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1 K14, involucrin, and TRP63, but negative for keratin 10.
2 cytes by double labeling for WNV antigen and keratin 10.
3 ntified including arginase 1, enolase 1, and keratin 10.
4 nation motif at the end of the rod domain of keratin 10.
5 on 10 in the 1A segment of the rod domain of keratin 10.
6 follicle and cyst, and ectopic expression of keratin 10, a marker of interfollicular differentiation
8 ter activity of keratin 5, increased that of keratin 10 and enhanced the effect of a differentiating
10 H18-1 cells form multiple layers and express keratin 10 and filaggrin predominantly in the upper laye
17 presence of the hair follicle marker Sox 9, keratins 10 and 14, and normal melanocyte distribution a
19 AFMK-stimulated expression of involucrin and keratins-10 and keratins-14 in the epidermis, indicating
20 pidermal differentiation markers involucrin, keratin 10, and filaggrin during tissue reconstruction.
21 l differentiation markers such as keratin 1, keratin 10, and loricrin, with or without the induction
23 sialoprotein-binding protein, fibrinogen and keratin-10 binding surface-anchored protein, fibrinogen-
24 f the differentiation markers involucrin and keratin 10 compared to cells with no cell-cell contact.
26 hich would spatially constrain the keratin 1/keratin 10 end domains to allow filament compaction and
27 ression in the stratum granulosum, a loss of keratin 10 expression in the stratum spinosum, and an in
29 inine-rich C-terminal peptide that redirects keratin 10 from the cytokeratin filament network to the
32 inocytes induces expression of keratin 1 and keratin 10 genes, early markers of terminal differentiat
33 ccur within the mutational "hot spot" of the keratin 10 (K10) 2B rod domain, adjacent to severe EI-as
34 rkers of differentiation, keratin 1 (K1) and keratin 10 (K10) but had a minimal effect on the express
35 zation studies determined that PsrP binds to Keratin 10 (K10) on the surface of lung but not nasophar
37 ese areas are composed of keratin 1 (K1) and keratin 10 (K10), and several K1 and K10 point mutations
38 351), human keratin 1 (K211 and K355), human keratin 10 (K163), bovine tubulin alpha (K60, K336, K163
39 We previously demonstrated that mutations in keratin 10 (KRT10) cause ichthyosis with confetti (IWC),
41 sease-causing mutations in the gene encoding keratin 10 (KRT10); all result in frameshifts into the s
43 ctivated transglutaminase 1, involucrin, and keratin 10 message and protein levels, demonstrating tha
44 8-1 cells synthesize considerable amounts of keratin 10 mRNA and protein when maintained in either su
45 criptase polymerase chain reaction assay for keratin 10 mRNA was developed to distinguish between exp
46 pressing mutant ras under the control of the keratin 10 or keratin 1 gene promoters, the formation of
47 from mutations affecting the tail domains of keratin-10 or keratin-1, and Suzuki et al. expand the mu
48 amplifying population and integrin-negative, keratin 10-positive cells left the basal layer exclusive
49 ferating compartment and an expansion of the keratin 10-positive layer of cells and was associated wi
50 press excess IGF-II delivered using a bovine keratin 10 promoter (k10Igf2/+) develop a disproportiona
51 connexin 26 [gjb2/connexin 26(D66H)], from a keratin 10 promoter, exclusively in the suprabasal epide
52 wed that SdrF mediates bacterial adhesion to keratin 10 through strong and weak bonds involving the A
53 cells staining with antibodies to suprabasal keratin 10, transglutaminase type I, involucrin, and fil
54 reduced tumorigenesis because keratin 1 and keratin 10, two keratins that indicate the commitment of
55 ntiation markers profilaggrin, loricrin, and keratin 10 was considerably downregulated in PF-N domain
56 , expression of the differentiation-specific keratin-10 was shown not to be required for HPV late fun
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