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1 nd that Shh is its direct target in the hair follicle.
2 Hair is also pigmented by melanocytes in the follicle.
3 to 11 MPa along the first millimeter of the follicle.
4 e main site of androgen activity in the hair follicle.
5 d receptor 5-positive stem cells in the hair follicle.
6 total follicles and percentages of advanced follicles.
7 ted heterogeneity among SCs and TACs of hair follicles.
8 near F4/80(+) mouse macrophages around hair follicles.
9 unilineage progenitors within TACs of mature follicles.
10 effective antiviral CD8 T cells from B-cell follicles.
11 m, and an increased number of cystic/atretic follicles.
12 g of Tfh cells and the development of B cell follicles.
13 endings wrapping the base of individual hair follicles.
14 ness, and decreased clustering of same stage follicles.
15 ystem leading to the formation of primordial follicles.
16 cation is concentrated in secondary lymphoid follicles.
17 cle localization, redirects them into B-cell follicles.
18 As that changed in the EVs of different size follicles.
19 ssociated in large clusters and formed small follicles.
20 y accessible human (mini-) organ: scalp hair follicles.
21 l germ cells, meiotic germ cells and ovarian follicles.
22 to reach the epidermis of the skin and hair follicles.
23 ses in vasculature and branching surrounding follicles.
24 nted layers, affects the survival of ovarian follicles.
25 es, germ cells remain arrested as primordial follicles.
26 n mice lead to de novo morphogenesis of hair follicles.
27 ssing cells toward the FDC-containing B cell follicles.
28 tor implicated in cellular entry into B-cell follicles.
29 bset of CD4(+) T cells in secondary lymphoid follicles.
30 estrogen and higher numbers of large ovarian follicles.
31 fects of chemotherapeutic agents on the hair follicle, a number of experimental models have been prop
32 unique characteristic of blocking primordial follicle activation that could be exploited to prevent t
33 nd expansion in vivo of PGCs and controlling follicle activation will be essential for continuing mai
35 ells, we found that SHH does not act on hair follicles, adipocytes, endothelial cells, and hematopoie
36 icroarray and qRT-PCR analysis of human hair follicles after Nrf2 activation using sulforaphane ident
40 tioxidant N-acetylcysteine rescued defective follicle and oocyte development resulting from Kat8 defi
42 iffusivity, especially when flux between the follicle and the surrounding stratum corneum is involved
43 allow imaging at increased depth through the follicle and transabdominal ultrasonography in vivo show
45 causes the stepwise miniaturization of hair follicles and eventual hair loss in wild-type mice and i
47 KO ovaries had a higher percentage of antral follicles and fewer corpora lutea; follicles progressed
48 sure to ATZ reduces the number of primordial follicles and increases the incidence of multi-oocyte fo
50 gradients observed experimentally in B cell follicles and interfollicular regions, building confiden
53 hogenic SIV infection, NK cells migrate into follicles and play a major role in viral reservoir contr
55 alence of relevant immune cells in tonsillar follicles and support the use of tonsils as lymphoid sit
57 resulted in high viral replication rates in follicles and the T cell zone and increased viral DNA in
58 ntestinal villus and colon-resident lymphoid follicle, and degeneration and atrophy of brain microvas
59 sphericity index, peripheral distribution of follicles, and absence of a dominant follicle were deter
61 st antiviral CD8 T cells do not enter B-cell follicles, and those that do fail to robustly control vi
63 ntal mechanisms of folliculogenesis, whereby follicles are formed by the reorganization of a non-stru
66 r were preferably taken up by M cells in the follicle-associated epithelium (FAE) region of Peyer's p
67 expression of IFN-lambda mRNA was higher in follicle-associated epithelium of animals that had clear
68 and nonstructural proteins were localized to follicle-associated epithelium of the dorsal soft palate
71 follicle, improved characterization of hair follicle biology, and methods development in precision m
72 t whole transcriptome RNA sequencing of hair follicle bulge melanocyte precursors and compared their
73 gulation of TNC, GJB6, and THBS1 in the hair follicle bulge melanocytes and of TYR in the epidermal m
74 populated by melanocyte precursors from hair follicle bulge that proliferate, migrate, and differenti
77 m cells (McSCs) located in the bulge of hair follicles can regenerate mature melanocytes for hair and
78 rom K14-H2B GFP mice led to significant hair follicle catagen transformation compared with controls.
