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1 observed when the mutant is expressed before connexin 32.
2 chimeras with the transmembrane portions of connexin 32.
3 -3, claudin-1, -2, -4, and -8, occludin, and connexin-32.
5 itivity of gap junction channels composed of connexin 32 and decreases their sensitivity to transjunc
10 nd expressed the hepatocyte-specific markers connexin-32 and hepatic nuclear factor-4alpha, but not c
12 ecular permeation through channels formed by connexin-32 and/or connexin-26 reconstituted into liposo
14 ff limits for permeability through homomeric connexin-32 channels and through heteromeric connexin-32
17 imately 420 nM) were twice those measured by connexin-32 chimera (approximately 200 nM); both chimera
19 rified homomeric connexin-32 and heteromeric connexin-32/connexin-26 channels were inhibited by expos
23 disease family with a novel mutation in the Connexin 32 (Cx32) P2 promoter region at position -526bp
26 n the gene encoding the gap junction protein connexin 32 (Cx32), which is expressed by Schwann cells.
30 hypothesis that the gap junctional proteins connexin 32 (Cx32; expressed by oligodendrocytes, intern
31 Madin-Darby canine kidney cells expressing connexin-32 (Cx32) and Cx43 were exposed to bradykinin (
32 eral myelin protein 22, myelin protein zero, connexin 32, early growth response factor 2, periaxin, m
33 nic increases in protein abundance, whereas, connexin-32 exhibited reciprocal decreases in abundance
35 ne, early growth response gene 2 (EGR-2) and connexin-32 gene, which are expressed in Schwann cells,
37 ntain low amounts of connexin 26 relative to connexin 32 in contrast to the equal connexin ratios det
38 ied that increased levels of glutaminase and connexin 32 in Mecp2-null microglia are responsible for
39 reviously that expression of connexin-43 and connexin-32 in an indolent prostate cancer cell line, LN
40 pendent state, we introduced connexin-43 and connexin-32 into an invasive, androgen-independent cell
41 In addition, other sequence elements of the connexin-32 IRES were characterized by mutation analysis
45 slated region (5'-UTR) of the nerve-specific connexin-32 mRNA, previously found in a family with Char
47 17p12 duplication (CMT1A duplication), 11 a connexin 32 mutation, 5 a myelin protein zero mutation,
48 reviously unreported mutant alleles: two for connexin 32, three for myelin protein zero, and two for
49 porter Npt2b, and the gap junction component connexin 32, usually expressed in secretory epithelia, w
50 and in acutely dissociated cells showed that connexin 32 was expressed in neurons and oligodendrocyte
51 rved cysteines in the extracellular loops of connexin 32 were moved individually and in all possible
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