ライフサイエンスコーパス: keratin

1 animals had aberrant disulphide cross-linked keratins.

2 3 downstream targets Gata3, Hoxc13, and hair keratins.

3 produce hair shafts expressing hair-specific keratins.

4 geneity co-expressing both basal and luminal keratins.

5 We identified a causal de novo mutation in keratin 1 (KRT1).

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

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

8 of epidermal differentiation markers such as keratin 1, keratin 10, and loricrin, with or without the

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

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

11 smoglein 1 (Dsg1), desmocollin 1 (Dsc1), and keratins 1 and 10 (K1/K10), in a dose-dependent manner i

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

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

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

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

16 ccur within the mutational "hot spot" of the keratin 10 (K10) 2B rod domain, adjacent to severe EI-as

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

18 We previously demonstrated that mutations in keratin 10 (KRT10) cause ichthyosis with confetti (IWC),

19 nant negative mutations in the gene encoding keratin 10 (KRT10).

20 We identified keratin 10 as a marker of suprabasal epithelial cells in

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

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

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

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

25 l differentiation markers such as keratin 1, keratin 10, and loricrin, with or without the induction

26 K14, involucrin, and TRP63, but negative for keratin 10.

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

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

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

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

31 4, N-Cadherin, DeltaNp63 and ABCG2, and less keratin 12, consistent with their less differentiated st

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

33 from dominant mutations in keratin 5 (K5) or keratin 14 (K14) genes, encoding the intermediate filame

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

35 ing membrane ovalbumin (mOVA), driven by the keratin 14 (K14) promoter, developed GVHD-like mucocutan

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

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

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

39 sified by markers keratin 8/18 (K18, KRT18), keratin 14 (K14, KRT14) and estrogen receptor (ER, ESR1)

40 d in the central alpha-helical rod domain of keratin 14 is necessary for the formation of a stable pe

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

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

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

44 is study, we crossed Fam20C(fl/fl) mice with keratin 14-Cre (K14-Cre) transgenic mice to specifically

45 generates mitochondrial oxidative stress in keratin 14-expressing epidermal stem/progenitor cells in

46 Keratin 14-mediated Cre recombinase expression induced e

47 se exostosin glycosyltransferase 1 (Ext1) in keratin 14-positive cells from P21.

48 on the Spdef promoter and that treatment of keratin 14-positive cells with TGFbeta inhibited SPDEF a

49 Gain of function of Spdef in keratin 14-positive epithelia resulted in the ectopic fo

50 g growth factor beta receptor II (Tgfbr2) in keratin 14-positive stratified epithelia causes ocular s

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

52 urface but increased total protein levels of keratin-14 and beta1 integrins.

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

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

55 rate in bitransgenic mice expressed from the keratin-14 promoter to enhance carcinoma development in

56 nail LRCs express the hair stem cell marker, keratin 15 (K15), and lineage tracing show that these K1

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

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

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

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

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

62 Mutations in the type I keratin 16 (Krt16) and its partner type II keratin 6 (Kr

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

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

65 synthetase-like [OASL]) and barrier (MKi67, keratin 16 [K16], and claudin 8 [CLDN8]) AD-related gene

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

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

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

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

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

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

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

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

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

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

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

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

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

79 this study, we show that high expression of keratin-17 (K17) predicts poor outcome in patients with

80 Human mutations in keratin 8 (K8) and keratin 18 (K18), the intermediate filament proteins of

81 sion in cardiomyocytes of keratin 8 (K8) and keratin 18 (K18), two epithelial-specific intermediate f

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

83 -5, suggesting that Krtap5-5 crosstalks with keratin 18 in E0771 cells.

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

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

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

87 er enzymes, insulin resistance, adiponectin, keratin 18, high-sensitivity C-reactive protein, or hyal

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

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

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

91 e demonstrate that the intermediate filament keratin-19 (Krt19) marks long-lived, radiation-resistant

92 chaperone Hsp72 with appearance of misfolded keratins; 2) elevated levels of the transglutaminase 2 (

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

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

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

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

97 5 and 14 but not the differentiation marker keratin 4.

