ライフサイエンスコーパス: connexin 26

1 0% were nonsyndromic (mainly associated with connexin 26).

2 and Gdel35, both of which likely inactivate connexin 26.

3 na occludens 2), nine gap junction proteins (connexin 26, 30, 30.3, 31, 32, 40, 43, 46, and 50), one

4 ar membrane integrity and early increases in connexin 26, a cochlear gap junction protein previously

5 GJB2 encodes connexin 26, a gap junction protein, which permits inter

6 genes not previously described in psoriasis--connexin 26, a gap junction protein; squamous cell carci

7 Human connexin 26 and connexin 30 are expressed in the same ce

8 sgene expression was associated with loss of Connexin 26 and Connexin 30 from epidermal keratinocyte

9 are knock-outs for the gap-junction channels connexin 26 and connexin 30 genes, we show that defects

10 are knockouts for the gap-junction channels connexin 26 and connexin 30 genes, we show that defects

11 lesional epidermis, but double labeling for connexin 26 and Ki67 showed that many connexin 26 positi

12 encoding heat shock proteins 40 and 110 and connexins 26 and 30 may point to novel molecules whose r

13 ontaining the GJB2 and GJB6 genes coding for connexins 26 and 30, are the most frequent cause of rece

14 Immunoprecipitation using antibodies to connexins 26 and 32 showed that liver gap junctions were

15 Oligomers of connexins 26 and 32 were extensively present in Golgi me

16 structed from approximately equal amounts of connexins 26 and 32.

17 mistry, we have compared the distribution of connexins 26 and 43 with that of proliferating cells (Ki

18 In three independent experiments connexin 26 appeared in a patchy intercellular distribut

19 Mutations in connexin 26 are responsible for approximately 20% of gen

20 study independently confirms the identity of connexin 26 as an NSRD gene.

21 eric connexin-32 and heteromeric connexin-32/connexin-26 channels were inhibited by exposure to nanom

22 channels and through heteromeric connexin-32/connexin-26 channels.

23 ubstantially higher than those reported by a connexin-26 chimera (approximately 130 nM).

24 ut diminished cellular levels of E-cadherin, connexin 26, connexin 43, and gap junction.

25 Connexin 26, connexin 43, and gap-junction activity were

26 onectin expression and repressed E-cadherin, connexin-26, connexin-43, and gap junction levels in CRC

27 rvations would be consistent with a role for connexin 26 containing gap junctions during both early a

28 Connexin-26 contributes to a narrowed pore.

29 se via canalostomy in adult mice with floxed connexin 26 (Cx26) alleles promoted Cre/LoxP recombinati

30 the genes encoding for gap junction proteins connexin 26 (Cx26) and connexin 30 (Cx30) have been link

31 the genes encoding for gap junction proteins connexin 26 (Cx26) and connexin 30 (Cx30) have been link

32 Here we show that the gap junction subunits connexin 26 (Cx26) and connexin 43 (Cx43) are expressed

33 Recent evidence suggests that connexin 26 (Cx26) and Cx30 are the major constituent pr

34 We found that connexin 26 (Cx26) and Cx30 GJs readily diffuse within t

35 (PCs), coupled by gap-junctions composed of connexin 26 (Cx26) and Cx30.

36 f genetic origin is common, and mutations of connexin 26 (Cx26) are the most frequent cause of this d

37 e encoding the cochlear gap junction protein connexin 26 (CX26) cause prelingual, nonsyndromic deafne

38 Mutations in the connexin 26 (Cx26) gene (GJB2) are associated with the t

39 Human connexin 26 (Cx26) has been considered to be a candidate

40 The gap junction protein connexin 26 (Cx26) has been detected previously in the p

41 Mutations in the gene (GJB2) encoding connexin 26 (cx26) have been linked to sensorineural hea

42 Mutations in the GJB2 gene-encoding connexin 26 (Cx26) have been linked to skin disorders an

43 Here we show that connexin 26 (Cx26) hemichannels, causally linked to resp

44 Because in the human skin connexin 26 (Cx26) is co-expressed with other connexins,

45 to demonstrate that in the medulla oblongata connexin 26 (Cx26) is preferentially expressed near the

46 n the gene encoding the gap-junction protein connexin 26 (Cx26) that segregates with the profound dea

47 Given the localization of connexin 26 (Cx26) to the chemosensing areas of the medu

48 by point mutations in the GJB2 gene encoding Connexin 26 (Cx26) which result in aberrant activation o

49 Because connexin 26 (Cx26), a tumor suppressor gene candidate, c

50 ant upregulation of the gap junction protein connexin 26 (Cx26).

