ライフサイエンスコーパス: AP4

1 AP4 downregulation by p53 was mediated indirectly by the

2 AP4 interacts with Runx1 in cells in which Cd4 is silenc

3 AP4 overexpression rendered the intrinsic growth capacit

4 AP4 was found only in the cytoplasmic fraction.

5 AP4 was induced by c-MYC during the T-B interactions, wa

6 conserved repressor of ATGL-1 called HLH-11/AP4.

7 ee genes encoding adaptor protein complex 4 (AP4) subunits: a nonsense mutation in AP4S1 (NM_007077.3

8 ry protein of the adaptor protein complex 4 (AP4).

9 Activator protein 4 (AP4) is a basic helix-loop-helix leucine-zipper transcri

10 331 of factor Va heavy chain (9 amino acids, AP4') contains a binding site for factor Xa.

11 In addition, AP4 induction was required for EMT, migration, and invas

12 OTX-008 showed significant decrease in p-Akt/AP4 and protein-promoter activity of Gal-1 and fibronect

13 Furthermore, although AP4-deficient CD8(+) T cells appeared to normally down-r

14 ive feedback loop involving miR-15a/16-1 and AP4 that stabilizes epithelial and mesenchymal states, r

15 ition, p300, Sox, nuclear factor-kappaB, and AP4 appear to be modulators of IEX-1 gene expression to

16 n kidneys of type 1 and 2 diabetic mice, and AP4 is a major transcription factor that activates Gal-1

17 metabolism were shared targets of c-Myc and AP4.

18 TGFbeta repression of SALL2 and AP4 is independent of the induction of connective tissue

19 Mouse monoclonal antibody AP4-24H11 was shown previously to blunt quorum sensing-m

20 trans-acting factors such as Sp1, AP1, AP2, AP4, and the glucocorticoid receptor, the hMTIIA promote

21 lococcal AIP receptors AgrC and the AIPs, as AP4-24H11.AIP-4 binding recapitulates features that have

22 In colorectal cancer cells, AP4 was downregulated by DNA damage in a p53-dependent m

23 interacting with the adaptor protein complex AP4 and Stargazin and possibly using recycling endosomes

24 nsfection of an expression vector containing AP4 coding sequence downregulates the expression of repo

25 nsfection of an expression vector containing AP4 coding sequence reduces estrogen-induced promoter ac

26 or by DL-2-amino-4-phosphonobutyric acid (DL-AP4).

27 es, which are depolarizing and blocked by DL-AP4.

28 Elevated AP4 expression in primary CRC significantly correlated w

29 ed to normally down-regulate CD4 expression, AP4 deficiency significantly increased the frequency of

30 conditions identified a transcription factor AP4 (TFAP4) construct that enhanced fitness of chronical

31 oter and identified the transcription factor AP4 as binding to the Gal-1 promoter to up-regulate its

32 The transcription factor AP4 increases along with SALL2 in quiescent cells and po

33 The transcription factor AP4 mediates epithelial-mesenchymal transition (EMT) in

34 ic helix-loop-helix ZIP transcription factor AP4 to have an important role in Cd4 regulation.

35 Here, we show that the transcription factor AP4 was required for sustained GC B cell proliferation a

36 basic helix-loop-helix transcription factor AP4/TFAP4/AP-4 is encoded by a c-MYC target gene and dis

37 ription factor HNF-3 and a ubiquitous factor AP4.

38 These results suggest important roles for AP4 and SP1 in the constitutive expression of mEPCR.

39 Furthermore, AP4 directly suppressed expression of miR-15a/16-1.

40 Here we identified AP4 as the transcription factor that was induced by c-My

41 These findings imply AP4 as a new regulator of EMT that contributes to metast

42 QP4-Ab positivity and physical disability in AP4-Ab negative relapsing cases.

43 of a double-negative feedback loop involving AP4 and miR-15a/16-1 that regulates EMT and metastatic p

44 L-AP4 exhibited high potency and a pharmacological profile

45 l-AP4 raised internal calcium concentration.

46 L-AP4-sensitive, but not insensitive, cells responded to a

47 onists L-2-amino-4-phosphono-butyric acid (L-AP4) and O-phospho-L-serine (L-SOP) both caused a concen

48 and L-(+)-2-Amino-4-phosphonobutyric acid (L-AP4) in the presence and absence of three distinct poten

49 ist L-(+)-2-amino-4-phosphonobutyric acid (L-AP4) inhibited these IPSCs through a presynaptic mechani

50 agonist L-2-amino-4-phosphonobutyric acid (L-AP4) produced an increase in visual response habituation

51 eptor, l-2-amino-4-phosphonobutanoic acid (l-AP4) was tested in slices of rat visual cortex.

