ライフサイエンスコーパス: anagen

1 on of an exaggerated, aberrant growth phase (anagen).

2 pression patterns in the Cl during postnatal anagen.

3 trix cells were positive for PS2 during late anagen.

4 , pre-cortex, and hair shaft during mid-late anagen.

5 activation of beta-catenin produced a normal anagen.

6 tion or proliferation of matrix cells during anagen.

7 growth cycle, the largest peak is coupled to anagen.

8 n and reentry of telogen hair follicles into anagen.

9 , however, appeared to remain blocked in pro-anagen.

10 to terminate precursor cell division during anagen.

11 n differentiating hair cortical cells during anagen.

12 ls, suggesting that 5-FU killed the cells in anagen.

13 an increased proportion in the growth phase, anagen.

14 s highly expressed in late telogen and early anagen.

15 tors Bmp2, Dkk1, and Sfrp4 increase in early anagen.

16 in human anagen HFs significantly prolonged anagen.

17 ferent stages of the hair cycle, telogen and anagen.

18 uiescent phase (telogen) before returning to anagen.

19 hinner hair follicles and shafts during late anagen.

20 Treatment of mice at 59 days of age (when in anagen 1) with topical 5-FU delayed hair regrowth by 10

21 Hairs irradiated in anagen and analyzed during the second cycle exhibited a

22 pression of miR-31 markedly increases during anagen and decreases during catagen and telogen.

23 ression was detected during early and middle anagen and during middle catagen stages.

24 s of the hair cycle, and in the bulge during anagen and early catagen, whereas Aldh1a3 expression was

25 panion layer of the outer root sheath during anagen and in the club hair sheath during catagen and te

26 hannel blockers act through Cav1.2 to induce anagen and overcome the TS phenotype.

27 P cells there was an increase in the size of anagen and telogen DP, but the proportion of tdTomato-la

28 in the epidermis and the epithelium of both anagen and telogen hair follicles.

29 e onset of catagen when the follicles are in anagen and the onset of anagen when the follicles are in

30 n of TGF-beta1 and its receptors during late anagen and the onset of catagen of the hair cycle.

31 ir follicles cycle between stages of growth (anagen) and metabolic quiescence (telogen) throughout li

32 licles cycle between stages of rapid growth (anagen) and metabolic quiescence (telogen) throughout li

33 periods of relative resting, active growth (anagen), and regression.

34 es induced in the dermal papilla (DP) during anagen as a result of the interaction with epithelial ma

35 that epithelial Wnt ligands are required for anagen, as loss of Wls in the follicular epithelium resu

36 hifted it towards a mild form of "dystrophic anagen", associated with a significant reduction in apop

37 ly proliferating hair-producing cells of the anagen bulb (matrix cells), while these cells were stron

38 In anagen bulbs, kazrin was expressed by a band of cells wi

39 of label-retaining cells to define the human anagen bulge.

40 es Shh target genes and epithelial tumors at anagen but not other stages, pointing to a restricted co

41 e., the follicular papilla cells, during the anagen but not the catagen phase.

42 and dermal papilla cells during early to mid-anagen but was highly upregulated throughout the catagen

43 Existing hair follicles entered anagen, but no ectopic follicles formed.

44 t manner, as it can be detected in FP during anagen, but not in catagen and telogen phases of the hai

45 r resulted in a delay in the first postnatal anagen, but subsequent hair cycles were normal.

46 al stem cell maintenance, and stimulation of anagen by hair plucking caused follicular proliferation

47 ained in the follicle following induction of anagen by plucking of the hairs.

48 ir germs through 48 h following induction of anagen by plucking, but instead remained in their subseb

49 ollicle melanocytes were examined during the anagen-catagen transformation, comparing spontaneous and

50 find that TNFalpha is required for a timely anagen-catagen transition in mouse pelage follicles, and

51 st values in anagen VI, decreased during the anagen-catagen transition phase.

52 r indirect promotion of apoptosis during the anagen-catagen transition.

53 staining was observed in this region at the anagen-catagen transition.

