ライフサイエンスコーパス: keratin

1 geneity co-expressing both basal and luminal keratins.

2 reflects the high cysteine content in human keratins.

3 We observed that keratin 1 and 10 end domains are likely to form a tetram

4 Keratin 1 expression is reduced throughout days 19-28.

5 olved in early KC differentiation, including keratin 1, keratin 10, and DSC-1, is reversed by p63 blo

6 esidues, which would spatially constrain the keratin 1/keratin 10 end domains to allow filament compa

7 Keratins 1 (K1) and 10 (K10) are the primary keratins ex

8 SdrF bound human keratins 1 and 10 and adhered to keratinocytes and epith

9 ns of the head and tail domains of epidermal keratins 1 and 10, based on all-atom 3D simulations of k

10 re altered in human skin diseases, including keratins 1 and 10, filaggrin, and loricrin.

11 howing that a polyarginine frameshift in the keratin-1 tail can also cause this disorder.

12 affecting the tail domains of keratin-10 or keratin-1, and Suzuki et al. expand the mutation spectru

13 ned the crystal structure of wild-type human keratin-1/keratin-10 helix 1B heterotetramer at 3.0 angs

14 Reduced expression of Keratin 10 (K10) resulting from Cdk5 knockdown may be re

15 ligase MDM2 are upregulated concomitant with keratin 10 (KRT10) downregulation.

16 hich would spatially constrain the keratin 1/keratin 10 end domains to allow filament compaction and

17 wed that SdrF mediates bacterial adhesion to keratin 10 through strong and weak bonds involving the A

18 follicle and cyst, and ectopic expression of keratin 10, a marker of interfollicular differentiation

19 rly KC differentiation, including keratin 1, keratin 10, and DSC-1, is reversed by p63 blockade.

20 pidermal differentiation markers involucrin, keratin 10, and filaggrin during tissue reconstruction.

21 presence of the hair follicle marker Sox 9, keratins 10 and 14, and normal melanocyte distribution a

22 ystal structure of wild-type human keratin-1/keratin-10 helix 1B heterotetramer at 3.0 angstrom resol

23 from mutations affecting the tail domains of keratin-10 or keratin-1, and Suzuki et al. expand the mu

24 pithelium, particularly keratin 3 (KRT3) and keratin 12 (KRT12).

25 ured by the decrease and increase in p63 and keratin 12 expression, respectively.

26 4, N-Cadherin, DeltaNp63 and ABCG2, and less keratin 12, consistent with their less differentiated st

27 rneal epithelial progenitor cells expressing keratin-12 originated from limbus, and gave rise to the

28 homotypic disulfide bond involving Cys367 in keratin 14 (K14) occurs in an atomic-resolution structur

29 The intermediate filament protein keratin 14 (K14) provides vital structural support in ba

30 and development, epithelial cells expressing keratin 14 (K14) Sox2, Sox9, Sox10, and Trp63 give rise

31 several Msx-regulated genes (Bmp4, Fgf8, and keratin 14 (K14)) in BlC groups, including MSX1, MSX2, a

32 in type II (KtyII) K5 and its type I partner keratin 14 (K14).

33 pressed the epithelial cytoskeletal protein, keratin 14 (K14).

34 ilized a transgenic mouse model in which the keratin 14 promoter drives expression of the entire HPV8

35 t affect injury severity or proliferation of keratin 14(+) (KRT14(+)) basal progenitors or other urot

36 n between invasion and protein expression of Keratin 14, a known biomarker for poor prognosis, with p

37 fter removal of rapamycin and expressed more keratin 14, N-Cadherin, DeltaNp63 and ABCG2, and less ke

38 and conditional deletion of Prdm1 in either Keratin 14- or Foxn1-expressing cells in mice resulted i

39 cer cells led to cell blebbing and a loss of keratins 14 and 18, in addition to the upregulation of v

40 terminal differentiation including decreased keratin-14 and increased involucrin expression.

41 he murine epidermis under the control of the keratin-14 promoter and showed that E7 is carcinogenic i

42 vivo models of metastasis, we establish that keratin-14+ breast cancer cells are vulnerable to NK cel

43 Keratin 15 (K15), a type I keratin, which pairs with K5

44 elium that is characterized by expression of keratin 15 (Krt15).

