ライフサイエンスコーパス: ZO-2

1 ne encoding the tight junction protein TJP2 (ZO-2).

2 xons 19-21 of 4.1R and residues 1054-1118 of ZO-2.

3 bound on the cytoplasmic surface to ZO-1 and ZO-2.

4 ubsequently phosphorylates the N-terminus of ZO-2.

5 inds to and phosphorylates the C-terminus of ZO-2.

6 r exportation and proteosomal degradation of ZO-2.

7 and for the efficient nuclear importation of ZO-2.

8 de the cell polarity proteins Dlg1, PATJ and ZO-2.

9 junction proteins Claudin-1, Claudin-7, and ZO-2.

10 sary for interaction with the PDZ2 domain of ZO-2.

11 tight junction proteins, occludin, ZO-1, and ZO-2.

12 enuated 3-NC-induced hyperphosphorylation of ZO-2.

13 hionine-labeled in vitro translated ZO-1 and ZO-2.

14 interacted with in vitro translated ZO-1 and ZO-2.

15 l calcium, the complexes ZO-2/14-3-3zeta and ZO-2/14-3-3sigma move to the cell borders and dissociate

16 transferred to normal calcium, the complexes ZO-2/14-3-3zeta and ZO-2/14-3-3sigma move to the cell bo

17 iously identified to interact with Cx43, and ZO-2, a potential novel interacting partner.

18 epithelial permeability via association with ZO-2, afadin, and PDZ-GEF1 to activate Rap2c and control

19 with a scaffold signaling complex containing ZO-2, Afadin, and the small GTPase Rap2.

20 , in addition to tyrosine phosphorylation of ZO-2, also stimulates threonine phosphorylation of ZO-1

21 lls and reveal the novel interaction between ZO-2 and 14-3-3 proteins, which is critical for ZO-2 pro

22 lular PDZ proteins, including MUPP1, MAGI-1, ZO-2 and Dlg1.

23 ed the expression of Cdx2 and Oct-4, but not ZO-2 and F-actin.

24 e report that JAM-A associates directly with ZO-2 and indirectly with afadin, and this complex, along

25 CH is accompanied by decreased expression of ZO-2 and nuclear expression of YAP.

26 4.1R is colocalized with ZO-2 and occludin at Madin-Darby canine kidney (MDCK) ce

27 nd in vivo binding assays indicate that both ZO-2 and occludin interact with specific domains within

28 ther of ZO-1, or one of the related proteins ZO-2 and ZO-3 (ZO proteins), or all three together.

29 ssumed that ZO-1, together with its homologs ZO-2 and ZO-3, serves as a platform to scaffold various

30 rks distinct from those of heterodimers with ZO-2 and ZO-3.

31 reviously, ZO-1 also forms heterodimers with ZO-2 and ZO-3.

32 on protein 2 (encoded by TJP2, also known as ZO-2) and bile acid Coenzyme A: amino acid N-acyltransfe

33 n-1, claudin-5, zonula occludens (ZO)-1, and ZO-2, and a TJ accessory protein annexin-ll.

34 of the TJ proteins, zonula occludens (ZO)-1, ZO-2, and cingulin, examination of the Triton X-100 solu

35 rmine tissue distribution of occludin, ZO-1, ZO-2, and claudin-1 in the rat cornea.

36 o Ser/Thr phosphorylation of occludin, ZO-1, ZO-2, and claudin-5.

37 PDZ proteins, including MUPP1, PATJ, MAGI-1, ZO-2, and Dlg1.

38 din, a second tight junction-specific MAGUK, ZO-2, and F-actin, although the nature and functional si

39 of Ad9 E4- ORF1 and the first PDZ domain of ZO-2, and in cells this interaction resulted in aberrant

40 The unique region 2 of ZO-2, and S261 located within a nuclear localization sig

41 Synaptojanin 1, PAK2, ZO-2, and TAFII70, which contain CIN85 SH3 recognition c

42 e for cytoplasmic proteins, presumably ZO-1, ZO-2, and ZO-3, in localizing occludin in tight junction

43 rier through disruption of TJs, and ZO-1 and ZO-2 are targets for the induction.

44 AmotL1 and ZO-2 are two candidates that could be harnessed to contr

45 the identification of tight junction protein ZO-2 as a bona fide substrate of c-Abl.