54 of the follicular pigmentary unit during HF anagen-catagen-telogen transition and may be used for th

55 or Dicer during an established growth phase (anagen) caused failure of hair follicles to enter a norm

56 During anagen, cell proliferation in the germinative matrix of

57 This production was associated with anagen-dependent expression of the tyrosinase gene and e

58 embled neonatal dermis than adult telogen or anagen dermis.

59 Furthermore, acceleration of wound-induced anagen development in Lhx2(+/-) mice is inhibited by adm

60 n contrast, BMP4 induces selective arrest of anagen development in the non-tylotrich (secondary) HF.

61 Anagen development is accompanied by down-regulation of

62 ses of the hair cycle results in accelerated anagen development, and altered differentiation of hair

63 a shorter telogen and a premature entry into anagen during the second phase of hair cycling without a

64 (catagen), rest (telogen), and regeneration (anagen) during postnatal life.

65 ing that fibroblasts migrate out of the late anagen/early catagen papilla and re-enter the proximal c

66 onstrate that forced MSI2 expression retards anagen entry and consequently delays hair growth, wherea

67 of EF epidermis was most similar to that of anagen epidermis, consistent with activation of beta-cat

68 r root sheath, hair fiber perforation of the anagen follicle base, and progressive follicular replace

69 g a prominent marker of sebaceous glands and anagen follicle bulbs.

70 receptor mice displayed the same pattern of anagen follicle formation as the wild-type mice.

71 that diffusible factors associated with the anagen follicle influence cell proliferation in the epid

72 a critical role of TSP-1 in the induction of anagen follicle involution, with potential implications

73 hin the dermal papilla regulates the telogen-anagen follicle transition and suggest that diffusible f

74 kely to contribute to the formation of a new anagen follicle.

75 Anagen follicles in mutants exhibit decreased proliferat

76 In anagen follicles, high levels of telomerase activity wer

77 sebaceous gland hypoplasia, abnormally long anagen follicles, retained inner root sheath, hair fiber

78 of all developing HFs and also by postnatal anagen follicles.

79 above telogen follicles to 7.0% above early anagen follicles.

80 he existence of quiescent noncycling KSCs in anagen follicles.

81 of the infundibulum; the companion layer in anagen follicles; and the single layer of outer root she

82 a single defined source; and possess a long anagen growth phase, we initiated a study of them in cul

83 rved in the outer root sheath throughout the anagen growth phase.

84 ed in telogen rather than transitioning into anagen growth, confirmed by retention of bromodeoxyuridi

85 growth cycle in 3 phases: telogen (resting), anagen (growth), and catagen (regression).

86 e RASopathy, Noonan-like syndrome with loose anagen hair (NS/LAH).

87 the subsequent hair cycle, i.e., after a new anagen hair bulb has been constructed, which points to t

88 rmatitis, and the proliferative cells of the anagen hair bulb.

89 idermis and, for the cyclic formation of new anagen hair bulbs.

90 layer of the inner root sheath of the lower anagen hair follicle and weak staining of the telogen fo

91 Shh target genes normally occurs only in the anagen hair follicle in response to expression of Shh.

92 /SPRR1 is localized to specific areas of the anagen hair follicle with weak staining in the telogen f

93 haracterized by a marked increase in size of anagen hair follicles (HFs) and by the replacement of zi

94 er, these models are based on the culture of anagen hair follicles and have only partially been used

95 the effects of TGF-beta1 injection on murine anagen hair follicles in vivo.

96 ntary unit during the cyclical involution of anagen hair follicles is unknown.

97 CD31 staining revealed that the late anagen hair follicles of the KrP mice were surrounded by

98 Dsg1 compensates for the loss of Dsg3 in the anagen hair follicles of these Dsg3-/- mice.

99 ession profiles revealed that in contrast to anagen hair follicles of wild-type mice, tumors of trans

100 marked proliferation of the root sheaths of anagen hair follicles, limited to the region within the

101 dian clock activity specific to regenerating anagen hair follicles, namely epithelial matrix and mese

102 Such observations indicate that, in anagen hair follicles, the fragments containing cells ac

103 s and Xenopus, being confined to the bulb of anagen hair follicles, the infundibulum, and parakeratot

104 In developing and mature anagen hair follicles, whn is expressed at high levels i

105 pilla, and connective tissue sheath of human anagen hair follicles.