45 t study has studied these characteristics of keratin 15+ (K15), CD200+ or CD34+ cells within anagen V

46 D) activation mutation and Smad4 deletion in keratin 15-positive stem cells and a human oral SCC cell

47 icular differentiation markers, expansion of keratin-15-positive cells from localization within the b

48 Keratin 16 (K16) is a cytoskeletal scaffolding protein h

49 a combined hyperplasia score [thickness and keratin 16 (K16) mRNA] at baseline and after cyclosporin

50 The type I intermediate filament keratin 16 (KRT16 gene; K16 protein) is constitutively e

51 Mice genetically null for keratin 16 (Krt16), one of the genes mutated in pachyony

52 sociated PPK are reproduced in mice null for keratin 16 (Krt16), which is commonly mutated in PC pati

53 atures (thickness, Ki67(+) keratinocytes and keratin 16 [KRT16] mRNA expression, and phosphorylated s

54 improvements in epidermal disease hallmarks (keratin 16 and loricrin) in lesional skin from responder

55 IL-19 and LL37) and epidermal proliferation (keratin 16 and S100As) markers (P < .001).

56 her, we report on the novel observation that keratin 16 can localize to the nucleus of epithelial cel

57 idermal hyperplasia (increased thickness and keratin 16 expression) and T-cell and dendritic cell inf

58 greater epidermal hyperplasia (thickness and keratin 16) and cellular infiltration (CD3(+), CD11c(+),

59 thickness, keratin 16, and Ki67; P < .05 for keratin 16) decreased.

60 nd hyperplasia markers (epidermal thickness, keratin 16, and Ki67; P < .05 for keratin 16) decreased.

61 ons in key inflammatory and barrier markers (keratin 16, IL-13, IL-22, CCL17, CCL18, PI3/elafin, S100

62 Hyperplasia measures (thickness/keratin 16/Ki67) showed greater reductions with GBR 830

63 We previously identified Keratin 17 (K17) as a negative prognostic biomarker in o

64 High levels of the intermediate filament keratin 17 (K17) correlate with a poor prognosis for sev

65 y in the cytoplasm, the cytoskeletal protein keratin 17 (K17) has been recently identified inside the

66 ression of the intermediate filament protein keratin 17 (K17) is robustly upregulated in inflammatory

67 eased expression of the inflammatory markers Keratin 17 (Ker17) and Ki67.

68 The intermediate filament protein keratin 17 (Krt17) shows highly dynamic and inducible ex

69 The cytoskeletal protein Keratin 17 (KRT17;K17) is robustly expressed in a broad

70 These cells were p63 negative, keratin 17 positive, and keratin 6 positive and present

71 ulation of PAX6 and DKK1 and upregulation of keratin 17 protein expression levels.

72 Finally, Keratin-17-expressing keratinocytes but not Merkel cells

73 Keratin 8 (K8) and keratin 18 (K18) are the intermediate filament proteins

74 in sensitivity increased, and serum level of keratin 18 decreased.

75 -5, suggesting that Krtap5-5 crosstalks with keratin 18 in E0771 cells.

76 intestinal epithelial intermediate filament keratin 18 interact with the C-terminus of the Shigella

77 Keratin 18 mutants where O-GlcNAcylation at Ser(30) was

78 We further demonstrate that knockdown of keratin 18 phenocopies the loss of Krtap5-5, suggesting

79 [miR-122]) or provide mechanistic insights (keratin-18 [K18], high mobility group box-1 [HMGB1], and

80 total (M65) and caspase-cleaved (M30) serum keratin-18 fragments (n = 204) with histological paramet

81 We identified keratin 19 (CK19 or K19) as a novel CFTR-interacting pro

82 Keratin 19 (K19) belongs to the keratin family of protei

83 g the biliary/hepatic progenitor cell marker keratin 19 (K19) have been linked with a poor prognosis

84 analyses indicate 14-3-3 is associated with Keratin 19 (K19) in the whole embryo and, more specifica

85 First, using keratin-19 (Krt19) to mark a heterogeneous population of

86 ls express the ductal markers, keratin-7 and keratin-19, and form lumenized spheroids.

87 n of both knob residues to alanine disrupted keratin 1B tetramer and full-length filament assembly.

88 rformed transcriptome studies and identified keratin 23 (KRT23) as a new ductular cell marker.

89 pression of hair follicle-related molecules (keratin 25, trichohyalin, ribonuclease, RNase A family,

90 ions of the corneal epithelium, particularly keratin 3 (KRT3) and keratin 12 (KRT12).

91 sue differentiation, decreased expression of keratin 4 (KRT4) and cornulin (CRNN), and increased expr

92 5 and 14 but not the differentiation marker keratin 4.

