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1 to a nonfluorescent core continuous with the hair shaft.
2 el (inner root sheath) cells surrounding the hair shaft.
3 bnormal profile of protein expression in the hair shaft.
4 e restricted to the cells giving rise to the hair shaft.
5 onfirmed by microscopical examination of the hair shaft.
6 d HOXC13, a transcriptional regulator of the hair shaft.
7 impaired formation of the hair canal and the hair shaft.
8 y due to urinary steroids diffusing into the hair shaft.
9  massive fungal invasion involving the whole hair shaft.
10 tem cells to initiate the formation of a new hair shaft.
11 particularly in controlling the shape of the hair shaft.
12 induced photosensitization by melanin in the hair shaft.
13 rogenitor cells of the inner root sheath and hair shaft.
14 formation of the outer cortex/cuticle of the hair shaft.
15 hair specific keratin genes and generate the hair shaft.
16 oduced efficient genetic modification of the hair shaft.
17  and in increased size of hair follicles and hair shafts.
18 ed to keratinocytes to produce normal mature hair shafts.
19 lity that is characterized by tightly curled hair shafts.
20  features including sparse and hypopigmented hair shafts.
21 ctional hair follicles that fail to generate hair shafts.
22  cycle resulted in the production of shorter hair shafts.
23 eratinocytes, and the formation of pigmented hair shafts.
24  pigmentation in the epidermis and in anagen hair shafts.
25 t follicles produced GFP-fluorescent growing hair shafts.
26 tered sebaceous gland differentiation, short hair shafts, aberrant catagen stage of the hair cycle, a
27 s, striking absence of sebaceous glands, and hair shaft abnormalities in KP lesions but not in unaffe
28 alized or generalized congenital ichthyosis, hair shaft abnormalities, immune deficiency, and markedl
29 rized by congenital erythroderma, a specific hair-shaft abnormality, and atopic manifestations with h
30 troscopy in vivo that human gray/white scalp hair shafts accumulate hydrogen peroxide (H(2)O(2)) in m
31 n from the proximal to the distal end of the hair shaft analyzed may indicate a change in the diet du
32 erstood about the mechanisms responsible for hair shaft anchorage.
33 ressing cells in the bulge area surround the hair shaft and are interconnected by short dendrites.
34  in KP pathogenesis, resulting in downstream hair shaft and epithelial barrier abnormalities.
35                                          The hair shaft and hair follicle inner root sheath (IRS) fai
36 s, the differentiating inner root sheath and hair shaft and in the most mature sebocytes of the sebac
37 in complete alopecia owing to failure of the hair shaft and inner root sheath to form, which is cause
38 ls in the postmitotic precursor cells of the hair shaft and inner root sheath.
39 ll types that keratinize as they move up the hair shaft and inner root sheath.
40 ritical roles played by Krt75 in maintaining hair shaft and nail integrity.
41 rkers of follicle differentiation, produce a hair shaft and progress through all stages of the hair f
42 mice displayed a normal hair coat, and their hair shaft and skin histology were indistinguishable fro
43 ng of the hair follicles and regrowth of the hair shaft and the inner root sheath resulted in subsequ
44  mice exhibit impaired de novo production of hair shafts and all temporary hair cell lineages, owing
45 llicles were complete with sebaceous glands, hair shafts and inner and outer root sheaths.
46                                              Hair-shaft and inner-root-sheath differentiation was ini
47 ion of the hair follicle, the medulla of the hair shaft, and in epithelia of the nail bed.
48 ing all hair follicle lineages including the hair shaft, and the inner and outer root sheaths in skin
49 genitors and their progeny that generate the hair shaft, and, subsequently, premature induction of th
50 ich are genetically deficient to grow normal hair shafts, and differentiated to keratinocytes to prod
51     Uncombable hair syndrome (UHS) is a rare hair shaft anomaly that manifests during infancy and is
52                                              Hair shafts are produced from stem cells located in the
53                              In contrast the hair shafts are shorter than normal, suggesting altered
54                               Msx2-deficient hair shafts are structurally abnormal.
55 he integrity of the sheaths that support the hair shaft, are expressed in the enamel organ and are es
56 f adhesional junctions, resulting in twisted hair shafts as well as an unusual deposition of hair cut
57 entire human hair follicle, inclusive of the hair shaft, as a key element in senile hair graying, whi
58 oval of upper skin layer exposed keratinized hair shafts at the skin surface.