106 a (AA) is an autoimmune disease that attacks anagen hair follicles.

107 s basal pigmentation in the epidermis and in anagen hair shafts.

108 sg1 and Dsg3 in this layer, in anchoring the anagen hair to the follicle.

109 +/+ or Dsg3+/- mice, showed striking loss of anagen hair, which was confirmed and quantitated by gent

110 d remained in the follicle after loss of the anagen hair.

111 mmune disease that targets actively growing (anagen) hair follicles in humans and other mammals.

112 mmune disease that targets actively growing (anagen) hair follicles in humans, mice, rats, dogs, hors

113 ry cell infiltrates around actively growing (anagen) hair follicles.

114 ut) mice lose hair during telogen, but their anagen hairs remain anchored to the follicle.

115 cells, rather than quiescent bulge SCs, for anagen HF repair can be a potential approach to prevent

116 knockout mice also show an increased size of anagen HFs associated with increased cell proliferation

117 cell proliferation and controls the size of anagen HFs by modulating the expression of cell-cycle-as

118 Markedly enlarged anagen HFs of TG mice show increased proliferation in th

119 nockdown of either BMAL1 or Period1 in human anagen HFs significantly prolonged anagen.

120 econdary hair germ of late telogen and early anagen HFs, suggesting a potential role for NF-kappaB in

121 r matrix and outer and inner root sheaths of anagen HFs.

122 StEpiDelta/StEpiDelta) mice presented solely anagen HFs.

123 eath (IRS) markers, with expression onset at anagen IIIa above the new hair bulb and subsequent sprea

124 curring in the Cl, mK6a expression begins at anagen IIIb in differentiating cells located proximal to

125 of Shh target gene transcription only during anagen in follicular and interfollicular keratinocytes.

126 tivation improved hair regrowth by promoting anagen in hair follicles and accelerated regrowth of car

127 More hair follicles were in anagen in mice fed high vitamin A.

128 were in anagen VI, whereas none (0%) were in anagen in the control group.

129 ostnatal skin would accelerate initiation of anagen in the hair follicle cycle, with concomitant acce

130 onic development of hair follicles, and that anagen in the postnatal cycling follicle has morphologic

131 human HF cycling and manipulate long-lasting anagen in vivo.

132 Genes induced in the DP during anagen included modulators of genes expressed additional

133 decreased Wnt/beta-catenin signaling during anagen induction compared with control hair follicles.

134 uired for Wnt/beta-catenin activation during anagen induction is unknown.

135 in HF stem/progenitor cell activation during anagen induction.

136 Loss of Fgf18 signaling markedly accelerates anagen initiation, whereas loss of Tgf-beta2 signaling s

137 nocytes demonstrated a defective response to anagen initiation.

138 lopecia--the last a consequence of defective anagen initiation.

139 In animals exposed during anagen, intermediate fluences induced nonscarring alopec

140 ely regulated cycles of active regeneration (anagen), involution (catagen), and relative quiescence (

141 follicles, transition from telogen back into anagen involves the activation, proliferation, and diffe

142 y accelerated entry into catagen and through anagen, irregular hair follicle orientation, and increas

143 e show that Wnt signaling is elevated during anagen, is reduced at the onset of catagen, and can be r

144 ting the apoptotic death of ORS cells during anagen leads to a more rapid termination of progenitor c

145 tro, and shows that P-cadherin is needed for anagen maintenance by regulating canonical Wnt signaling

146 om the middle back region of the spontaneous anagen mice that received PTH (7-34) revealed that 19 +/

147 Similarly, in induced anagen mice treated with PTH (7-34), 22.3 +/- 1.4 (mean

148 At mid-anagen, NF-kappaB activity was observed in the inner roo

149 The onset of anagen of the first postnatal hair follicle cycle was al

150 llicle development and for the growth phase (anagen) of postnatal follicles.