93 perkeratotic surface (45 [33.6%]), yellowish keratin (42 [31.3%]), comedo-like openings (41 [30.5%]),

94 kinase (ERK)-driven proliferation of mostly keratin 5 (KRT5)(+)/KRT14(-) intermediate cells.

95 in pigmentation associated with mutations in keratin 5 (KRT5), protein O-fucosyltransferase 1 (POFUT1

96 the undifferentiated epithelial cell markers keratin 5 and 14 but not the differentiation marker kera

97 cantly higher total E-cadherin and decreased keratin 5 staining than epithelium of placebo-treated mi

98 Specifically, after low-dose IR, keratin 5(+) basal hair bulb progenitors, rather than bu

99 xpressing mouse strains under the control of keratin 5, CD4, and retinoic acid receptor-related orpha

100 Using either a keratin 5-Cre recombinase (K5-Cre) cross or an MMTV-NIC

101 mutants display premature differentiation of keratin 5-positive (Krt5(+)) basal cells and ectopic exp

102 ng a desmoglein-3 mouse model (Dsg3(-/-)) or keratin 5-specific reporter mice, the investigators show

103 lumen layer of multi-ciliated and a layer of Keratin-5-positive basal cells.

104 were p63 negative, keratin 17 positive, and keratin 6 positive and present at sites of adhesion, alt

105 ifferentiate, as demonstrated by the lack of keratin 6, a marker of the periderm.

106 maintained periderm-like cells that express keratin 6, but we observed abnormal expression of GRHL3.

107 We reported that the intermediate filament keratin 6a (K6a) is constitutively processed into antimi

108 rent in protein profiles and histopathology: keratin 6a+ precancerous cells gave rise to adenocarcino

109 ed to address this question, we identified a keratin 6a-expressing precancerous stem cell (PcSC) subs

110 One AS, designated Homo sapiens keratin 7 (KRT7-AS), was selected due to its marked upre

111 nt with KRT9 loss is a gain of the primitive keratin 7 and a signature of dsRNA sensing, including th

112 (but not its non-KRT7-OL portions) increased keratin 7 protein levels in cells.

113 mSG-DUC1 cells express the ductal markers, keratin-7 and keratin-19, and form lumenized spheroids.

114 Keratin 8 (K8) and keratin 18 (K18) are the intermediate

115 ectopic expression of the Merkel cell marker keratin 8 (K8) throughout the epidermis.

116 y molecule-1 (Kim1), lipocalin 2 (Lcn2), and keratin 8 (Krt8)-and of several novel genes (Ahnak, Sh3b

117 Liver disease-associated keratin 8 and 18 mutations modulate keratin acetylation

118 Keratins 8/18 (K8/18) are phosphoglycoproteins and form

119 rates expression of NP markers FoxF1, Pax-1, keratin-8/18, carbonic anhydrase-12, and NC markers brac

120 inhibitors (AI)-resistant cells, leading to Keratin-80 (KRT80) upregulation.

121 We show that KERATIN 9 (KRT9) is the most uniquely enriched transcrip

122 lar) epidermis is globally unique, including Keratin 9 (KRT9).

123 Keratin 9 (Krt9/K9), the most robustly expressed gene in

124 examine blood plasma expression patterns of Keratin 9 and its relationship to other AD-associated pr

125 Our findings suggest that dysregulated Keratin 9 expression is a consequence of AD pathology bu

126 and propose that the abnormal expression of Keratin 9 in AD blood and cerebrospinal fluid may be a r

127 Keratin 9 is highly enriched in volar keratinocytes, and

128 le pathways through which the involvement of Keratin 9 may take place.

129 Keratin 9 was recently identified as an important compon

130 ity of the surface protein SdrF to adhere to keratin, a major molecule expressed on the skin surface.

131 se-associated mutations in keratins modulate keratin acetylation and methylation, which may contribut

132 sociated keratin 8 and 18 mutations modulate keratin acetylation and methylation.

133 We compared keratin acetylation/methylation in liver disease-associa

134 raction of water ions from the volume of the keratin active layer, while the figures of merit of the

135 12-Leu132Pro mutation results in cytoplasmic keratin aggregates.

136 Finally, results of keratin and bioapatite delta(13)C indicate that the pred

137 odies reduced adherence of S. epidermidis to keratin and keratinocytes.

