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1 nner root sheaths and later in the secondary hair germ.
2 al and suprabasal cells above and around the hair germ.
3 found in the hair canal, sebaceous gland, or hair germ.
4 between early superficial BCCs and embryonic hair germs.
5 illa and neighboring stem cells (SCs) in the hair germ and bulge regulate new follicle growth in the
6 y negatively regulates Lgr5 in the secondary hair germ and inhibits HF cycling.
7 press keratin 79 (K79) and stream out of the hair germ and into the epidermis prior to lumen formatio
8 ed epithelial compartments (bulge, secondary hair germ) and co-express selected stem cell markers (So
9 f hair follicles, including HFSCs, secondary hair germ, and dermal papilla.
10 Lgr5 and cell proliferation in the secondary hair germ are increased.
11  Keratin 16 initially localizes within early hair germs, but rapidly shifts to a subset of cells at t
12 ulation in the dermal papilla, the secondary hair germ cells, and the epidermis.
13 de novo epithelial buds resembling embryonic hair germs, collections of epidermal cells whose develop
14 se skin, lacking laminin-10, contained fewer hair germs compared with controls, and after transplanta
15 et of cells in the lower bulge and secondary hair germ compartments.
16                                              Hair germs comprising epidermal placodes and associated
17 5, is required for hair cycle regulation and hair germ-dermal papilla anchoring.
18 The epithelial-fibroblast interface, namely, hair germ-dermal papilla interface, makes asymmetrically
19 lls of the hair-follicle bulge and secondary hair germ does not induce robust Hh signaling or produce
20 antation, Lama5 -/- skin showed a failure of hair germ elongation followed by complete hair follicle
21                 Notably, however, developing hair germs evaginate rather than invaginate, thereby per
22  Wnt signaling tilts each stem cell toward a hair germ fate and, vice versa, based on a continuous sc
23               From the "infundibular cysts", hair germs form centrifugally followed by follicular bud
24 tility and resistant to size change, whereas hair germ (HG) progenitors are soft and periodically enl
25 lly, a horizontal plexus under the secondary hair germ (HPuHG) transiently neighbors the HFSC activat
26                         Similar to embryonic hair germs, human BCC buds showed increased levels of cy
27 o proliferate and become activated to form a hair germ is reduced.
28 cytes during catagen suggests that secondary hair germ of late catagen HF is most likely repopulated
29 appaB activity was detected in the secondary hair germ of late telogen and early anagen HFs, suggesti
30 lls migrate out of the reactivated secondary hair germ prior to formation of a new hair canal.
31 ly undescribed dermal papilla, bulge SC, and hair germ SC genes in mouse and human counterparts.
32 signatures of dermal papilla, bulge SCs, and hair germ SCs, but low detection sensitivity limited the
33 riptomes of dermal papilla cells, bulge SCs, hair germ SCs, epidermal and follicle epithelial cells a
34 Cs) in the hair follicle bulge and secondary hair germ (sHG).
35 s required for normal advancement beyond the hair germ stage of development.
36  RA, resulting in arrest of hf growth at the hair germ stage.
37 markedly increases during telogen (bulge and hair germ stem cell compartments).
38 f aPKClambda altered the fate of lower bulge/hair germ stem cells.
39 majority of cells in the bulge and secondary hair germ that proliferate in response to skin injury.
40 heir labeled daughters were not found in the hair germs through 48 h following induction of anagen by
41 til the early dermal papilla stage for guard hair germs to make follicles, but is dispensable for the
42              As in embryologically initiated hair germs, transgenic follicles induce Lef-1, but folli
43 esent in the basement membrane of elongating hair germs, when other laminins were downregulated, sugg
44 hibit molecular profiles resembling those of hair germs, yet still possess multipotentiality in vivo.