151 d each other's effects on the growing phase (anagen) of scalp follicles cultured in media with and wi

152 w premature termination of the growth phase (anagen) of the hair cycle, an event that is regulated in

153 lar vascularization during the growth phase (anagen) of the hair cycle, followed by regression of ang

154 ninER expressing hair follicles also entered anagen on 4OHT treatment.

155 we demonstrate its direct role in promoting anagen onset and HFSC proliferation.

156 terozygous Lhx2 knockout (+/-) mice, whereas anagen onset in the HFs located closely to the wound is

157 naling in the dermal papilla is required for anagen onset in the murine hair cycle.

158 ycle abnormalities, driven by the dystrophic anagen or dystrophic catagen pathway, play important par

159 During early anagen or growth phase of the hair follicle, nestin-expr

160 f pelage follicles during catagen but not in anagen or telogen.

161 -expressing lower outer root sheath cells in anagen, our studies indicate an alternative origin, and

162 he suprabasal cells of the telogen bulge and anagen outer root sheath (ORS).

163 n in the field is whether the bulb region of anagen pelage follicles contains multipotential progenit

164 gnificant acceleration of healing during the anagen phase of HF cycling in vivo, associated with alte

165 rement for the vitamin D receptor during the anagen phase of the first (developmental) hair cycle, bu

166 und healing and those upregulated during the anagen phase of the hair cycle in unwounded skin.

167 heath and medulla of the follicle during the anagen phase of the hair growth cycle.

168 s repressed by R-spondin2 injection, and the anagen phase persists.

169 ing the hair cycle, Msx2 deficiency shortens anagen phase, but prolongs catagen and telogen.

170 ches were characterized by hair follicles in anagen phase, implicating keratinocytes in the aberrant

171 hair follicle, and for inciting the growth (anagen) phase of the hair cycle.

172 ehog monoclonal antibody during the growing (anagen) phase of the hair cycle.

173 During its growth (anagen) phase, the proximal-distal axis of the mouse coa

174 ation that resides in the lower hair bulb of anagen-phase follicles and expresses Hopx.

175 Wnts, but not Sonic hedgehog (Shh), maintain anagen-phase gene expression in vitro and hair inductive

176 erin silencing reduced the expression of the anagen-promoting growth factor, IGF-1, whereas that of t

177 hair follicle stem cells and contributes to anagen re-entry but does so in a calcium flux-independen

178 sed hair density, altered hair types, faster anagen re-entry, and formation of compound vibrissa foll

179 , and spares the progenitor cells needed for anagen re-entry, is poorly understood.

180 hair follicles may affect each other during anagen re-entry, thus forming propagating regenerative h

181 t were either spontaneously in or induced to anagen received either PTH (7-34) or placebo.

182 s further, and the probability of successful anagen reentry decreases, leading to progressive alopeci

183 ollicle generation and regeneration, telogen-anagen reentry, and extra-follicular macro-environmental

184 progressing through stages of rapid growth (anagen), regression (catagen), and relative "quiescence"

185 deled mini organ that cycles between growth (anagen), regression (catagen), and relative quiescence (

186 lly recognized to comprise phases of growth (anagen), regression (catagen), and rest (telogen).

187 evels in VDR(-/-) keratinocytes and restored anagen responsiveness in vivo in VDR(-/-) mice, resultin

188 cles with a Gsdma3 mutation enter the second anagen simultaneously as WT mice.

189 blasts from neonatal skin, adult telogen and anagen skin and adult skin in which ectopic hair follicl

190 The circadian transcriptomes of telogen and anagen skin are largely distinct, with the former domina

191 Mouse anagen skin fragments, maintained in histoculture, were

192 his issue, Ansell et al. show that wounds on anagen skin heal faster than those on telogen skin, sugg

193 s can lead to the identification of not only anagen-specific genes (e.g., nexin 1), but also a catage

194 roxylase activities during the telogen/early anagen stage (days 0-1).

195 Actively growing and pigmented anagen stage hair follicles were sensitive to hair remov

196 tive mesenchymal expression during postnatal anagen stage hair-follicle cycling.

197 logen hair follicles into the hair-producing anagen stage in mature skin remain incompletely understo

198 FM is stringently coupled to the anagen stage of the hair cycle, being switched-off in ca

199 by histology that these follicles are in the anagen stage of their first hair growth cycle.