138 strate that SdrF mediates adherence to human keratin and suggest that SdrF may facilitate S. epidermi

139 l characteristics of sauropsid-specific beta-keratin and tropomyosin were detected in tissues contain

140 ic features of nonalcoholic steatohepatitis, keratin and ubiquitin aggregates within cytoplasmic Mall

141 Our data revealed that keratin and vimentin are nonconventional kinesin-1 cargo

142 the kinesin heavy chain tail is involved in keratin and vimentin IF transport, strongly suggesting t

143 keratinocyte (KC)-specific molecules such as keratins and adhesion molecules could be detected in the

144 tal interplay of intermediate filament alpha keratins and corneous beta-proteins that is employed in

145 1B knob/pocket mechanism is conserved across keratins and many non-keratin intermediate filaments.

146 ach for suppressing the expression of mutant keratins and related phenotypes in the epidermis.

147 f mutations in the end domains of suprabasal keratins and so contribute to understanding of the mecha

148 arious isoforms of casein kinase 1 (CK1) and keratins and to mediate organization of keratin cytoskel

149 uated adhesion to human-derived fibronectin, keratin, and fibrinogen.

150 ), mitochondria, acidic organelles, F-actin, keratin, and soluble fluorescein.

151 DTCs were immunostained with the pan-keratin antibody A45-B/B3.

152 Unlike F-actin or microtubules, keratins are the first major components of the cytoskele

153 e multifunctional system exclusively made by keratin as a bendable sensor for monitoring the humidity

154 the simultaneous use of naturally extracted keratin as both active ionic electrolyte for water ions

155 establish that K17 functions specially among keratins as an oncoprotein by controlling the ability of

156 ilaments which can be reconstituted by other keratins as well as by K15.

157 We identified keratin-associated protein 5-5 (Krtap5-5) as a candidate

158 greater body location-specific variation in keratin-associated proteins and intracellular proteins,

159 o test whether this was a result of enhanced keratin association, we used the desmoplakin mutant S284

160 Whale baleen is a keratin-based biological material; it provides life-long

161 oxidative stress observed in PC and related keratin-based skin disorders.

162 Live-embryo imaging shows that keratins become asymmetrically inherited by outer daught

163 of the CPC caused disassembly of F-actin and keratin between asters and local softening of the cytopl

164 16 with robust downregulation of its type II keratin binding partner, K6.

165 microridge morphogenesis, whereas periplakin-keratin binding was required to elongate microridges.

166 sensor pave the way for the effective use of keratin biopolymer in wearable or edible electronics whe

167 Disruption of the keratin cytoskeleton by perturbing Krtap5-5 function bro

168 n led to a striking abnormality in the major keratin cytoskeleton filaments structure in both in vivo

169 sion structures that are associated with the keratin cytoskeleton.

170 and keratins and to mediate organization of keratin cytoskeletons and desmosomes.

171 f degranulation/depolarization near sites of keratin deposition, as well as an ROS-generating paraxia

172 nse that directly up-regulates production of keratin-derived AMPs (KAMPs) by the ubiquitin-proteasome

173 >25%) was associated with greater immune and keratin dysregulation and larger abnormalities in nonles

174 pe ErbB2-derived tumors that express luminal keratins, ErbB2DeltaEx16-derived tumors exhibit high deg

175 Keratins 1 (K1) and 10 (K10) are the primary keratins expressed in differentiated epidermis.

176 An altered keratin expression profile was observed in the cornea of

177 es, mediated by asymmetric cell junction and keratin expression.

178 Keratin 19 (K19) belongs to the keratin family of proteins, which maintains structural i

179 The dissociation of cten from tension-free keratin fibers depends on the duration of cell stretch,

180 atin network interactions over time and that keratin fibers retain remarkable structural memory of a

181 the (supra)molecular organization within the keratin fibers.

182 ing disease epidermolysis bullosa simplex is keratin filament (KF) network collapse caused by aggrega

183 like KGs whose coalescence was restricted by keratin filament bundles.

184 6R mutant showed the enhanced sensitivity of keratin filament collapse upon okadaic acid treatment.

185 Electron microscopy revealed disruption of keratin filament cytoskeleton and accumulation of melano

186 g extensibility to ensure flexibility of the keratin filament network in the differentiating epidermi

187 f keratin subunits into filaments and blocks keratin filament recruitment toward cell-cell contacts.

188 diated by C-cadherin, the mechanism by which keratin filament reorganization occurs remains poorly un

189 le of microtubules and microtubule motors in keratin filament transport.