52 and L-(+)-2-amino-4-phosphonobutyric acid (L-AP4), agonists for group-II and group-III mGluRs, respec

53 und L-(+)-2-Amino-4-phosphonobutyric acid (L-AP4), are often used for receptor activation and compoun

54 ist, L(+)-2-amino-4-phosphonobutyric acid (L-AP4), decreased the evoked EPSCs by 71 % with an EC50 of

55 and L(+)-2-amino-4-phosphonobutyric acid (L-AP4), respectively) decreased the frequency of miniature

56 st, l-(+)-2-Amino-4-phosphonobutyric acid (l-AP4), slightly decreased the frequency of the pyloric rh

57 ist L-(+)-2-amino-4-phosphonobutyric acid (L-AP4); however, full activation was apparent when both li

58 nist L(+)-2-amino-4-phosphonobutyric acid (L-AP4); it was blocked by the broadly acting mGluR antagon

59 nist (S)-2-amino-4-phosphonobutanoic acid (L-AP4; 10 microM) were without effect, indicating that the

60 ate monohydrate) and the group III agonist L-AP4 (L-(+)-2-amino-4-phosphonobutyric acid) failed to al

61 ory actions of the group III mGluR agonist L-AP4 on depolarizing GABA activity were found in developi

62 tal cells, we found that an mGluR agonist (L-AP4) reduced cone-driven light responses and mEPSC frequ

63 a solution containing the mGluR6 agonists L-AP4 or glutamate.

64 Also, l-AP4 had little effect on membrane potential and input im

65 ively reversed the inhibition by L-CCG and L-AP4 to 81.3 +/- 12% and 65.3 +/- 6.6% of predrug, respec

66 The effects of L-CCG and L-AP4 were fully reversible.

67 er mGluR agonists (ACPD, DHPG, L-CCG-1 and L-AP4) did not induce a significant inward current at the

68 These effects were not mimicked by L-AP4 (100-200 microM).

69 the magnitude of the depression caused by L-AP4 indicates that any physiological activation of group

70 The depression of the CT EPSP caused by L-AP4 was reversed using the group III antagonist (S)-2-am

71 recordings of cones and horizontal cells, L-AP4 slightly reduced cone ICa ( approximately 10%) and c

72 4.4 +/- 3.8 % and 88.0 +/- 24.7 microM for L-AP4, and 42.0 +/- 2.5 % and 958 +/- 492 microM for L-SOP

73 SNAP-25 cleaving protease BoNT/A inhibited L-AP4 effects on synaptic transmission, as did introductio

74 no [3H]glutamate binding to group 3-like (L-AP4 sensitive) sites could be demonstrated.

75 Neither L-CCG (0.0001-10 microM) nor L-AP4 (0.001-50 microM) caused membrane currents or change

76 efore and after intravitreal injections of L-AP4 (not APB) (2-amino-4-phosphonobutyric acid, 1.6-2.0

77 and LY341495 indicate that this action of L-AP4 is mediated via mGlu7 and mGlu8 and not mGlu4 recept

78 Furthermore, the effect of L-AP4 on striatopallidal transmission was absent in mGluR4

79 that intracerebroventricular injections of L-AP4 produce therapeutic benefit in both acute and chroni

80 The inhibitory effect of l-AP4 was blocked by MPPG and partially blocked by APICA.

81 ed in vitro and in vivo in the presence of L-AP4, a blocker of retinal ON-bipolar cells.

82 s not elicited by intraseptal injection of L-AP4, cysteine sulfinic acid or DHPG.

83 The potencies of L-AP4, L-SOP and LY341495 indicate that this action of L-A

84 e acting as a noncompetitive antagonist of L-AP4, XAP044 and derivatives act as apparent competitive

85 Brainstem microinjection of APDC or L-AP4 decreased plasma insulin secretion, whereas only APD

86 e agonist, L-2-amino-4-phosphonobutanoate (L-AP4).

87 II agonist L-2-amino-4-phosphonobutanoate (L-AP4).

88 luR agonist L-2-amino-4-phosphonobutyrate (L-AP4) was less potent, with EC50 values of 297 nM (contro

89 ts (such as L-2-amino-4-phosphonobutyrate (L-AP4)) potently inhibit transmitter release, but their au

90 hat MSG and L-2-amino-4-phosphonobutyrate (L-AP4), a ligand for mGluR4, elicit similar tastes in rats

91 responding to 2-amino-4-phosphonobutyrate (L-AP4), presumably metabotropic L-glutamate receptors, do

92 tor was the L-2-amino-4-phosphonobutyrate (L-AP4)-sensitive, group III receptor.