59                        Interestingly, zigzag hair shaft bending depends on noncanonical NF-kappaB sig
60                       Differentiation of the hair shaft but not the inner root sheath is severely imp
61 s plays a major role in specification of the hair shaft, but little is known about how the equally im
62 f-1/Wnts at the crossroads of the IRS versus hair shaft cell fate decision in hair follicle morphogen
63 or of proliferation, acting on LEF1-positive hair shaft committed progenitor cells.
64  genes specific for cells of the three major hair shaft compartments (cuticle, cortex, and medulla) a
65 rs and the mechanisms by which they regulate hair shaft components are poorly understood.
66 er root sheath and in precursor cells of the hair shaft cortex and cuticle which lie immediately adja
67 showed ragged and dilapidated cuticle of the hair shaft (CUH, a hair anchoring structure), poor hair
68 keratin that is exclusively expressed in the hair shaft cuticle during anagen phase, and its expressi
69 ed by congenital ichthyosiform erythroderma, hair shaft defects and atopy, caused by mutations within
70 the profile of single gene mutations causing hair shaft defects were profound.
71 sease, characterized by severe skin disease, hair shaft defects, atopic diathesis, and increased susc
72 red for severity of skin condition, specific hair shaft defects, atopy, and recurrent infections.
73  is because of strikingly similar defects in hair shaft differentiation and that both mutants suffer
74 egulators of the genetic program controlling hair shaft differentiation in postnatal hair follicles.
75 3) has been shown to be essential for proper hair shaft differentiation, as Hoxc13 gene-targeted (Hox
76  14-3-3sigma mutation have severe defects in hair shaft differentiation, resulting in destruction of
77 ard-keratin-containing portion of the murine hair shaft displays a positive immunoreactivity with an
78 arily in the dermal papilla, pre-cortex, and hair shaft during mid-late anagen.
79 erentiation, resulting in destruction of the hair shaft during morphogenesis.
80  a KRT15(+) stem cell population and produce hair shafts expressing hair-specific keratins.
81 g programs the epidermis towards placode and hair shaft fate at the expense of epidermal differentiat
82 ition to promoting hair follicle placode and hair shaft fate, beta-catenin signaling actively suppres
83 her genes known to play an important role in hair shaft formation (trichohyalin and involucrin, ultra
84 P-2alpha expression during the initiation of hair shaft formation and active hair follicle downward g
85 al papilla in these mice, yet the subsequent hair shaft formation was inhibited.
86 f primary hair follicle development prior to hair shaft formation.
87  structural protein TCHH are all involved in hair shaft formation.
88 erentiation of hair matrix keratinocytes and hair shaft formation.
89 ncodes a protein that is essential to proper hair-shaft formation, were associated with CCCA.
90 odifies other proteins that are essential to hair-shaft formation.
91  the first week post-birth, correlating with hair shaft fragility and untimely apoptosis in the hair
92                                              Hair shafts from AKR/J mice were deficient in these proj
93  shotgun proteomic profiling can distinguish hair shafts from different inbred mouse strains.
94 jumping whisker HAP stem cells produced long hair shafts from numerous hair follicles for least 2 hai
95          This resulted in a complete loss of hair shafts from the nontylotrich hair follicles in thes
96 ted compartments of the human hair follicle: hair shaft, gland-containing fragment, upper intermediat
97                            As a consequence, hair shafts grow longer.
98 JMD patients, P-cadherin silencing inhibited hair shaft growth, prematurely induced HF regression (ca
99  the lower and middle cortical region of the hair shaft in both developing and cycling hair.
100 erized by the development of blebs along the hair shaft in mice.
