 sumoylation is regulate

68 These results provide a molecular explanation for how Mtb impairs the adaptive immune resp

69 nt kinetics in both cell types, providing an explanation for how mutations in the ubiquitously expres

70 alpha control provides a potential molecular explanation for how N-terminal Rb loss-of-function delet

71 e measured orientation provides a structural explanation for how neck surface residues enhance proces

72 Altogether, these data provide a mechanistic explanation for how newborns may cope with an immunosupp

73 Our model provides a mechanistic explanation for how nucleotides regulate the p97-ataxin3

74 although not necessarily mutually exclusive, explanation for how oncogenes initiate and sustain tumor

75 he cyclin-binding motif of p21, providing an explanation for how p21 is found associated with active

76 ycle checkpoint is activated and provides an explanation for how p53 is protected from degradation in

77 Our findings provide an elegant molecular explanation for how PAS sequences are recognized for mRN

78 They also provide an explanation for how pathologically increased TGF-beta si

79 weight of evidence by providing a plausible explanation for how PCBs can cause NHL through immune dy

80 se interdomain contacts provide a functional explanation for how PIP(2) binding and tyrosine phosphor

81 ses lamina dynamics, providing a mechanistic explanation for how PKC activity influences nuclear size

82 ty of natural small molecules represents one explanation for how plants may rapidly recruit enzymes f

83 , with the dynein motor complex may offer an explanation for how poliovirus hijacks the cellular tran

84 These data provide a mechanistic explanation for how PPARgamma activation facilitates amy

85 -B at Ser(523) provides a possible molecular explanation for how pressor hormones inhibit CNP signali

86 Our results provide a novel explanation for how primates uniquely concentrate xantho

87 s psychologically and biologically plausible explanations for how psychological factors might influen

88 ural and biochemical results thus provide an explanation for how receptor recognition, phospholipid b

89 They also give a molecular explanation for how rising CO(2) concentrations elicit i

90 This can provide a novel explanation for how risk influences action selection and

91 In this paper, we offer an explanation for how selectivity for orientation could be

92 during the cell cycle, thereby providing an explanation for how 'silent' heterochromatin can be tran

93 These findings provide a mechanistic explanation for how Smk1 activity thresholds are generat

94 These findings suggest a possible structural explanation for how so many commonly used medications bl

95 ound apolipoprotein A-I which may provide an explanation for how specific domains of apolipoprotein A

96 These studies provide a simple mechanistic explanation for how stromal cell signals regulate both t

97 Our results provide an explanation for how structurally similar spectrin-like r

98 aureus entry into the dermis and provide an explanation for how such dermal dysbiosis results in inc

99 Here we provide an explanation for how Tax induces some Chk2 activities but

100 Our findings offer an explanation for how telomerase is recruited to telomeres

101 In this paper, we develop a theoretical explanation for how temperature robustness can emerge fr

102 We provide an explanation for how the AMO may drive physical changes i

103 This deformation pattern may provide an explanation for how the Arabidopsis leaf maintains a rel

104 and network theories to offer a mechanistic explanation for how the brain moves between cognitive st

105 These results provide a new and novel explanation for how the calpain/calpastatin network is o

106 ptosis in thymocytes and provide a molecular explanation for how the cAMP stimulators, including the

107 nt ABC transporter activities and provide an explanation for how the comparable transporter in native

108 This provides one mechanistic explanation for how the epithelial-mesenchymal transitio

109 These findings offer a molecular-level explanation for how the HCM mutation cTnI-R145G reduces

110 This study represents the first detailed explanation for how the islet facilitates inhibitory act

111 t serves to protect the genome, providing an explanation for how the loss of a survival pathway leads

112 Missing was an explanation for how the movements of these domains are c

113 at a peripheral location, which provides an explanation for how the NAT protein structure is not sig

114 ctivities in homologues of OSBS and a likely explanation for how the OSBS from Amycolaptosis also can

115 r protease recognition provides a compelling explanation for how the oxidation-induced conformational

116 cognition specificity provides a mechanistic explanation for how the same effector function can be us

117 s (scleractinian corals) provides a possible explanation for how the site of gastrulation has changed

118 omewhat cross-reactive, thereby providing an explanation for how the specific recognition of a limite

119 Our data provide an explanation for how the stromal ECM encodes architectura

120 These data provide a mechanistic explanation for how the SUMOylation status of Drp1 acts

121 Our results provide an explanation for how the unique domain architecture of JA

122 emical shift mapping results also suggest an explanation for how the unstable dnaQ49 mutator phenotyp

123 lated receptors by Nef is rising, so are the explanations for how their downregulation could contribu

124 nic in geothermal systems, offer a molecular explanation for how these algae tolerate arsenic in thei

125 e of the two compounds provided a structural explanation for how these compounds are able to effectiv

126 yl)propane 1-phosphate provided a structural explanation for how these compounds are able to effectiv

127 The evolutionary explanation for how these polymorphisms are maintained h

128 ped strand displacement model as a potential explanation for how these stutter products are generated

129 tory and excitatory CIN pathways and suggest explanations for how these pathways maintain alternating

130 nd the cell surface and provide a functional explanation for how this association occurs.

131 , the 'ABC model' is a simple and satisfying explanation for how this conserved floral architecture i

132 They also provide an explanation for how this small molecule can direct diver

133 These studies provide a mechanistic explanation for how this therapeutic strategy can select

134 on of the skin-homing receptor, providing an explanation for how thymic selection is coordinated with

135 conformational ensemble model, providing an explanation for how VDR and possibly the estrogen recept

136 cancer cells, providing a direct mechanistic explanation for how VEGF-C expression is upregulated in