79 emphysema severity; (4) there were lymphoid follicles (CD20(+)IgM(+)) with active B cells (phosphory
82 Hnt upregulates Mmp2 expression in posterior follicle cells (essential for the breakdown of the folli
83 he follicle wall) and Oamb expression in all follicle cells (the receptor for receiving adrenergic si
84 o requires Torso-like, which is expressed by follicle cells adjacent to the ends of the developing oo
85 r data strongly suggest that 20E produced in follicle cells before ovulation activates EcR.B2 to prim
86 Hnt is not expressed in immature stage-13 follicle cells but is upregulated in mature stage-14 fol
88 ion of the Ecdysone receptor (EcR) in mature follicle cells mimicked shd-knockdown defects, which wer
91 ydroxyecdysone (20E), specifically in mature follicle cells, blocked follicle rupture, which was resc
92 cells but is upregulated in mature stage-14 follicle cells, which is essential for follicle rupture/
95 mall interfering RNA) in cultured human hair follicles confirmed the regulation of key Nrf2 target ge
98 r granzyme B production, and expanded B-cell follicles correlated with protection from reactivation.
99 on preserves the ovarian reserve, primordial follicle counts, serum anti-Mullerian hormone levels (a
101 during epidermal ontogenesis and normal hair follicle cycling and that its absence may aggravate the
102 5-dihydroxyvitamin D3 and/or calcium in hair follicle cycling is not clear despite their impact on ke
103 dent function of activated prostasin in hair follicles, dependent on zymogen conversion by matriptase
105 fficiency is chemotherapy-induced primordial follicle depletion, which has been proposed to be mediat
107 indings identify WNT5a as a key regulator of follicle development and gonadotropin responsiveness.-Ab
108 dotropin hormones, which are responsible for follicle development and maturation and ovarian function
109 eletion resulted in female infertility, with follicle development failure in the secondary and preant
113 rschmidt et al. (2017) show that during hair follicle development, commensals induce regulatory T cel
114 d the most marked defect is abnormal ovarian follicle development, resulting in impaired fertility.
124 rbid acne inversa (AI), an inflammatory hair follicle disorder, and had a history of nicotine abuse a
126 al stem cell (eSC) niche of human scalp hair follicles, during the inflammatory permanent alopecia, l
128 ng and partially reversing EMT in human hair follicles eSCs ex vivo, including in lichen planopilaris
129 this enzyme is highly expressed in the hair follicle, especially the inner root sheath, and that the
131 es, including the first concrete examples of follicles, feather tracts and apteria in Cretaceous avia
134 natal germline cyst breakdown and primordial follicle formation by regulating E-cadherin junctions be
137 ency reduces spleen weights, restores B-cell follicle formation, impedes cell cycle progression of pr
140 ssed in the alveolar epithelium and lymphoid follicles from patients with IPF, and AKAP13 mRNA expres
143 onstrate that (i) the response of human hair follicles grafted onto immunodeficient mice to cyclophos
145 netic protein 15 (BMP15) are secreted during follicle growth and play pivotal roles in this local reg
150 ch is produced by granulosa cells of growing follicles, has been proposed as a negative regulator of
151 sic polycystic ovaries, reduced large antral follicle health, and several metabolic traits including
153 ctor NF-kappaB controls key features of hair follicle (HF) development, but the role of NF-kappaB in
155 egulated in dermal papilla cells during hair follicle (HF) morphogenesis and the postnatal hair cycle