51 t genetic forms of deafness, including GJB2 [connexin 26 (Cx26)], GJB3 (Cx31), GJB6 (Cx30) and GJB1 (

52 Mutations in one gene, connexin 26 (CX26GJB2), are responsible for most cases o

53 between individuals (man and mouse) carrying Connexin 26(D66H) and those carrying insertional mutants

54 derma similar to that in humans carrying the Connexin 26(D66H) mutation (true Vohwinkel syndrome).

55 ced which expressed mutant connexin 26 [gjb2/connexin 26(D66H)], from a keratin 10 promoter, exclusiv

56 ll have contributed to the high frequency of connexin-26 deafness in the USA, and could represent a n

57 These new findings also show that connexin 26 deficiency can reduce active cochlear amplif

58 Mutations in one gene, connexin 26 (encoding the gap junction protein beta 2),

59 The gene for the connexin 26 gap junction protein, recently shown to be m

60 ly occurs at a mutational hotspot within the connexin 26 gene.

61 Recessive mutations at the connexin-26 gene locus are now recognised as the cause o

62 ed by heterozygous missense mutations in the connexin-26 gene, GJB2.

63 in (TECTA), the transcription factor POU4F3, connexin 26 (GJB2), and two unconventional myosins (MYO7

64 erconnected through gap junctions containing connexin 26 (Gjb2).

65 ic mice were produced which expressed mutant connexin 26 [gjb2/connexin 26(D66H)], from a keratin 10

66 c deafness have been mapped and mutations in connexin 26 have been identified as a cause of non-sydro

67 f the gap-junction beta-2 subunit gene GJB2 (connexin 26) have suggested that the 101T-->C (M34T) nuc

68 We find that targeted-deletion of connexin 26 in Deiters cells and outer pillar cells, whi

69 the suprabasal epidermis (the cells in which Connexin 26 is up-regulated in epidermal hyperproliferat

70 for heteromeric connexin channels containing connexin-26; it does not occur significantly for homomer

71 cells were nonproliferative, suggesting that connexin 26 may be related to differentiation rather tha

72 pontaneous neural activity in the absence of connexin 26 may increase the effectiveness of early ther

73 In situ hybridizations showed that connexin 26 mRNA was expressed 10-fold higher in psoriat

74 progression of deafness for a boy with GJB2 (CONNEXIN 26) mutations.

75 9 and DNFB21, have been identified, encoding connexin-26, myosin VIIA, myosin XV, pendrin, otoferlin

76 protein expression, while transfection with connexins 26 or 43 led to functional gap junction membra

77 ng for connexin 26 and Ki67 showed that many connexin 26 positive basal cells were nonproliferative,

78 The increase in connexin 26 preceded that in cell proliferation.

79 Immunohistochemistry showed that connexin 26 protein was strongly expressed in spinous ke

80 hrough channels formed by connexin-32 and/or connexin-26 reconstituted into liposomes.

81 mbranes were shown to contain low amounts of connexin 26 relative to connexin 32 in contrast to the e

82 blots confirmed the increased expression of connexin 26, SCCA1, and NAD6 genes in psoriatic skin.

83 GJB2 gene encoding the gap junction protein connexin-26, suggesting an etiological relationship.

84 uding the human gap junction channel protein connexin 26, the ATP binding cassette transporter MsbA,

85 athways that may account for the delivery of connexin 26 to the plasma membrane and explain the heter

86 ion of mutations in the gene (Gjb2) encoding connexin 26, using archives established from the UK ENU

87 Connexin 26 was absent from the interfollicular and inte

88 In psoriatic lesional epidermis connexin 26 was also located mainly in suprabasal, nonpr

89 Connexin 26 was present in a patchy distribution in the

90 Connexin 26 was prominent in lesional psoriatic epidermi

91 ithelium, buccal epithelium, and viral warts connexin 26 was restricted mainly to suprabasal, nonprol

92 Although aequorin fused to connexin-26 was nonfunctional, its ability to report Ca2

93 tol 3-kinase, and the gap junction component connexin 26 were specifically labeled.

94 and oligomeric intermediates, especially of connexin 26, were detected in the endoplasmic reticulum-

95 e adult CC was paralleled by upregulation of connexin 26, which correlated with the resumption of pro