190 but the rapid transport of fully polymerized keratin filaments has not been reported.

191 c envoplakin from intracellular vimentin and keratin filaments in cultured cells.

192 14-3-3 colocalizes with keratin filaments near cell-cell junctions in migrating

193 Keratin filaments stabilized microridges, and overexpres

194 tering the primary structure and function of keratin filaments underlie genetic diseases typified by

195 1614Y recognises a conformational epitope on keratin filaments which can be reconstituted by other ke

196 cytoplasmic particles became associated with keratin filaments, a feature not seen in conventional mo

197 We found that long keratin filaments, like other types of IFs, are transpor

198 nts for the A(11) mode of axial alignment in keratin filaments.

199 ebrafish skin cells contained both actin and keratin filaments.

200 s the ability to fluidize amino acids in the keratin filaments.

201 ng and loose network interconnections of the keratin filaments.

202 Kinesin-dependent transport of keratin filaments: a unified mechanism for intermediate

203 how that intermediate filaments assembled by keratins function as asymmetrically inherited fate deter

204 patial chromatin looping of the feather beta-keratin gene cluster on chromosome 27.

205 , we find two major strategies regulate beta-keratin gene clusters.

206 yonychia congenita is caused by mutations in keratin genes and typified by dystrophic lesions affecti

207 Dominant mutations in keratin genes can cause a number of inheritable skin dis

208 show that in chicken, the difference in beta-keratin genes expressed in feathered and scaly skin is r

209 w-density lipoprotein receptor (LDLR) and of keratin genes known to be expressed in the outer root sh

210 through allele-specific silencing of mutant keratin genes.

211 additional acetylation of highly methylated keratins has a synergistic effect on prolonged stability

212 More importantly, however, studies of keratin have seeded the discovery of the genetic basis f

213 MSCs implantation with high-molecular-weight keratin hydrogel was selected as the inner core.

214 he iron chelator-loaded low-molecular-weight keratin hydrogel with quick degradation property was sel

215 Marked remodeling of the keratin IF network accompanies collective cellular morph

216 perphosphorylation-dependent collapse of the keratin IF network results in a similar hyper-SUMOylatio

217 sential for the proper reorganization of the keratin IF network.

218 these findings indicate that 14-3-3 acts on keratin IFs and is involved in their reorganization to s

219 The dynamics of keratin IFs have been described to depend mostly on the

220 bonding in the organization and dynamics of keratin IFs in skin keratinocytes.

221 n in dynamic reorganization and stability of keratin IFs.

222 s if the counter surface is soft relative to keratin in a dry state.

223 To characterize keratin intermediate filament assembly mechanisms at ato

224 Reversion of the keratin intermediate filament fragility phenotype associ

225 The mechanical resilience of the keratin intermediate filament network itself is determin

226 Keratin intermediate filaments (IFs) are the major cytos

227 we suggest a detailed model for bundling of keratin intermediate filaments based on interfilament el

228 Here we show that keratin intermediate filaments directly regulate the mor

229 in family that is implicated in crosslinking keratin intermediate filaments during hair formation, ye

230 Keratin intermediate filaments form dynamic intracellula

231 f mechanical integrity in the mesendoderm by keratin intermediate filaments is required to balance st

232 n providing the first credible evidence that keratin intermediate filaments play a unique and essenti

233 not actin fibers; instead, these fibers are keratin intermediate filaments.

234 sm is conserved across keratins and many non-keratin intermediate filaments.

235 PC1 proteins included keratin intermediate filaments; proteins associated with

236 inoid regulation of differentiation-specific keratins involves post-transcriptional mechanisms as we

237 While this reorganization of keratin is initiated by force transduction on cell-cell

238 Keratin is one of the most important structural proteins

239 al and disease states, and how this 'stress' keratin is regulated.

240 73 in K14, which is conserved in a subset of keratins, is revealed as a novel regulator of keratin or

241 atoderma, prompted us to examine the role of Keratin (K) 16 protein and its partner K6 in regulating

242 press expression of differentiation-specific keratins K1, K10 and K2 in normal human epidermal kerati

243 genes, which encode the cytoskeletal protein keratins K3 and K12, respectively.

244 ia expression of a transposase driven by the keratin K5 promoter in a p53(+/-) background.

245 Hair keratin (KRT) expressions (ie, KRT86 and KRT85) were sig

246 Depletion of keratin (krt8) with antisense morpholinos results in hig

247 s stabilized microridges, and overexpressing keratins lengthened them.

