ライフサイエンスコーパス: afadin

1 h protein harbors a cryptic binding site for afadin.

2 ll junction regulators including the protein Afadin.

3 tion proteins vinculin, alpha-E-catenin, and afadin.

4 vated contractility by increasing junctional afadin.

5 AJ reannealing mediated by the Rap1 effector afadin.

6 ynapses through the scaffolding protein AF-6/afadin.

7 y associates with the nectin-binding protein afadin.

8 d with the cytoplasmic actin-binding protein afadin.

9 It was also previously shown that AF-6 (afadin), a PDZ domain-containing protein, associates wit

10 In this study, we find that afadin, a component of N-cadherin.beta-catenin.alpha-N-c

11 osphoproteomics for S6K1 substrates revealed Afadin, a known component of cell-cell junctions require

12 that lumen formation and elongation require afadin, a nectin adaptor protein implicated in adherens

13 Infectious-center growth is facilitated by afadin, a protein connecting the adherens junction and t

14 We propose that afadin acts as a robust protein scaffold that maintains

15 Together, these results suggest that afadin acts upstream of the Par complex to regulate the

16 neuroblasts), the scaffolding protein Canoe (Afadin/Af-6 in mammals) regulates spindle orientation, b

17 vo and phosphorylates Canoe, the ortholog of Afadin/AF-6, in vitro.

18 that palatal epithelial conditional loss of afadin (Afdn) - an obligate nectin- and actin-binding pr

19 Loss of Afadin also impairs the ability of breast cancer cells t

20 cell adherens junctions and interacts with l-afadin, an F-actin-binding protein.

21 to thrombin or APC signaling, a function for afadin and adducin-1 actin binding proteins in thrombin-

22 through their cytoplasm-associated proteins, afadin and catenins, it is not fully understood how nect

23 we show that the adherens junction proteins afadin and CDH2 are critical for the control of cell pro

24 ll-cell adhesion sites after both the nectin-afadin and E-cadherin-catenin systems had been assembled

25 nin-binding protein that connects the nectin-afadin and E-cadherin-catenin systems through alpha-acti

26 hat LMO7 was associated with both the nectin-afadin and E-cadherin-catenin systems.

27 The most apical is populated with nectins/afadin and lined with F-actin; the second is populated w

28 Both Afadin and PDZ-GEF2 colocalized and coimmunoprecipitated

29 tion facilitates formation of a complex with Afadin and PDZ-GEF2 that activates Rap1A, which regulate

30 ted with the PDZ domain-containing molecules Afadin and PDZ-guanine nucleotide exchange factor (GEF)

31 Our study uncovers essential roles of Afadin and RhoA in pancreatic central lumen morphogenesi

32 In this issue, Choi et al. show that afadin and ZO-1 regulate tension and maintain zonula adh

33 lial permeability via association with ZO-2, afadin, and PDZ-GEF1 to activate Rap2c and control contr

34 physical interactions between MAGI-1, AFD-1/afadin, and SAX-7/L1CAM, which are part of a functional

35 scaffold signaling complex containing ZO-2, Afadin, and the small GTPase Rap2.

36 iates directly with ZO-2 and indirectly with afadin, and this complex, along with PDZ-GEF1, activates

37 These results indicate that LMO7 is an afadin- and alpha-actinin-binding protein that connects

38 of the human LIM domain only 7 (LMO7) as an afadin- and alpha-actinin-binding protein.

39 Here, we observed dynamic polarization of afadin- and alpha-actinin-interacting protein (ADIP) in

40 e Rap1 and the actin-junctional linker Canoe/afadin are essential for polarity establishment, as both

41 the synaptic localization of nectin-1 and l-afadin are F-actin-dependent and that the shedding of ne

42 er metastatic breast cancer cells, including Afadin, Arhgap21, Pdlim2, Pdlim7, Rims2, Scrib, and ZO-1

43 We specifically examined the role of Afadin as a potential Claudin-2-interacting partner that

44 Our findings identify nectins and afadin as components of the reelin signaling pathway and

45 Moreover, combining Claudin-2 and Afadin as prognostic markers better predicts the potenti

46 Afadin associates with Claudin-2, an interaction that re

47 data demonstrate that activation of the Rap1-afadin axis is a physiological mechanism driving restora

48 de the first direct evidence that the nectin-afadin axis is essential for proper palate shelf elevati

49 elix bundles, both of which are required for afadin binding.

50 also generated a nectin-4 mutant without the afadin-binding site in its cytoplasmic tail.

51 lpha-catenin, residues 385-651, contains the afadin-binding site.

52 supra-complex bound to F-actin reveals that afadin-CC bridges adjacent alphaE-catenin actin-binding

53 adherin-beta-catenin-alphaE-catenin-vinculin-afadin-CC supra-complex bound to F-actin reveals that af

54 upts the synaptically localized nectin-1 and afadin cluster at an early stage and elicits nectin-1 ec

55 Nectin-1 and afadin cluster at developing synapses between hippocampa

56 These nectin-afadin clusters uniformly colocalize with N-cadherin-cat

57 The nectin-afadin complex also localizes to AJs and links to the cy

58 elial cells, MV spread requires the nectin-4/afadin complex and is based on cytoplasm transfer betwee

59 e that signaling downstream from a Claudin-2/Afadin complex enables the efficient formation of breast

60 its role in promoting cadherin recruitment, afadin deletion resulted in 70% fewer and less intense N

61 However, while Afadin depletion led to reduced Ucp1 mRNA induction by c

62 Afadin depletion resulted in enhanced thrombin-promoted

63 ether, these results support a model whereby afadin determines lumen placement by directing apical-ba

64 We further demonstrate that afadin directly interacts with AMPA receptors and that l

65 We show that loss of the scaffolding protein Afadin disrupts de novo lumenogenesis and lumen continui

66 age and roles of the linkage regulator Canoe/afadin during Drosophila germband extension (GBE), a con

67 we studied the distribution of nectin-1 and afadin during hippocampal synapse formation using cultur

68 nohistochemical analysis of Claudin-2 and/or Afadin expression in 206 metastatic breast cancer tumors

69 ratus and the dual-belt organization rely on afadin expression.