157 re generally well differentiated, while hair follicle (HF) stem cell-derived SCCs frequently exhibit
161 egs) in skin preferentially localize to hair follicles (HFs), which house a major subset of skin SCs
163 ls are uniquely defined by expression of the follicle-homing receptor CXCR5, the guidance receptor pr
164 re OV, FPO-9, and peripheral distribution of follicles; however, reproducibility of these measures wa
165 in patients with diseases affecting the hair follicle, improved characterization of hair follicle bio
169 83) directs B-cell migration in the lymphoid follicles in response to its endogenous ligands, oxyster
171 the submucosa and ectopic tertiary lymphoid follicles in the ectocervix and vagina; and 3) concentra
172 represents the stock of quiescent primordial follicles in the ovary which is gradually depleted durin
176 eiotic progression in mammalian preovulatory follicles is controlled by the granulosa cells around th
177 d that mesenchymal cell condensation at hair follicles is locally directed by an epidermal prepattern
178 domain activity operating in the first hair follicles is responsible for a delay in follicular destr
179 0.89), substantial for absence of a dominant follicle (kappa, 0.74), moderate for FPO-9 (ICC, 0.54) a
182 e origin of repeating patterns, such as hair follicles, limb digits, and intestinal villi, during dev
183 okine receptor on TFH associated with B-cell follicle localization, redirects them into B-cell follic
184 ical studies showed markedly dystrophic hair follicles, loss of hair shafts with increased apoptosis,
186 re characterized by the presence of the hair follicle marker Sox 9, keratins 10 and 14, and normal me
188 is narrow-band UVB (NBUVB), but how the hair follicle melanocyte precursors are activated by UV light
192 be expressed in both the epidermis and hair follicle of normal skin, but its expression was dramatic
193 CD4(+) T cells were found outside the B cell follicle of the LN, predicted the size of the persistent
195 concentrated within CD4(+) T cells in B cell follicles of secondary lymphoid tissues during asymptoma
196 rees scaffolds provide corners that surround follicles on multiple sides while 90 degrees scaffolds h
197 ression of the BMP antagonist Noggin in hair follicles or deletion of the BMP receptor in myofibrobla
198 s known about the energetics of growing hair follicles, particularly in the mitochondrially abundant
199 enchymal self-organisation processes in hair follicle patterning, identifying a network of fibroblast
200 characteristic curve [AUC]) of the number of follicles per ovary (FPO) measuring 9 mm or smaller (FPO
201 itical for the normal development of ovarian follicles, perturbations in oocyte-GC communication duri
204 Physiologically, the size of the primordial follicle pool determines the reproductive lifespan of fe
206 of antral follicles and fewer corpora lutea; follicles progressed to the antral stage but many were u
208 anscription factor Gata6 in adult mouse hair follicle regeneration where it controls the renewal of r
212 lper CD4 T cells, TFH, present inside B-cell follicles represent a major source of this residual viru
214 ations impairing TBX3 expression in the hair follicle, resulting in a more circumferential distributi
216 rictor that is transiently produced prior to follicle rupture by granulosa cells of periovulatory fol
218 ecifically in mature follicle cells, blocked follicle rupture, which was rescued by ectopic expressio
227 tem cells in affected tissues including hair follicles, sebaceous glands, taste buds, nails and sweat
230 he amount of scaffold interaction increases, follicle spreading is limited and survival increases.