248 kin family cytolinkers that bind F-actin and keratins, localized to microridges, and were required fo

249 oncomitant to an increase in diameter of the keratin macrofibrils, their continuous compaction, and i

250 onditions of the free-standing insoluble all-keratin made microelectrode array ionic sensor pave the

251 ults from nanostructural organization of the keratin matrix feather barbs of the crown.

252 4 expression at the PM, suggesting that this keratin may regulate the apical expression of other ATP-

253 nding of how disease-associated mutations in keratins modulate keratin acetylation and methylation, w

254 Keratin mutation (Arg-to-Lys/Ala) at the methylation sit

255 These results establish the keratin network as an integral part of force-sensing ele

256 observations, we observed disassembly of the keratin network between asters in zygotes fixed before a

257 r follicle as a model to link changes in the keratin network composition and architecture to the mech

258 -lacking (KtyII(-/-)) keratinocytes prevents keratin network formation altogether.

259 The mechanisms governing keratin network formation and collapse due to EBS mutati

260 the external force favors maturation of cten-keratin network interactions over time and that keratin

261 hesions that stably anchor the intracellular keratin network to the extracellular matrix.

262 istence of a mechanotransduction pathway via keratin network.

263 plasmic stiffness by disassembling actin and keratin networks.

264 ss of microscopic junctions made between the keratin of the stratum corneum of the skin and the glass

265 The terminal domains of suprabasal keratins of the skin epithelium are very resistant to ev

266 eratins, is revealed as a novel regulator of keratin organization and YAP function in early different

267 ity with defects in desmosome morphology and keratin organization, thus demonstrating the utility of

268 t epithelial cells in the connective tissue, keratin pearls in the OSCC, and ducts of salivary glands

269 d with epithelial metaplasia, sometimes with keratin pearls, consistent with squamous cell carcinomas

270 Here, we examine the role of keratin phosphorylation in KF network rearrangement and

271 s containing remnant melanosomes and decayed keratin plates.

272 r of hydrophobic residues in the constituent keratin polypeptides, and the extent to which the electr

273 conversely induces the localization of this keratin population to the region of cell-cell contacts.

274 and 10, based on all-atom 3D simulations of keratin primary amino acid sequences, and tyrosine phosp

275 tochemistry demonstrated a similarly altered keratin profile in corneal tissue from a K12-Leu132Pro M

276 e liver disease-associated variants regulate keratin protein stability.

277 ion sites, led to decreased stability of the keratin protein.

278 The abundance of keratin proteins and the filaments they form in surface

279 This said, the remarkable diversity of keratin proteins and the notion that they are encoded by

280 ass influence lineage fate, via differential keratin regulation, and identify an early function for i

281 of other post-translational modifications in keratins related to liver diseases have not been fully e

282 clustered in immunologic, cell adhesion, and keratin-related processes.

283 we demonstrate that 14-3-3 proteins regulate keratin reorganization dynamics in embryonic mesendoderm

284 , cells to promote expression of specialized keratins required for normal tissue structure and integr

285 SSIM) of 0.925 and 0.920 for amylase and pan-keratin respectively.

286 lmoplantar thickening to modulate the stress keratin response and to mediate context-dependent stress

287 ghtly regulated by dynamic reorganization of keratin-rich intermediate filaments.

288 Finally, we report that a K14:K5->K14:K79 keratin shift occurs during SG differentiation.

289 of K1 and K10 to better understand how human keratin structure correlates with function.

290 -3 results in both the decreased exchange of keratin subunits into filaments and blocks keratin filam

291 the functional and structural properties of keratin such as bendability and insolubility were obtain

292 RNA interference reduced keratin synthesis in keratinocytes and, as a result, Sdr

293 d AURKB-dependent disassembly of F-actin and keratin that propagated ~40 mum without microtubules and

294 er, robust GVP markers derive primarily from keratins that do not exhibit body location-specific diff

295 Allele-specific silencing of mutant keratins through RNA interference is a promising therape

296 this study, we demonstrate that the type II keratin topological associating domain undergoes epigene

297 caused by aggregation of the basal epidermal keratin type II (KtyII) K5 and its type I partner kerati

298 Adherence to keratin types 1 and 10, human foreskin keratinocytes, an

299 tion/methylation in liver disease-associated keratin variants.

300 Keratin 15 (K15), a type I keratin, which pairs with K5 in epidermis, has been used