93 dominant input to the cell was stimulated, l-AP4 generally reduced the EPSP that was produced.

94 For 8.3-Hz stimulation, L-AP4 eliminated the steady state PERG and reduced simulat

95 For 2-Hz stimulation, L-AP4 reduced both negative- and positive-going (N95 and P

96 Several characteristics of these L-AP4-resistant light responses suggested that they were d

97 All neurones responsive to L-AP4 were also responsive to APDC, but not vice versa.

98 variances in response to glutamate versus L-AP4.

99 Further, in neurones where L-AP4 decreased mIPSC frequency, exendin-4 increased, whil

100 ferent maximal levels of potentiation with L-AP4 versus glutamate, but there appear to be common stab

101 ollowing disruption of the ON pathway with L-AP4.

102 Mice lacking AP4 specifically in CD8+ T cells showed enhanced suscept

103 ndings unveil a distinct aspect of the c-Myc-AP4 axis and highlight a previously unrecognized intrins

104 Here, we reveal a role for the c-Myc-AP4 axis in axon regeneration and the intrinsic growth c

105 Accordingly, activation of AP4 induced EMT and enhanced migration and invasion of C

106 Here a genome-wide characterization of AP4 DNA binding and mRNA expression was performed using

107 B-cell-specific deletion of AP4 resulted in reduced GC sizes and reduced somatic hyp

108 The downregulation of AP4 was necessary for induction of MET and cell cycle ar

109 Inhibition of AP4 in CRC cells resulted in decreased lung metastasis i

110 Neuronal-specific knockdown of AP4 abolished the regenerative phenotype induced by c-My

111 yses, we demonstrated that overexpression of AP4 in mice not only accelerated in vivo axon regenerati

112 Moreover, down-regulation of AP4 by small interfering RNA resulted in a significant d

113 Conversely, down-regulation of AP4 resulted in mesenchymal-epithelial transition and in

114 a previously unrecognized intrinsic role of AP4 in axon regeneration, with potential therapeutic imp

115 d carrying mutations in the binding sites of AP4 to Gal-1 promoter resulted in decreased protein func

116 geted the 3' untranslated region (3'-UTR) of AP4 mRNA, induced mesenchymal-epithelial transition (MET

117 thelial protein C receptor gene contains one AP4 site and one SP1 site.

118 alian clathrin adaptor complex AP1 and plant AP4 but not that of plant and mammalian AP2.

119 Despite normal priming, AP4-deficient CD8+ T cells failed to continue transcript

120 hibits expression of SALL2 and its regulator AP4 when added to quiescent fibroblasts.

121 eration and tumor cell migration like REPIN1/AP4, ST3GAL6, TRNAU1AP and PFKM are degraded upon loss o

122 Thereby, hundreds of induced and repressed AP4 target genes were identified.

123 We demonstrate that AP4-TgTEP is essential for the actin-dependent transport

124 s, these results support the hypothesis that AP4-complex-mediated trafficking plays a crucial role in

125 These results indicate that AP4 integrates T-cell-mediated selection and sustained e

126 Kinetic analyses revealed that AP4' is a noncompetitive inhibitor of prothrombinase wit

127 Our results suggest that AP4 contributes to Cd4 silencing both in DN and CD8(+) T

128 A new study reveals a key role for the AP4 adaptor protein complex in the Golgi-to-endosome tra

129 ndings reveal that, unlike in metazoans, the AP4 complex in T. gondii utilizes clathrin as a coat pro

130 Mutations in the core sequence of the AP4 and SP1 sites impaired both nuclear protein binding

131 cognizable syndrome due to deficiency of the AP4 complex.

132 have elucidated the crystal structure of the AP4-24H11 Fab in complex with AIP-4 at 2.5 A resolution

133 nvolved in the control of proliferation, the AP4 target genes included markers of stemness (LGR5 and

134 Thus, AP4 maintains c-Myc-initiated cellular activation progra

135 yclic AMP-responsive elements [CREs] and two AP4 sites) reported by others to be important for Tax-me

136 ning amino acid region 323-331 of factor Va (AP4') was found to be a potent inhibitor of prothrombina

137 er, miR-15a levels inversely correlated with AP4 protein levels shown previously to correlate with di