ライフサイエンスコーパス: hair cycle

1 an abnormal anagen (the growth phase of the hair cycle).

2 ells within the hair follicle throughout the hair cycle.

3 ption complex required for initiation of the hair cycle.

4 ene expression during specific phases of the hair cycle.

5 rgoes dramatic remodeling during adult mouse hair cycle.

6 late the anagen to catagen transition of the hair cycle.

7 melanocyte apoptosis and survival during the hair cycle.

8 but not in catagen and telogen phases of the hair cycle.

9 gene expression when compared with a normal hair cycle.

10 only after the start of the first postnatal hair cycle.

11 overexpression of the peptide on the murine hair cycle.

12 ing cells in the hair follicle vary with the hair cycle.

13 remature entry into the catagen phase of the hair cycle.

14 e shafts that shed arise during the previous hair cycle.

15 a distinct shedding, or exogen, phase of the hair cycle.

16 ies were detected before the first postnatal hair cycle.

17 late anagen and the onset of catagen of the hair cycle.

18 ody during the growing (anagen) phase of the hair cycle.

19 y at the onset of a new growing stage of the hair cycle.

20 uring telogen delays the initiation of a new hair cycle.

21 duration of anagen, the growth phase of the hair cycle.

22 g increase in dermal fibrosis and an altered hair cycle.

23 ble role for 6BH4 in the synchronized murine hair cycle.

24 uld be of major functional importance in the hair cycle.

25 lieved to regulate catagen remodeling in the hair cycle.

26 H4 de novo synthesis at the beginning of the hair cycle.

27 to C57 BL/6 mice at different stages of the hair cycle.

28 C2-R) gene was similar throughout the entire hair cycle.

29 major factor responsible for controlling the hair cycle.

30 atterns during the depilation-induced murine hair cycle.

31 HFSC activation and accelerate initiation of hair cycle.

32 lly in HFSCs, promoted the activation of the hair cycle.

33 lly in HFSCs, promoted the activation of the hair cycle.

34 air follicle stem cell (HFSC) activation and hair cycle.

35 a is required for anagen onset in the murine hair cycle.

36 nd bulge regulate new follicle growth in the hair cycle.

37 or inciting the growth (anagen) phase of the hair cycle.

38 is not essential for the initiation of a new hair cycle.

39 licle stem cell activation during the murine hair cycle.

40 e to proliferation and launch the subsequent hair cycle.

41 ut did not detect significant changes in the hair cycle.

42 for FGF13 in hair follicle growth and in the hair cycle.

43 tic shortening of the quiescent phase of the hair cycle.

44 ted with the K15- upper bulge throughout the hair cycle.

45 are heterogeneous and dynamic throughout the hair cycle.

46 re induction of the destructive phase of the hair cycle.

47 n, and proposed to be an active phase of the hair cycle.

48 to a prolonged quiescent phase of the first hair cycle.

49 o markedly shortened resting periods between hair cycles.

50 r follicles (HFs) regeneration by regulating hair cycles.

51 ession was similar in normal human and mouse hair cycles.

52 s two novel and interdependent regulators of hair cycling.

53 al communication that is required for normal hair cycling.

54 iety of disorders related to disturbances of hair cycling.

55 tissue regeneration and degeneration during hair cycling.

56 e signaling cues during HF morphogenesis and hair cycling.

57 ages and thus exhibited defects in postnatal hair cycling.

58 atrix keratinocytes and chemotherapy-induced hair-cycle abnormalities, driven by the dystrophic anage

59 ratinization, epidermis development, and the hair cycle (absolute log2-fold change > 4), with concomi

60 The enhanced hair cycling accelerates HFSC expenditure, and impacts h

61 Paradoxically, Kras(G12D) also prevented hair cycle activation.

62 air loss phenotype that involves an aberrant hair cycle, altered sebaceous gland differentiation with

63 mination of the growth phase (anagen) of the hair cycle, an event that is regulated in part by FGF5.

64 protein activation is regulated through the hair cycle and coincides with HFSC activation.

65 elayed anagen entry during the physiological hair cycle and compromised HF regeneration upon transpla

66 Remarkably, this happens not by perturbing hair cycle and follicle architecture, but rather by prom

67 ts suggest that vitamin A regulates both the hair cycle and immune response to alter the progression

68 strictly coupled to the growth stage of the hair cycle and is interrupted during follicle regression

69 Understanding of the hair cycle and its regulation would shed light on many o

70 The deregulated hair cycle and severely diminished fertility in Cutl1(tm

71 chemotherapy drug, induces disruption of the hair cycle and subsequent alopecia.

