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 melanocyte apoptosis and survival during the hair cycle.

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

4 gene expression when compared with a normal hair cycle.

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

6 overexpression of the peptide on the murine hair cycle.

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

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

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

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

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

12 ies were detected before the first postnatal hair cycle.

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

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

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

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

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

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

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

20 lieved to regulate catagen remodeling in the hair cycle.

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

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

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

24 major factor responsible for controlling the hair cycle.

25 atterns during the depilation-induced murine hair cycle.

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

27 licle stem cell activation during the murine hair cycle.

28 e to proliferation and launch the subsequent hair cycle.

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

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

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

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

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

34 are heterogeneous and dynamic throughout the hair cycle.

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

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

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

38 ells within the hair follicle throughout the hair cycle.

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

40 ption complex required for initiation of the hair cycle.

41 ene expression during specific phases of the hair cycle.

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

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

44 o markedly shortened resting periods between hair cycles.

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

46 s two novel and interdependent regulators of hair cycling.

47 al communication that is required for normal hair cycling.

48 iety of disorders related to disturbances of hair cycling.

49 e signaling cues during HF morphogenesis and hair cycling.

50 ages and thus exhibited defects in postnatal hair cycling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 follicular epithelium resulted in a profound hair cycle arrest.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 Hair cycle domains are different from regional specifici

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

138 The hair cycle is a dynamic process where follicles repeated

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

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

141 Hair cycling is modulated by factors both intrinsic and

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

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

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

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

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

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

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

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

150 he physiological changes associated with the hair cycle phase.

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

152 ferentiation along different lineages as the hair cycle progresses.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 The hair cycle transition is strictly regulated by the auton

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

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

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

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

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

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

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

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

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

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

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

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

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