200 on from the resting (telogen) to the growth (anagen) stage of the hair cycle in adult mouse skin.

201 essed in the upper matrix and medulla of the anagen-stage hair.

202 telogen hair follicles into a proliferative (anagen) state, whereas 100% of the hair follicles in the

203 generalized follicular hamartoma, and loose anagen syndrome, may be associated with developmental de

204 resting phase of the hair follicle cycle) to anagen (the active phase), thereby facilitating robust h

205 od) and remained continuously in an abnormal anagen (the growth phase of the hair cycle).

206 However, in mid- and late anagen, the GFP-expressing cells are located in the uppe

207 During telogen or resting phase and in early anagen, the GFP-positive cells are mainly in the bulge a

208 orrelated with a decrease in the duration of anagen, the growth phase of the hair cycle.

209 tein-alpha and -beta were upregulated during anagen, then downregulated in catagen follicles.

210 telogen, significantly upregulated in early anagen, then gradually declined, and reappeared again in

211 the hair follicles to exit telogen and enter anagen, thereby initiating hair growth.

212 d the progression of the hair follicles from anagen to catagen (hair follicle maturation and regressi

213 and fibroblast growth factor-5 regulate the anagen to catagen transition by independent pathways.

214 gand receptor combination might regulate the anagen to catagen transition of the hair cycle.

215 other signaling molecules that regulate the anagen to catagen transition.

216 o be switched off during the transition from anagen to catagen, which implies a regulatory role for I

217 in grafts of null skin did not progress from anagen to telogen and scanning electron micrografts reve

218 Transition from anagen to telogen involves an intermediate stage, catage

219 The transition from anagen to telogen is marked by downregulation of hair co

220 repetitively progresses from a growth phase (anagen) to a rapid apoptosis-driven involution (catagen)

221 As the anagen-to-catagen transformation of microdissected human

222 is involved in hair cycle control, i.e., the anagen-to-catagen transformation, was tested.

223 NF-kappaB participates in telogen-anagen transition in awl and zigzag HFs, and is required

224 JAK-inhibition is able to induce telogen-to-anagen transition in wild-type mice.

225 ecome increasingly clear that the telogen-to-anagen transition is controlled jointly by at least the

226 as a crucial proximal signal for the telogen-anagen transition.

227 te of HFSCs in the process of the telogen-to-anagen transition.

228 During mid-anagen, two types of deleted in colon carcinoma staining

229 cells were created by Atoh1 induction during anagen versus telogen and following disruption of Notch

230 ultured, human scalp hair follicles (HFs) in anagen VI can be exploited for dissecting and manipulati

231 1.4 (mean +/- SEM) of the follicles were in anagen VI compared to only 1.3 +/- 0.7% in the control m

232 topical application of dexamethasone during anagen VI decreased the concentration of POMC, MC1-R, an

233 atin 15+ (K15), CD200+ or CD34+ cells within anagen VI hHFs by immunohistomorphometry, using Ki-67 an

234 umber and total papilla size were maximal by anagen VI, but intriguingly, decreased by 25% during thi

235 h, and, after reaching the highest values in anagen VI, decreased during the anagen-catagen transitio

236 - 4% (mean +/- SEM) of the follicles were in anagen VI, whereas none (0%) were in anagen in the contr

237 dShh, but not in controls, acceleration into anagen was evident, since hair follicle size and melanog

238 When anagen was induced by hair depilation at day 20 after bi

239 p of follicles put into culture when in late anagen were attempting to cycle in vitro.

240 the follicles are in anagen and the onset of anagen when the follicles are in telogen.

241 The second peak was observed at mid-anagen, when melanogenesis takes place.

242 a dominant-negative manner to markedly delay anagen, while L-type channel blockers act through Cav1.2

243 that induces resting hair follicles to enter anagen with consequent hair growth.

244 Hair follicles cannot enter the second anagen with ectopic WT Gsdma3 overexpression.

245 air follicles cycle from catagen to the next anagen without transitioning through a morphologically t