101         Both proteins play critical roles in hair shaft integrity.
102  variant predisposition leading to disrupted hair shaft integrity.
103 quences of DSG4 dysfunction on epidermal and hair shaft integrity.
104 tion and suggests that K17 expression in the hair shaft is a general trait in this species.
105                                 Although the hair shaft is derived from the progeny of keratinocyte s
106 to the inner layers of the hair follicle and hair shaft is impaired.
107 ion are associated with the structure of the hair shaft itself, while evolutionary rate shifts in non
108 opted hair follicle fate, broadly expressing hair shaft keratins in place of epidermal stratification
109 me differentiation of hair matrix cells into hair-shaft-like material, no hair was formed.
110 nd that lipids accelerated the elongation of hair-shaft-like structures.
111 ull progenitor cells expressed mixed IRS and hair shaft markers.
112 atin protein is the major component of scalp hair shaft material and it is composed of 21 amino acids
113                                              Hair shaft melanin components (eu- or/and pheomelanin) a
114 e distribution of keratin 6hf protein in the hair shaft mirrors that of keratin 17, and the observati
115                          We demonstrate that hair shaft mtDNA sequencing provides a simple but reliab
116 e numerous within dermal papillae and around hair shafts (n = 4).
117 s without nuclear DNA, i.e. thrombocytes and hair shafts, only showed the mitotype of haplogroup (hg)
118 rly and efficiently, resulting in diminished hair shaft outgrowth.
119 which results in efficient alteration of the hair shaft phenotype.
120 rized by abnormal flattening and twisting of hair shafts (pili torti) and hearing problems.
121  phenotype due to altered differentiation of hair shaft precursor cells, and cyclical balding resulti
122                               In contrast to hair shaft precursor cells, postnatal outer root sheath
123 ation patterns (HPPs) along individual human hair shafts, producing quantifiable physical timescales
124          Ex vivo, dWAT tendentially promoted hair shaft production, and significantly stimulated hair
125 entify upregulated BMP signaling in knockout hair shaft progenitors and demonstrate that Bmp6 inhibit
126        Here, we report the identification of hair shaft progenitors in the matrix that are differenti
127 uced migration and increased BMP activity of hair shaft progenitors.
128 trols the migration speed of differentiating hair shaft progenitors.
129  (ie, genes that encode functionally related hair shaft proteins).
130            To investigate the application of hair-shaft proteomics to the study of such diseases, pel
131        For this purpose, analyzing the total hair shaft provided better discrimination than analyzing
132                                    Since the hair shaft provides a discrete sampling of the species p
133 rmal papilla, are found in the precortex and hair shaft region.
134 onilethrix is a rare inherited defect of the hair shaft resulting in hair fragility and dystrophic al
135 nce; scanning electron microscopy of patient hair shafts reveals deformities (longitudinal grooves) a
136                        Proteomic analysis of hair shaft samples from one of the families revealed no
137  of the hair, and amino acid analysis of the hair shafts show levels of sulfur-containing proteins in
138 ned in vitro for a minimum of 20 d after the hair shaft stopped growing.
139 r cells, and cyclical balding resulting from hair shaft structural defects and associated with an abn
140 e expression of a mutant Krt75, which causes hair shaft structural defects characterized by the devel
141 eveux incoiffables" is a rare anomaly of the hair shaft that occurs in children and improves with age
142                              Besides forming hair shafts, the highly organized, metabolically vigorou
143 e the ratio of shed overfur to shed underfur hair shafts varies with the cycle phase and that the she
144  keratinocytes responsible for producing the hair shaft were below the split and remained in the foll
145                                       Normal hair shafts were not produced in the Dicer mutant, and t
146 intained in hair follicles such that growing hair shafts were phenotypically altered.
147 1 concentrated in the precursor cells to the hair shaft, where TOPGAL expression was co-induced with
148 imal region of the inner root sheath and the hair shaft, where Trpv3 is highly expressed, and correla
149  markedly dystrophic hair follicles, loss of hair shafts with increased apoptosis, and hyperplastic e

 
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