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

99 lex (EBS) results from dominant mutations in keratin 5 (K5) or keratin 14 (K14) genes, encoding the i

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

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

102 the expression of the proliferation markers keratin 5 and cyclin D1.

103 mSG cells exhibited progenitor cell markers (keratin 5 and nanog) as well as acinar-specific markers-

104 al component of the NF-kappaB pathway, under keratin 5 promoter (K5-Ikkbeta).

105 nic (Tg) mice over-expressing Cx26 driven by keratin 5 promoter had an unexpected mammary phenotype:

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

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

108 k of keratin filaments (with type II partner keratin 5) in skin keratinocytes analyzed by static and

109 ress a subset of basal cell genes, including keratin 5, but no longer express high levels of either T

110 airway stem cells expressing Trp63 (p63) and keratin 5, called DASC(p63/Krt5), to this process.

111 ing loss of gangliogenesis, innervation, and keratin 5-positive (K5+) epithelial progenitors in the S

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

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

114 For IFs comprised of keratins 5 and 14 (K5 and K14), which occur in basal ker

115 amous phenotype with increased expression of keratins 5/6 and beta-catenin.

116 nocyte-specific CtBP1 transgenic mice with a keratin-5 promoter (K5.CtBP1) to probe the pathological

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

118 I keratin 16 (Krt16) and its partner type II keratin 6 (Krt6a, Krt6b) cause pachyonychia congenita (P

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

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

121 2 and 3: EGF, FGF-2, IFNalpha2, IL-1RA, HSA, keratin-6, and involucrin; cortisol was significantly hi

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

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

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

125 ssociated polymorphisms in the gene encoding keratin 75 (KRT75), KRT75(A161T) and KRT75(E337K), are p

126 Human mutations in keratin 8 (K8) and keratin 18 (K18), the intermediate fi

127 ated ectopic expression in cardiomyocytes of keratin 8 (K8) and keratin 18 (K18), two epithelial-spec

128 Absence of keratin 8 (K8) in mice leads to colitis, decreased Na/Cl

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

130 ne sites on the simple epithelial IF protein keratin 8 (K8).

131 Tumors were further classified by markers keratin 8/18 (K18, KRT18), keratin 14 (K14, KRT14) and e

132 Ballooned hepatocytes were quantified by keratin 8/18 and ubiquitin (K8/18/Ub) staining.

133 Consistent with DNAJB6 dysfunction, keratin 8/18, a DNAJB6 client also accumulated in DNAJB6

134 Keratins 8 and 18 (K8/K18) are the intermediate filament

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

136 otein aggregates consisting of ubiquitinated keratins 8/18 (K8/K18).

137 ge-committed basal Lgr5-positive and luminal keratin-8-positive cells of the adult mouse mammary glan

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

139 Keratin 9 (K9) is a type I intermediate filament protein

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

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

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

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

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

145 Keratin 9 was recently identified as an important compon

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

147 Keratin acetylation provides a new mechanism to regulate

148 widespread formation of EBS-like cytoplasmic keratin aggregates in epithelial and non-epithelial fly

149 12-Leu132Pro mutation results in cytoplasmic keratin aggregates.

150 cytes through concurrent binding of SPP with keratin and CsA.

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

152 rmined refractive index dispersion values of keratin and melanin.

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

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

155 identification of pathways altered by mutant keratins and for the development of EBS therapies.

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

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

158 ssion by significant upregulation of luminal keratins and tight-junction proteins such as claudins.

159 cles are K15 positive, but mature hair fiber keratins are absent.

160 Simple-type epithelial keratins are intermediate filament proteins important fo

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

162 tensive barrier defects persist, identifying keratins as essential CE scaffolds.

