ライフサイエンスコーパス: hair shaft

1 bnormal profile of protein expression in the hair shaft.

2 e restricted to the cells giving rise to the hair shaft.

3 massive fungal invasion involving the whole hair shaft.

4 tem cells to initiate the formation of a new hair shaft.

5 formation of the outer cortex/cuticle of the hair shaft.

6 particularly in controlling the shape of the hair shaft.

7 to a nonfluorescent core continuous with the hair shaft.

8 induced photosensitization by melanin in the hair shaft.

9 rogenitor cells of the inner root sheath and hair shaft.

10 hair specific keratin genes and generate the hair shaft.

11 oduced efficient genetic modification of the hair shaft.

12 el (inner root sheath) cells surrounding the hair shaft.

13 and in increased size of hair follicles and hair shafts.

14 lity that is characterized by tightly curled hair shafts.

15 features including sparse and hypopigmented hair shafts.

16 ctional hair follicles that fail to generate hair shafts.

17 cycle resulted in the production of shorter hair shafts.

18 eratinocytes, and the formation of pigmented hair shafts.

19 pigmentation in the epidermis and in anagen hair shafts.

20 t follicles produced GFP-fluorescent growing hair shafts.

21 tered sebaceous gland differentiation, short hair shafts, aberrant catagen stage of the hair cycle, a

22 s, striking absence of sebaceous glands, and hair shaft abnormalities in KP lesions but not in unaffe

23 alized or generalized congenital ichthyosis, hair shaft abnormalities, immune deficiency, and markedl

24 rized by congenital erythroderma, a specific hair-shaft abnormality, and atopic manifestations with h

25 troscopy in vivo that human gray/white scalp hair shafts accumulate hydrogen peroxide (H(2)O(2)) in m

26 n from the proximal to the distal end of the hair shaft analyzed may indicate a change in the diet du

27 erstood about the mechanisms responsible for hair shaft anchorage.

28 ressing cells in the bulge area surround the hair shaft and are interconnected by short dendrites.

29 in KP pathogenesis, resulting in downstream hair shaft and epithelial barrier abnormalities.

30 The hair shaft and hair follicle inner root sheath (IRS) fai

31 s, the differentiating inner root sheath and hair shaft and in the most mature sebocytes of the sebac

32 in complete alopecia owing to failure of the hair shaft and inner root sheath to form, which is cause

33 ls in the postmitotic precursor cells of the hair shaft and inner root sheath.

34 ll types that keratinize as they move up the hair shaft and inner root sheath.

35 ritical roles played by Krt75 in maintaining hair shaft and nail integrity.

36 rkers of follicle differentiation, produce a hair shaft and progress through all stages of the hair f

37 mice displayed a normal hair coat, and their hair shaft and skin histology were indistinguishable fro

38 ng of the hair follicles and regrowth of the hair shaft and the inner root sheath resulted in subsequ

39 mice exhibit impaired de novo production of hair shafts and all temporary hair cell lineages, owing

40 llicles were complete with sebaceous glands, hair shafts and inner and outer root sheaths.

41 Hair-shaft and inner-root-sheath differentiation was ini

42 ion of the hair follicle, the medulla of the hair shaft, and in epithelia of the nail bed.

43 ing all hair follicle lineages including the hair shaft, and the inner and outer root sheaths in skin

44 genitors and their progeny that generate the hair shaft, and, subsequently, premature induction of th

45 Hair shafts are produced from stem cells located in the

46 In contrast the hair shafts are shorter than normal, suggesting altered

47 Msx2-deficient hair shafts are structurally abnormal.

48 he integrity of the sheaths that support the hair shaft, are expressed in the enamel organ and are es

49 f adhesional junctions, resulting in twisted hair shafts as well as an unusual deposition of hair cut

50 entire human hair follicle, inclusive of the hair shaft, as a key element in senile hair graying, whi

51 oval of upper skin layer exposed keratinized hair shafts at the skin surface.

52 Interestingly, zigzag hair shaft bending depends on noncanonical NF-kappaB sig

53 Differentiation of the hair shaft but not the inner root sheath is severely imp

54 s plays a major role in specification of the hair shaft, but little is known about how the equally im

55 f-1/Wnts at the crossroads of the IRS versus hair shaft cell fate decision in hair follicle morphogen

56 genes specific for cells of the three major hair shaft compartments (cuticle, cortex, and medulla) a

57 rs and the mechanisms by which they regulate hair shaft components are poorly understood.

58 er root sheath and in precursor cells of the hair shaft cortex and cuticle which lie immediately adja

59 showed ragged and dilapidated cuticle of the hair shaft (CUH, a hair anchoring structure), poor hair

60 ed by congenital ichthyosiform erythroderma, hair shaft defects and atopy, caused by mutations within

61 the profile of single gene mutations causing hair shaft defects were profound.

62 is because of strikingly similar defects in hair shaft differentiation and that both mutants suffer

63 egulators of the genetic program controlling hair shaft differentiation in postnatal hair follicles.