46 Our results reveal a novel role of ZO-2 as a modulator of cell size.

47 Collectively, our data uncover ZO-2 as a novel mediator for c-Abl-dependent regulation

48 We examined Cx43 interaction with ZO-1 and ZO-2 at different stages of the cell cycle and found tha

49 CaSR) with Gd(3+) triggers the appearance of ZO-2 at the cell borders.

50 racellular Ca(2+) triggers the appearance of ZO-2 at TJs in epithelial cells and reveal the novel int

51 ilized ZO-2 suggest the presence of multiple ZO-2 binding sites in this domain.

52 ssed 4.1R containing the spectrin/actin- and ZO-2-binding domains was recruited to tight junctions in

53 Occludin, ZO-1, and ZO-2, but not claudin-1, are components of corneal epith

54 -2 in cells, and overexpression of wild-type ZO-2, but not mutant ZO-2 lacking the second and third P

55 ial cells than the up-regulation of ZO-1 and ZO-2 by itself.

56 rescence studies indicate that both ZO-1 and ZO-2 can co-localize with Cx43 within the plasma membran

57 Far Western analysis revealed that ZO-2 can directly bind to Cx43 independent of other inte

58 cause other tight junction components, ZO-1, ZO-2, cingulin, and the adherens junction protein E-cadh

59 distribution of TJ proteins (occludin, ZO-1, ZO-2, claudin-5) by CCL2.

60 lted in a decrease in the levels of ZO-1 and ZO-2 compared with untreated cells.

61 Co-immunoprecipitation of this domain with ZO-2 demonstrated preservation of the specificity of the

62 ZO-2 departure from the nucleus requires intact S257, an

63 xin exposure did not induce translocation of ZO-2, dephosphorylation or translocation of occludin, or

64 In cells cultured in low calcium (LC), ZO-2 displays a diffuse cytoplasmic distribution, but ac

65 lts show that double knockdown (dKD) of ZO-1/ZO-2 elevates the apical epithelial tension and effectiv

66 ibits pro-apoptotic function of YAP, whereas ZO-2 enhances it.

67 This phosphorylation induces ZO-2 entry into the nucleus and accumulation in speckles

68 ZO-2 expression demonstrated a direct correlation with i

69 onclude that claudin-1, claudin-5, ZO-1, and ZO-2 expression exhibit differential developmental regul

70 ZO-2 expression was 45% and 70% lower (P<0.01) in the pl

71 IL-15-mediated up-regulation of ZO-1 and ZO-2 expression was independent of the IL-2Rbeta subunit

72 ocorticoids are associated with increases in ZO-2 expression, but not with occludin, claudin-1, claud

73 r morphology and migration through targeting ZO-2 for phosphorylation.

74 We report here that AmotL1 and ZO-2 form a tripartite complex with YAP and regulate its

75 leled by dissociation of occludin, ZO-1, and ZO-2 from the lateral TJ membrane without influencing th

76 that in confluent cultures newly synthesized ZO-2 goes directly to the plasma membrane.

77 Zona occludens 2 (ZO-2) has a dual localization.

78 pressed the TJ proteins claudin-5, ZO-1, and ZO-2; HIV-1 decreased TJ proteins expression and induced

79 ted impaired binding to and sequestration of ZO-2 in cells, and overexpression of wild-type ZO-2, but

80 However, further depletion of ZO-2 in Eph4 ZO-1KO cells, which do not express ZO-3, ca

81 iminishes expression of claudin-5, ZO-1, and ZO-2 in HBMECs.

82 showed an increase in the amount of ZO-1 and ZO-2 in high density fractions following ATP depletion,

83 f TJ-associated proteins occludin, ZO-1, and ZO-2 in LPS-treated THCE cells.

84 mely, occludin, zonula occludens (ZO)-1, and ZO-2 in the caveolar fraction of HBMECs.

85 enous glucocorticoids regulate claudin-5 and ZO-2 in vivo at some, but not all ages, and increases in

86 TJP2/ZO-2-inactivating mutations cause progressive cholestati

87 with no lysine kinase-4 that phosphorylates ZO-2 inducing its concentration at TJs.