72 zed to regenerate the new follicle with each hair cycle and to reepithelialize epidermis during wound

73 ved in the follicular papilla throughout the hair cycle and was accompanied by weak staining of the m

74 However, hair cycle and wound healing processes were severely com

75 is essential for skin remodeling, including hair cycle and wound healing.

76 the importance of the shedding phase of the hair cycle and, in the context of current literature, an

77 skin is accompanied by a marked reduction in hair cycling and appearance of bald patches, leading res

78 es of the hair follicles are responsible for hair cycling and contribute to the regeneration of the n

79 Thus, the combinatorial defects in hair cycling and differentiation, together with conceale

80 suggest that Hh signaling may play a part in hair cycling and in epidermal mesenchymal interactions i

81 ortant role for mature dermal adipocytes for hair cycling and wound healing.

82 t hair shafts, aberrant catagen stage of the hair cycle, and eventual loss of the hair follicle.

83 DP cell numbers fluctuate over the hair cycle, and hair loss is associated with gradual dep

84 n 16 during skin morphogenesis, in the adult hair cycle, and in challenged epidermis.

85 basal/spinous layer during all stages of the hair cycle, and in the bulge during anagen and early cat

86 rs of different sizes or types in successive hair cycles, and this shift is accompanied by a correspo

87 he regulation of mK6a during mouse postnatal hair cycling, and compare it to mK75, a companion layer

88 remarkable regenerative capacity throughout hair cycling, and display fate plasticity during cutaneo

89 layers in the context of development, adult hair cycling, and wound repair.

90 and tail follicles occurs after two to three hair cycles, apparently by necrosis.

91 follicular epithelium resulted in a profound hair cycle arrest.

92 R(-/-)) mice exhibit lack of postmorphogenic hair cycles as a result of impaired keratinocyte stem ce

93 less (hr) genes play a role in the mammalian hair cycle, as inactivating mutations in either result i

94 dependent regulatory modules for ventral and hair cycle ASIP expression, and we characterize their ac

95 d genes that were not previously known to be hair cycle-associated and confirmed their temporal and s

96 air follicle mesenchyme exhibits significant hair cycle-associated plasticity.

97 ringently coupled to the anagen stage of the hair cycle, being switched-off in catagen to remain abse

98 Scd3 expression changes during the mouse hair cycle but not as dramatically as Scd1.

99 Protection was maintained after a second hair cycle, but at a lower level (hairs and follicles).

100 These transgenic mice have a normal first hair cycle, but lose their hair completely beginning 2-3

101 he anagen phase of the first (developmental) hair cycle, but with earlier effects on the terminal dif

102 e data suggest that LGR4 promotes the normal hair cycle by activating HF stem cells and by influencin

103 The regression phase of the hair cycle (catagen) is an apoptosis-driven process acco

104 ether mpAGA-associated HF transformation and hair cycle changes are primarily driven by the HF mesenc

105 g and are an integral component of the human hair cycle clock.

106 but reappeared at the start of the postnatal hair cycle, concomitant with precortex formation.

107 ogenesis, Edar signaling is also involved in hair cycle control and regulates apoptosis in HF keratin

108 t the peripheral clock system is involved in hair cycle control, i.e., the anagen-to-catagen transfor

109 good model system with which to investigate hair cycle control.

110 Throughout the hair cycle, DCC expression was confined to the basal ker

111 and that its ablation partially rescues the hair cycling defect of K17-null mice.

112 n Lgr4(-/-) mice can effectively reverse the hair cycle delay.

113 duced by transcutaneous DNA immunization was hair cycle dependent, because the plasmid needed to be a

114 , and CDKN1A), with Period1 expression being hair cycle dependent.

115 beta may, in turn, play a part in regulating hair cycle-dependent gene expression.

116 FP-1 protein is expressed in vivo in a hair cycle-dependent manner, as it can be detected in FP

117 us gland, and interfollicular epidermis in a hair cycle-dependent manner, suggesting that RA biosynth

118 AAT/enhancer-binding protein-delta showed no hair cycle-dependent variation in immunoreactivity.

119 estrogen receptor in the dermal papilla was hair cycle-dependent with the highest levels of expressi

120 was markedly reduced, but again demonstrated hair-cycle-dependent expression.

