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1 extracellular spaces (positioned to activate transglutaminase-1).
2 s differentiation-dependent genes, primarily transglutaminase 1.
3 ucocerebrosidase, acid sphingomyelinase, and transglutaminase 1.
4 ldren tested positive for IgA against tissue transglutaminase (1.0%; 95% confidence interval, 0.4%-1.
5 crin, ultra-high sulfur matrix proteins, and transglutaminases 1, 2, and 3) did not provide any evide
8 into the pathophysiology of TGM1 ichthyoses, transglutaminase-1 enzymatic activity, and potential the
9 b, -2f, and -2g proteins), the cross-linking transglutaminase 1 enzyme (Tg-1) and Muc5AC mRNA transcr
12 strate that mutations of both alleles of the transglutaminase 1 gene are the cause of lamellar ichthy
13 onse element in the proximal promoter of the transglutaminase 1 gene to transcription in normal epide
16 le gene mutated in lamellar ichthyosis (LI), transglutaminase-1, in rat keratinocytes, we created an
20 mRNA and protein levels of involucrin and transglutaminase 1, markers of differentiation, increase
21 tion in the coding region leading to reduced transglutaminase 1 mRNA levels rather than mutation of t
25 sed in keratinocytes transfected with either transglutaminase 1 or involucrin promoter-luciferase con
29 mutations in the TGM1 gene that encodes the transglutaminase 1 (TGase 1) enzyme, which is critical f
31 as been associated with loss of keratinocyte transglutaminase 1 (TGase1), an enzyme believed necessar
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