88 ns are then degraded in proteosomes, whereas ZO-2 integrates to TJs.

89 for interaction with ZO-1 during G0, whereas ZO-2 interaction occurred approximately equally during G

90 ins, hyperphosphorylated occludin, ZO-1, and ZO-2 into the tight junctional protein complex.

91 From the plasma membrane residual ZO-2 is endocyted and degradaded in lysosomes.

92 These results show that ZO-2 is implicated in regulating the nuclear shuttling o

93 with the candidate tumor suppressor protein ZO-2 is key to defining the unique transforming and tumo

94 At the plasma membrane ZO-2 is not O-GlcNAc, and instead, as TJs mature, it bec

95 In confluent epithelia, ZO-2 is present at tight junctions (TJs), whereas in spa

96 In LC, ZO-2 is protected from degradation by association to 14-

97 Zonula occludens-2 (ZO-2) is a tight junction (TJ) cytoplasmic protein, whos

98 the tight junction protein zona occludens 2 (ZO-2 KD) induces cell hypertrophy by two mechanisms: pro

99 ZO-2 knockdown did not replicate either the permeability

100 expression of wild-type ZO-2, but not mutant ZO-2 lacking the second and third PDZ domains, interfere

101 Reduction of the ZO-2 level was associated with the disappearance of ZO-2

102 ecture to develop, as cells transfected with ZO-2 mutant S257A or S257E form aberrant cysts with mult

103 ed domains critical for the interaction with ZO-2, occludin, and F-actin.

104 entified by the rescue experiment with tjp-2/ZO-2 or the PAR complex (par-3, par-6, and prkci/atypica

105 meability, suggesting a relationship between ZO-2 phosphorylation and tight junction permeability.

106 2 and 14-3-3 proteins, which is critical for ZO-2 protection and intracellular traffic.

107 Further, with loss of ZO-1, ZO-2 protein was increased significantly in ventricular

108 ing motif to interact with zona occludens-2 (ZO-2) protein, which promotes YAP's translocation to the

109 Only depletion of ZO-2 reduced the nuclear import of YAP.

110 hat sustain the interaction between 4.1R and ZO-2 reside within the amino acids encoded by exons 19-2

111 We also asked if AmotL1, YAP and ZO-2 signal together.

112 vel was associated with the disappearance of ZO-2 staining from cell borders in 6-hour LPS-treated ce

113 nction, and binding studies with immobilized ZO-2 suggest the presence of multiple ZO-2 binding sites

114 eal novel posttranslational modifications of ZO-2 that regulate the intracellular fate of this protei

115 tro (along with claudins, occludin, ZO-1 and ZO-2), the tight junctional networks that form were disc

116 vities are required for membrane assembly of ZO-2 TJ protein, while only PKCzeta activity is involved

117 d that in sparse cultures, newly synthesized ZO-2 travels to the nucleus before reaching the plasma m

118 o AA or 15(S)-HETE led to Src-Pyk2-dependent ZO-2 tyrosine phosphorylation, tight junction disruption

119 ZO-2 was higher at 90% gestation, in newborn and adult s

120 examethasone than placebo-treated lambs, and ZO-2 was higher in fetuses of dexamethasone than placebo

121 Occludin, ZO-1, and ZO-2 were found at the cell borders of the superficial l

122 f endogenous ZO-1 and another family member, ZO-2, were disrupted.

123 otein kinase 1, which in turn phosphorylates ZO-2, which contains 16 SR repeats.

124 here that the PDZ domain-containing protein ZO-2, which is a candidate tumor suppressor protein, is

125 and activity, whereas depletion of ZO-1 and ZO-2, which is associated with reduced ZO-3 expression,

126 We confirmed the interaction of ZO-2 with Cx43 by using a combination of fusion protein

127 fically bind and sequester MUPP1, MAGI-1 and ZO-2 within insoluble complexes whereas trimers specific

128 action resulted in aberrant sequestration of ZO-2 within the cytoplasm.

129 oteins that organize tight junctions such as ZO-2, ZO-1, and occludin.

130 also bind to the scaffolding proteins ZO-1, ZO-2, ZO-3, cingulin, the membrane trafficking protein V

131 0 kDa specifically interact with the protein ZO-2 (zonula occludens-2).