121 for and minimize the impact of physiological hair cycle differences when designing and interpreting n

122 Hair cycle domains are different from regional specifici

123 As mice age, multiple hair cycle domains form, each with its own regeneration

124 wn, wave propagation becomes restricted, and hair cycle domains fragment into smaller domains.

125 ew these regenerative hair waves and complex hair cycle domains, which were recently reported in tran

126 ctate how dynamic hair waves lead to complex hair cycle domains.

127 fts from numerous hair follicles for least 2 hair cycles during 36 days, demonstrations that HAP stem

128 In the hair cycle, during follicle regression, the niche traver

129 ized hypotrichosis, associated with abnormal hair cycle, epidermal and sebaceous gland hyperplasia, h

130 bset of DS cells are retained following each hair cycle, exhibit self-renewal, and repopulate the DS

131 tions are given for designing human-on-mouse hair cycle experiments.

132 During the hair cycle, follicle stem cells (SCs) residing in a spec

133 tion during the growth phase (anagen) of the hair cycle, followed by regression of angiogenic blood v

134 o be localized to the inner bulge during the hair cycle growth phase.

135 In the resting phase of the hair cycle, hair follicle stem cells are maintained in a

136 During the first hair cycle, hairs are lost and replaced by dystrophic ha

137 inhibitors of angiogenesis in the control of hair cycling, however, has remained unknown.

138 DR) are required for normal post-morphogenic hair cycles; however, the molecular mechanisms by which

139 entation recovers only during the subsequent hair cycle, i.e., after a new anagen hair bulb has been

140 tment, it was stimulated at the start of the hair cycle in a fashion that appeared to be dependent up

141 ically regulated as a function of the murine hair cycle in a way similar to other signaling molecules

142 telogen) to the growth (anagen) stage of the hair cycle in adult mouse skin.

143 During the induced hair cycle in C57BL/6 mice, administration of anti-c-kit

144 receptors, show the capacity to activate the hair cycle in mice.

145 rkedly changes during distinct stages of the hair cycle in mice.

146 e upregulated during the anagen phase of the hair cycle in unwounded skin.

147 igher replicate variance during asynchronous hair cycles in comparison with synchronous cycles.

148 ollicle development as well as in subsequent hair cycles in young and adult mice.

149 demonstrate a specialized role for Acvr1b in hair cycling in addition to hair follicle development.

150 dependent 1 and LIM homeobox 2 during normal hair cycling in adult skin.

151 required for VDR-DNA interactions and normal hair cycling in mice.

152 ion patterns of stem cell markers during the hair cycle, in addition to aberrant behavior of the mela

153 romote the regression phase of the mammalian hair cycle, in vivo in mice and in organ culture of huma

154 se skin collected at different phases of the hair cycle; in hamster melanomas; in normal and immortal

155 observed in follicles throughout the murine hair cycle, including the dermal papilla and lower epith

156 sufficient to induce HFSC proliferation and hair cycle induction.

157 The mammalian hair cycle involves periodic regeneration of a tiny orga

158 The hair cycle involves remodeling of cells and of cell grou

159 The human hair cycle is a complex, dynamic organ-transformation pr

160 The hair cycle is a dynamic process where follicles repeated

161 Cs, replenishment of primed SCs for the next hair cycle is compromised, delaying regeneration and eve

162 ndings suggest that PTHrP's influence on the hair cycle is mediated in part by its effects on angioge

163 ) development, but the impact of LGR4 on the hair cycle is still unclear.

164 Hair cycling is modulated by factors both intrinsic and

165 h mild, moderate, or severe CA compared with hair cycle-matched mice with no disease.

166 In the subsequent adult hair cycle, MED1 ablation activated the initiation of HF

167 During the hair cycle, Msx2 deficiency shortens anagen phase, but p

168 However, the influence of the hair cycle on wound healing has not previously been addr

169 m skin in the resting or growth phase of the hair cycle or skin with beta-catenin-induced ectopic fol

170 g pathways responsible for each phase of the hair cycle, or elucidate which proteolysis products from

171 ow that when the old bulge is lost with each hair cycle, overall levels of SC-inhibitory factors are

172 tryptamine) acetylation varied according to hair cycle phase and anatomic location.

173 he physiological changes associated with the hair cycle phase.

174 ollicle (HF) morphogenesis and the postnatal hair cycle, preceding dermal Wnt/beta-catenin activation

175 ferentiation along different lineages as the hair cycle progresses.