64 3) has been shown to be essential for proper hair shaft differentiation, as Hoxc13 gene-targeted (Hox

65 14-3-3sigma mutation have severe defects in hair shaft differentiation, resulting in destruction of

66 ard-keratin-containing portion of the murine hair shaft displays a positive immunoreactivity with an

67 arily in the dermal papilla, pre-cortex, and hair shaft during mid-late anagen.

68 erentiation, resulting in destruction of the hair shaft during morphogenesis.

69 a KRT15(+) stem cell population and produce hair shafts expressing hair-specific keratins.

70 g programs the epidermis towards placode and hair shaft fate at the expense of epidermal differentiat

71 ition to promoting hair follicle placode and hair shaft fate, beta-catenin signaling actively suppres

72 her genes known to play an important role in hair shaft formation (trichohyalin and involucrin, ultra

73 P-2alpha expression during the initiation of hair shaft formation and active hair follicle downward g

74 al papilla in these mice, yet the subsequent hair shaft formation was inhibited.

75 erentiation of hair matrix keratinocytes and hair shaft formation.

76 structural protein TCHH are all involved in hair shaft formation.

77 f primary hair follicle development prior to hair shaft formation.

78 the first week post-birth, correlating with hair shaft fragility and untimely apoptosis in the hair

79 Hair shafts from AKR/J mice were deficient in these proj

80 shotgun proteomic profiling can distinguish hair shafts from different inbred mouse strains.

81 This resulted in a complete loss of hair shafts from the nontylotrich hair follicles in thes

82 ted compartments of the human hair follicle: hair shaft, gland-containing fragment, upper intermediat

83 As a consequence, hair shafts grow longer.

84 JMD patients, P-cadherin silencing inhibited hair shaft growth, prematurely induced HF regression (ca

85 the lower and middle cortical region of the hair shaft in both developing and cycling hair.

86 erized by the development of blebs along the hair shaft in mice.

87 quences of DSG4 dysfunction on epidermal and hair shaft integrity.

88 tion and suggests that K17 expression in the hair shaft is a general trait in this species.

89 Although the hair shaft is derived from the progeny of keratinocyte s

90 to the inner layers of the hair follicle and hair shaft is impaired.

91 opted hair follicle fate, broadly expressing hair shaft keratins in place of epidermal stratification

92 me differentiation of hair matrix cells into hair-shaft-like material, no hair was formed.

93 ull progenitor cells expressed mixed IRS and hair shaft markers.

94 atin protein is the major component of scalp hair shaft material and it is composed of 21 amino acids

95 Hair shaft melanin components (eu- or/and pheomelanin) a

96 e distribution of keratin 6hf protein in the hair shaft mirrors that of keratin 17, and the observati

97 e numerous within dermal papillae and around hair shafts (n = 4).

98 rly and efficiently, resulting in diminished hair shaft outgrowth.

99 which results in efficient alteration of the hair shaft phenotype.

100 phenotype due to altered differentiation of hair shaft precursor cells, and cyclical balding resulti

101 In contrast to hair shaft precursor cells, postnatal outer root sheath

102 entify upregulated BMP signaling in knockout hair shaft progenitors and demonstrate that Bmp6 inhibit

103 Here, we report the identification of hair shaft progenitors in the matrix that are differenti

104 uced migration and increased BMP activity of hair shaft progenitors.

105 trols the migration speed of differentiating hair shaft progenitors.

106 To investigate the application of hair-shaft proteomics to the study of such diseases, pel

107 For this purpose, analyzing the total hair shaft provided better discrimination than analyzing

108 Since the hair shaft provides a discrete sampling of the species p

109 rmal papilla, are found in the precortex and hair shaft region.

110 onilethrix is a rare inherited defect of the hair shaft resulting in hair fragility and dystrophic al

111 Proteomic analysis of hair shaft samples from one of the families revealed no

112 of the hair, and amino acid analysis of the hair shafts show levels of sulfur-containing proteins in

113 ned in vitro for a minimum of 20 d after the hair shaft stopped growing.

114 r cells, and cyclical balding resulting from hair shaft structural defects and associated with an abn

115 e expression of a mutant Krt75, which causes hair shaft structural defects characterized by the devel

116 eveux incoiffables" is a rare anomaly of the hair shaft that occurs in children and improves with age

117 Besides forming hair shafts, the highly organized, metabolically vigorou

118 e the ratio of shed overfur to shed underfur hair shafts varies with the cycle phase and that the she

119 keratinocytes responsible for producing the hair shaft were below the split and remained in the foll

120 Normal hair shafts were not produced in the Dicer mutant, and t

121 intained in hair follicles such that growing hair shafts were phenotypically altered.

122 1 concentrated in the precursor cells to the hair shaft, where TOPGAL expression was co-induced with

123 markedly dystrophic hair follicles, loss of hair shafts with increased apoptosis, and hyperplastic e