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1 and Gdel35, both of which likely inactivate connexin 26.
2 na occludens 2), nine gap junction proteins (connexin 26, 30, 30.3, 31, 32, 40, 43, 46, and 50), one
3 ar membrane integrity and early increases in connexin 26, a cochlear gap junction protein previously
5 genes not previously described in psoriasis--connexin 26, a gap junction protein; squamous cell carci
7 sgene expression was associated with loss of Connexin 26 and Connexin 30 from epidermal keratinocyte
8 are knock-outs for the gap-junction channels connexin 26 and connexin 30 genes, we show that defects
9 are knockouts for the gap-junction channels connexin 26 and connexin 30 genes, we show that defects
10 lesional epidermis, but double labeling for connexin 26 and Ki67 showed that many connexin 26 positi
11 encoding heat shock proteins 40 and 110 and connexins 26 and 30 may point to novel molecules whose r
12 ontaining the GJB2 and GJB6 genes coding for connexins 26 and 30, are the most frequent cause of rece
16 mistry, we have compared the distribution of connexins 26 and 43 with that of proliferating cells (Ki
20 eric connexin-32 and heteromeric connexin-32/connexin-26 channels were inhibited by exposure to nanom
25 onectin expression and repressed E-cadherin, connexin-26, connexin-43, and gap junction levels in CRC
26 rvations would be consistent with a role for connexin 26 containing gap junctions during both early a
28 se via canalostomy in adult mice with floxed connexin 26 (Cx26) alleles promoted Cre/LoxP recombinati
29 the genes encoding for gap junction proteins connexin 26 (Cx26) and connexin 30 (Cx30) have been link
30 the genes encoding for gap junction proteins connexin 26 (Cx26) and connexin 30 (Cx30) have been link
31 Here we show that the gap junction subunits connexin 26 (Cx26) and connexin 43 (Cx43) are expressed
35 f genetic origin is common, and mutations of connexin 26 (Cx26) are the most frequent cause of this d
36 e encoding the cochlear gap junction protein connexin 26 (CX26) cause prelingual, nonsyndromic deafne
44 to demonstrate that in the medulla oblongata connexin 26 (Cx26) is preferentially expressed near the
45 n the gene encoding the gap-junction protein connexin 26 (Cx26) that segregates with the profound dea
49 t genetic forms of deafness, including GJB2 [connexin 26 (Cx26)], GJB3 (Cx31), GJB6 (Cx30) and GJB1 (
51 between individuals (man and mouse) carrying Connexin 26(D66H) and those carrying insertional mutants
52 derma similar to that in humans carrying the Connexin 26(D66H) mutation (true Vohwinkel syndrome).
53 ced which expressed mutant connexin 26 [gjb2/connexin 26(D66H)], from a keratin 10 promoter, exclusiv
54 ll have contributed to the high frequency of connexin-26 deafness in the USA, and could represent a n
61 in (TECTA), the transcription factor POU4F3, connexin 26 (GJB2), and two unconventional myosins (MYO7
62 ic mice were produced which expressed mutant connexin 26 [gjb2/connexin 26(D66H)], from a keratin 10
63 c deafness have been mapped and mutations in connexin 26 have been identified as a cause of non-sydro
64 f the gap-junction beta-2 subunit gene GJB2 (connexin 26) have suggested that the 101T-->C (M34T) nuc
66 the suprabasal epidermis (the cells in which Connexin 26 is up-regulated in epidermal hyperproliferat
67 for heteromeric connexin channels containing connexin-26; it does not occur significantly for homomer
68 cells were nonproliferative, suggesting that connexin 26 may be related to differentiation rather tha
71 9 and DNFB21, have been identified, encoding connexin-26, myosin VIIA, myosin XV, pendrin, otoferlin
72 protein expression, while transfection with connexins 26 or 43 led to functional gap junction membra
73 ng for connexin 26 and Ki67 showed that many connexin 26 positive basal cells were nonproliferative,
77 mbranes were shown to contain low amounts of connexin 26 relative to connexin 32 in contrast to the e
78 blots confirmed the increased expression of connexin 26, SCCA1, and NAD6 genes in psoriatic skin.
80 uding the human gap junction channel protein connexin 26, the ATP binding cassette transporter MsbA,
81 athways that may account for the delivery of connexin 26 to the plasma membrane and explain the heter
82 ion of mutations in the gene (Gjb2) encoding connexin 26, using archives established from the UK ENU
87 ithelium, buccal epithelium, and viral warts connexin 26 was restricted mainly to suprabasal, nonprol
90 and oligomeric intermediates, especially of connexin 26, were detected in the endoplasmic reticulum-
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