176 icle stem cells from aging by ensuring their hair cycle progression.

177 bulge maintains stem cell potency throughout hair cycle quiescence and growth, whereas paracrine Wnt

178 Axin2 is constantly expressed throughout the hair cycle quiescent phase in outer bulge stem cells tha

179 Through recurrent bouts synchronous with the hair cycle, quiescent melanocyte stem cells (McSCs) beco

180 ration in the outer root sheath, accelerated hair cycle, reduction of hair follicle stem cells, and m

181 phogenesis were later disrupted by delays in hair cycle reentry.

182 the microbiome in human organ remodeling and hair cycle regulation and define major open research que

183 nt of these BMs, laminin a5, is required for hair cycle regulation and hair germ-dermal papilla ancho

184 genes with detectable skin expression showed hair-cycle-related changes in expression, suggesting tha

185 The timing mechanism of the hair cycle remains poorly understood.

186 HrP trangene expression limited to the adult hair cycle resulted in the production of shorter hair sh

187 ture hair loss at early telogen phase of the hair cycle, resulting in cyclic alopecia.

188 n during the telogen phases of the postnatal hair cycle results in accelerated anagen development and

189 uring the early- and midanagen phases of the hair cycle results in accelerated anagen development, an

190 ry satisfactorily explains the origin of the hair cycle rhythm.

191 ed three major phenotypes--irregularities of hair cycle, sebaceous glands hypoplasia, and a thinner e

192 Here, we show that, during the hair cycle, Shh expression and the ability of skin cells

193 vi-LOF mice lost their hair during the first hair cycle, showing a reddish skin with impaired skin ba

194 shared with Arctic white wolves and that its hair cycle-specific module probably originated from an e

195 aligning sample collection with the desired hair cycle stage and animal age.

196 erm follicle pathology reflected the initial hair cycle stage at the time of isolation.

197 s guide seeks to offer a benchmark for human hair cycle stage classification, for both hair research

198 ries by skin location, developmental age and hair cycle stage, and that the Notch pathway plays a key

199 ve guide on how to recognize different human hair cycle stages in vivo is lacking.

200 than those on telogen skin, suggesting that hair cycle stages may influence healing outcome.

201 s show arrays of follicles in a continuum of hair cycle stages.

202 cally examine the influence of the different hair-cycle stages on murine skin wound healing.

203 achieved such that upon initiation of a new hair cycle, stem cells of each type activate lineage com

204 Dynamic Ppargc1a expression in the mouse hair cycle suggests a possible role in regulating hair g

205 ere, we have exploited spontaneous postnatal hair-cycle synchronicity in mice to systematically exami

206 of mouse skin at two different stages of the hair cycle, telogen and anagen.

207 Here, we show that during the murine hair cycle the expression of Eda A1, Edar, Edaradd, and

208 m a new bulge that houses HFSCs for the next hair cycle, the older bulge is left unanchored.

209 However, in the next hair cycle, the previously treated animals grow fully pi

210 , supporting key roles for these pathways in hair cycle timekeeping.

211 progeny sense BMPs at defined stages of the hair cycle to control their proliferation and differenti

212 The hair cycle transition is strictly regulated by the auton

213 Changes in the hair cycle underlie age-related alopecia, but the causat

214 g and other growth factors that regulate the hair cycle was examined by cross-breeding experiments em

215 ngation in telogen, the resting phase of the hair cycle, was also observed in adult animals.

216 Given the cyclic nature of the hair cycle, we felt it was important to consider a subse

217 the precise role of PTHrP and the PPR in the hair cycle, we have evaluated hair growth in the traditi

218 ptosis of epithelial cells during the murine hair cycle, we identified active TGF-beta responses usin

219 rmatogenesis, intestinal maintenance and the hair cycle, we review the role of dynamic heterogeneity

220 he produced cofactor during the synchronized hair cycle were determined employing the murine model C5

221 n the first postnatal anagen, but subsequent hair cycles were normal.

222 These become the primary SCs for the next hair cycle, whereas initial bulge SCs become reserves fo

223 D receptor null mice failed to initiate the hair cycle, whereas the vitamin D receptor null/human vi

224 brane potential oscillates during the normal hair cycle, with hyperpolarization specifically associat

225 entry into anagen during the second phase of hair cycling without a detectable change in the number o

226 s include antimicrobial defense and roles in hair cycling, wound healing, and thermogenesis.

227 follicle are critical for hair development, hair cycling, wound healing, and tumorigenesis.