163 chy in how Cys-4/Cys-40 and Cys-367 regulate keratin assembly in vitro and filament dynamics in live

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

165 eptors 1/2), as well as of a large number of keratin-associated protein genes, were seen after DXR tr

166 model for the cortex suggests that the alpha-keratin- based intermediate filaments (IFs) align with t

167 Interaction between SPP and keratin best correlated with measured CsA skin transport

168 16 with robust downregulation of its type II keratin binding partner, K6.

169 access the mechanical properties of both the keratin bundles themselves and the surrounding cytosol.

170 etae were assumed to be composed entirely of keratin, but analysis of footprints left behind by gecko

171 rks and determine mechanisms by which mutant keratins cause pathology.

172 argeting, and longer crypts, suggesting that keratins contribute to intestinal homeostasis.

173 The mechanisms by which type I and II keratins contribute to these functions remain incomplete

174 e identified highly expressed genes encoding keratin cross-linking proteins associated with rumen evo

175 ntrated network of keratin filaments, normal keratin cycling, and the sessile behavior of the nucleus

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

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

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

179 port that mice lacking all type I or type II keratins display severe barrier defects and fragile skin

180 Cys-4 and Cys-40, also participate in inter-keratin disulfide bonding and tandemly play a key role c

181 We recently showed that inter-keratin disulfide bonding plays an important role in the

182 plexity of a novel determinant, namely inter-keratin disulfide bonding, for the regulation of several

183 ila as a genetic model system to investigate keratin dynamics.

184 >25%) was associated with greater immune and keratin dysregulation and larger abnormalities in nonles

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

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

187 Molecular characteristics were measured by keratin expression patterns, which were nearly identical

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

189 However, owing to compensatory keratin expression, the overall contribution of keratins

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

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

192 P point mutation (S2849G) exhibits increased keratin filament association and fosters Ca(2+) insensit

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

194 t show an obvious liver phenotype or altered keratin filament distribution, whereas K8 G62C/R341C ani

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

196 ohesion via modulation of p38 MAPK-dependent keratin filament reorganization.

197 We show that loss of cell adhesion and keratin filament retraction induced by Dsg3 depletion is

198 letal (Triton X-100 insoluble) fraction, and keratin filament retraction, a hallmark of PV, was effic

199 formation of a stable perinuclear network of keratin filaments (with type II partner keratin 5) in sk

200 Additionally, keratin filaments fail to organize at the rear of cells

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

202 the assembly, organization, and dynamics of keratin filaments in skin keratinocytes in primary cultu

203 ng, for the regulation of several aspects of keratin filaments in surface epithelia.

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

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

206 mainly consists of 3 elements: intracellular keratin filaments, intercellular lipids, and the cornifi

207 sis of a perinuclear-concentrated network of keratin filaments, normal keratin cycling, and the sessi

208 ylation provides a new mechanism to regulate keratin filaments, possibly via modulating keratin phosp

209 hal alleles are enriched for genes affecting keratin filaments, suggesting that Neanderthal alleles m

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

211 portance of context-dependent regulation for keratin genes and proteins in vivo.

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

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

214 ny upregulated immune and downregulated hair keratin genes.

215 ult to examine in vivo on deletion of single keratin genes.

216 through allele-specific silencing of mutant keratin genes.

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

218 vealed that the striking defects observed in keratin IF bundling, cytoarchitecture, and mitochondria

219 mice to assess the functional importance of keratin IF self-organization in vivo.

220 ontribution of self-mediated organization of keratin IFs to structural support and cytoarchitecture i

221 ipids and investigate their association with keratin in 'pristine' sheds, or natural molts of the adh

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

223 t and molecular-level behavior of lipids and keratin in the setae is still not known.