70 between nectin-1 and the cytoplasmic protein afadin for HSV entry and spread as well as the effects o

71 ed to dissociation of cell junction scaffold afadin from the adherens junctions.

72 oncomitant shuttling of the scaffold protein afadin from the cytosol to the nucleus and synapses.

73 Mammalian afadin has been suggested to be essential for adhesion a

74 In contrast, the Afadin homolog Canoe acts in parallel to alpha-Catenin a

75 In contrast, Drosophila melanogaster's afadin homologue Canoe (Cno) has suggested roles in sign

76 Knockdown of Afadin in brown pre-adipocytes does not alter adipogenes

77 Mice that lack afadin in nephron precursors show evidence of Par3-expre

78 ealed that high levels of both Claudin-2 and Afadin in primary tumors were associated with poor disea

79 Forced expression of recombinant afadin in pulmonary endothelium attenuated CS-induced VE

80 Collectively, we demonstrate a role for Afadin in supporting the adrenergic response in brown ad

81 Absence of afadin in vivo leads to misorientation of apical-basal c

82 Thus, afadin is a key intracellular signaling molecule for cad

83 Afadin is a Rap-regulated, actin-binding protein that pr

84 Phosphorylation studies demonstrate that afadin is a substrate for AMPK.

85 Afadin is directly phosphorylated by S6K1 and abnormally

86 Here we show that the scaffold protein Afadin is dynamically regulated by cold in BAT, and part

87 Here, we demonstrate that Afadin is recruited for dephosphorylation by directly bi

88 Here, we demonstrate that afadin is required for lumen continuity by orienting the

89 ently found that the F-actin-binding protein afadin is required for lumen continuity in developing re

90 Furthermore, we demonstrate that afadin is required for Par complex formation.

91 Collectively, these data suggest that afadin is required for the maintenance of dendritic stru

92 that define PTP specificity, explaining how Afadin is selectively dephosphorylated by PTPRK yet not

93 noe (Cno), the Drosophila orthologue of AF-6/Afadin, is essential for Slit-Robo signaling.

94 Although ZO/afadin knockdown did not prevent contractile array assem

95 acts with the putative actin regulator AFD-1/afadin; knocking down magi-1 or afd-1 function in a hypo

96 cold tolerance was observed in fat-specific Afadin knockout mice.

97 lysis revealed that fat-specific ablation of Afadin led to decreased functional enrichment of gene se

98 Absence of afadin led to delayed and diminished integration of nect

99 is paradigm, arguing instead that the nectin-afadin linkage plays the more important role in mature j

100 that LMO7 localized at cell-cell AJs, where afadin localized, in epithelial cells of rat gallbladder

101 sing an in vitro 3D cyst model, we find that afadin localizes to the cell cortex adjacent to the spin

102 ether with the intracellular binding partner afadin, mediate adhesion and signaling at a variety of i

103 including Discs Large1, Mud/NuMA, and Canoe/Afadin, mislocalize in dividing Eph mutant neuroepitheli

104 role in mediating synaptogenesis, we deleted afadin (mllt1), using a conditional allele, in postmitot

105 The alpha-catenin fragment 385-651 binds afadin more strongly than the full-length protein, sugge

106 Critically, blocking afadin nuclear accumulation attenuated activity-dependen

107 Moreover, activity-dependent afadin nuclear translocation coincides with phosphorylat

108 Activity-dependent afadin nuclear translocation peaked 2 h post-stimulation

109 Inactivation of afadin or CDH2 in the dorsal telencephalon leads to a ph

110 Loss of JAM-A, Afadin, or PDZ-GEF2, but not ZO-1 or PDZ-GEF1, similarly

111 orylates at least five substrates, including Afadin, PARD3 and delta-catenin family members, which ar

112 Canoe's mammalian homologue Afadin plays similar roles in cultured cells, working in

113 equired for the colocalization of the nectin/afadin/ponsin adhesion system to adherens junctions, and

114 Cold exposure acutely increases Afadin protein levels and its phosphorylation in BAT.

115 Drosophila Canoe and mammalian Afadin provide superb entry points to explore how their

116 pletion of the actomyosin regulator RhoA and Afadin results in defects in the central lumens and arre

117 Here, we show that afadin's coiled-coil (CC) domain and vinculin synergisti

118 Furthermore, the nectin-afadin system is required for the deposition of tight ju

119 ing a mutant form of the Rap1 effector Canoe/Afadin that cannot bind Rap1, we found that Rap1 signals

120 ion to a putative coiled coil (CC) domain in Afadin that is separated by more than 100 amino acids fr

121 involving the Abl tyrosine kinase and Canoe/Afadin that stabilizes cell adhesion under tension at tr

122 motes neuronal Cdh2 function via nectin3 and afadin, thus directing the broadly expressed homophilic

123 mechanistic framework by which vinculin and afadin tune cadherin-catenin complex-cytoskeleton coupli

124 Furthermore, association of PDZ-GEF2 with Afadin was dependent on the expression of JAM-A.

125 To assess the relevance of the protein afadin, which connects nectin-4 to the actin cytoskeleto

126 n orientation in a manner dependent on Canoe/Afadin, which links actomyosin to adherens junctions.