234 eg cells preferentially localize to the hair follicle stem cell (HFSC) niche to control HFSC-mediated
235 l epithelium were compared to epidermal hair follicle stem cell RNA-Seq to identify genes representin
236 both germline stem cells (GSCs) and somatic follicle stem cells (FSCs) in the Drosophila germarium,
238 ovariole of a Drosophila ovary, contains two follicle stem cells (FSCs) that undergo neutral competit
241 In mammalian hair, it is unclear how hair follicle stem cells can enter an extended period of quie
245 soft keratinocyte matrix at the base of the follicle stiffens by a factor of approximately 360, from
247 GnRH regulates the pituitary gonadotropin's follicle-stimulating hormone (FSH) and luteinizing hormo
248 an inhibitor of prostaglandin signaling and follicle-stimulating hormone (FSH) and luteinizing hormo
249 one, testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and sex hormone-bindi
250 ts the beta-subunit of the pituitary hormone follicle-stimulating hormone (Fsh) increases bone mass i
252 serum level of antimullerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and ur
253 e sulfate (DHEAS), luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin, fasting p
255 tography and tandem mass spectrometry assay; follicle-stimulating hormone levels were measured at bas
256 Although follicles responded to initial follicle-stimulating hormone stimulation and developed n
257 s do not support the use of urinary or blood follicle-stimulating hormone tests or antimullerian horm
258 y end point was POF, defined as at least one follicle-stimulating hormone value of > 40 IU/L after 2
260 ned 12-month analysis evaluated E2, E1, E1S, follicle-stimulating hormone, and luteinizing hormone le
261 tory findings (insulin-like growth factor 1, follicle-stimulating hormone, luteinizing hormone, and t
263 vo imaging, we observe disruption in thyroid follicle structure that occurs early in thyroid developm
264 (1) their stem cells are contained within a follicle structure, (2) they undergo cyclic regeneration
265 es in large skin wounds that regenerate hair follicles, suggesting a new source of adipogenic progeni
266 a greater proportion of quiescent primordial follicles than control ExECs, indicating suppression of
267 ta (AA) is an autoimmune disease of the hair follicle that results in hair loss of varying severity.
269 cific antiviral immune responses in lymphoid follicles that limit SIV replication in this particular
270 9%), respectively; for absence of a dominant follicle, they were 90% (95% CI: 76%, 97%) and 27% (95%
271 ation occurs in germinal centers in lymphoid follicles through a critical interaction between B cells
272 5(+) and entered and persisted in lymph node follicles throughout the follow-up (240 d post-infection
273 essential roles of vasculature in organizing follicles to allow future studies on normal and diseased
274 e ovulation activates EcR.B2 to prime mature follicles to be responsive to neuronal ovulatory stimuli
275 R cells, which then migrated into the B cell follicles to prevent the expansion of self-reactive B ce
276 microfluidic system supports murine ovarian follicles to produce the human 28-day menstrual cycle ho
277 zation of unselected CD8 T cells into B-cell follicles using CXCR5 expression provides a strategy to
278 m (p<0.001) and the imaging of the skin hair follicles using multiphoton microscopy showed that it op
280 reamplified in the skin and surrounding hair follicles via intradermal injection of recombinant R-spo
281 isted in wild-type mice when thinning of the follicle wall was prevented by infusion of protease inhi
282 le cells (essential for the breakdown of the follicle wall) and Oamb expression in all follicle cells
283 imply a response to reduced thickness of the follicle wall; vasoconstriction persisted in wild-type m
284 ther subset of T cells in secondary lymphoid follicles was described, follicular regulatory T (TFR) c
286 T cells could be engineered to enter B-cell follicles, we genetically modified unselected CD8 T cell
288 tion of follicles, and absence of a dominant follicle were determined, with girls who were highly sus
289 t sphericity index and absence of a dominant follicle were significantly associated with the level of
290 d specificity for peripheral distribution of follicles were 33% (95% CI: 19%, 49%) and 95% (95% CI: 8
291 DHT-induced ovarian steroidogenesis, antral follicles were isolated from wild type and CMKLR1 knocko
293 e microscopy to be localized around the hair follicles, when applied to the skin using hypobaric stre
294 ically largely excluded from lymphoid B cell follicles, where HIV- and SIV-producing cells are most h
295 T-box 3 (TBX3) transcription factor in hair follicles, which in turn determines the distribution of
296 roblast reprogramming required neogenic hair follicles, which triggered bone morphogenetic protein (B
297 ization of CD8(hCXCR5) T cells within B-cell follicles with only rare cells in extrafollicular locati
298 (hCXCR5) T cells were present throughout the follicles with some observed near infected TFH In contra
299 helper CD4 T cells, TFH, residing in B-cell follicles within secondary lymphoid tissues, are readily
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