224 n K8(-/-) colonocytes, suggesting a role for keratins in colonocyte energy metabolism and homeostasis

225 findings provide radically new insight into keratin intermediate filament and Aire function, along w

226 cial role of structural support fulfilled by keratin intermediate filaments (IFs) in surface epitheli

227 Keratin intermediate filaments (KIFs) protect the epider

228 ponsive cadherin adhesion complex containing keratin intermediate filaments and the catenin-family me

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

230 In cells, keratin intermediate filaments form networks of bundles

231 the assembly, organization, and dynamics of keratin intermediate filaments in skin keratinocytes.

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

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

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

235 Here we show that suprabasal type II keratins, K1 and K2, are expressed in a mutually exclusi

236 d developed massive aggregates of the type I keratin, K10.

237 Keratin K2 is one of the most abundant structural protei

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

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

240 differentiation, and abnormal expression of keratins K5, K14, and K2.

241 e absence of K9 induces the stress-activated keratins K6 and K16.

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

243 -associated genes including wound-associated keratins (Krt16, Krt17) and Myosin VA (Myo5a), in the ep

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

245 tion factors through its intervening (I) and keratin-like (K) domains.

246 portion of the intervening and the complete keratin-like domain of SEP3.

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

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

249 Keratin mutations predispose to human liver disorders, w

250 ility that AMA may be found in patients with keratin mutations that associate with liver and other di

251 n is not observed with other disease-causing keratin mutations, the results of this study implicate K

252 nce of Q in the alpha-helical core domain of keratins, neighboring residues and steric hindrance prev

253 racellular forces and cross-talk between the keratin network and other cytoskeletal components, are m

254 y tissues with phosphatase inhibitors caused keratin network collapse, validating Drosophila as a gen

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

256 eratin solubility; and prominent pericentral keratin network disruption.

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

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

259 ied continuously by controlling the time the keratin network is allowed to phase separate before mobi

260 namel hardness, suggesting that a functional keratin network is required for the mechanical stability

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

262 ull' environment to examine the formation of keratin networks and determine mechanisms by which mutan

263 nd K5 resulted in the formation of extensive keratin networks in Drosophila epithelial and non-epithe

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 similar to that observed when expression of keratin or plakoglobin is inhibited.

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

268 e beta-keratin rather than that of the alpha-keratin phase.

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

270 e keratin filaments, possibly via modulating keratin phosphorylation.

271 s containing remnant melanosomes and decayed keratin plates.

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

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

274 he amino acid determination in hair included keratin protein acid hydrolysis using 6 M hydrochloric a

275 Keratin protein is the major component of scalp hair sha

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

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

278 les, we identified eight peptides from alpha-keratin proteins in sheep wool that could potentially be

279 absent, indicating the presence of the beta-keratin rather than that of the alpha-keratin phase.

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

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

282 ouse and that unbalanced expression of these keratins results in aggregate formation.

283 Therefore, absence of the hepatocyte keratins results in production of anti-mitochondrial aut

284 lar pathway, enhancing its partitioning into keratin-rich corneocytes through concurrent binding of S

285 accompanied by barrier disorders by linking keratin scaffolds to mitochondria, adhesion, and CE form

286 ural evidence that the cuticle contains beta-keratin sheets.

287 perphosphorylation at S74/S432 with enhanced keratin solubility; and prominent pericentral keratin ne

288 Keratin staining was significantly associated with ER st

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

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

291 Keratins that are overexpressed selectively in human car

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

293 croorganisms through the addition of feather keratin to compost enhanced degradation of PrP(263K) and

294 atin expression, the overall contribution of keratins to cell mechanics was difficult to examine in v

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

296 Proteomics analysis identifies keratin type II cytoskeletal 1 (KRT1) as a protein pulle

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

298 a indicated that deamidation in wool's alpha-keratin was influenced by primary and higher-order struc

299 ar localization signal (NLS), specific among keratins, where it bound p27(KIP1) during G1 phase of th

300 Here, we determined that epithelial hair keratins, which are crucial for maintaining the integrit