ライフサイエンスコーパス: crystallin

1 merization was effectively reduced by alphaB-crystallin.

2 ract in a nonspecific manner with the alphaB-crystallin.

3 f R3Abeta2m was potently prevented by alphaB-crystallin.

4 concentration excess with respect to alphaB-crystallin.

5 ens extracts as one multimeric entity, alpha-crystallin.

6 haB toward the lens-specific protein beta(L)-crystallin.

7 1-162) enhanced the degradation of wt alphaA-crystallin.

8 ins, including C-terminally truncated alphaA-crystallin.

9 ide, as well as an oligomeric form of alphaB-crystallin.

10 treated with the heat shock protein alpha-B crystallin.

11 t shock protein (HSP) homolog of human alpha-crystallin.

12 duction was inhibited by knockdown of alphaB-crystallin.

13 n but was inhibited by suppression of alphaB-crystallin.

14 ficient to inhibit aggregation of lens gamma-crystallin.

15 gregation of various cataract-causing mutant crystallins.

16 h to treating cataracts by stabilizing alpha-crystallins.

17 of the major chaperones, alphaA- and alphaB-crystallins.

18 n of beta-crystallin in the absence of alpha-crystallins.

19 phosphorylation, and the expression of beta-crystallins.

20 uding Prox1, p57(KIP2), aquaporin 0 and beta-crystallins.

21 , and cell transduction properties of alphaB-crystallins.

22 cts the degradation of wt alphaA- and alphaB-crystallins.

23 hetero-oligomers with wt alphaA- and alphaB-crystallins.

24 c-Maf, Prox1, and alphaA-, alphaB-, and beta-crystallins.

25 ression of the lens structural proteins, the crystallins.

26 eased levels of the stress-responsive alphaB-crystallins.

27 l experiments on in vitro alphaB- and gammaD-crystallin, 2D IR spectroscopy can identify the highly o

28 codon variants in the gene encoding gamma-B crystallin, a mammalian eye-lens protein, modulate the r

29 idual unfolding pathways of the human gammaD-crystallin, a multidomain protein that must remain corre

30 pairs exosome secretion by decreasing alphaB-crystallin, a protein that is expressed mainly in glial

31 strocytes decreased the expression of alphaB-crystallin, a small heat shock protein that is enriched

32 st abundant sHSPs in human tissue are alphaB-crystallin (ABC) and HSP27; here we present high-resolut

33 In contrast to wild-type, modified alpha-crystallins accumulated in HLE B3 cells.

34 Both alphaA- and alphaB-crystallin act as chaperones and anti-apoptotic proteins

35 yed by luciferase refolding and human gammaD-crystallin aggregation suppression and refolding.

36 orescence intensity of Smad7 and the corneal crystallin aldehyde dehydrogenase 3A1.

37 dopsis reductase ornithine cyclodeaminase/mu-crystallin, alias SYSTEMIC ACQUIRED RESISTANCE-DEFICIENT

38 degradation of C-terminally truncated alphaA-crystallin (alphaA(1-162)) and vice versa.

39 alphaA-Crystallin (alphaA) and alphaB-crystallin (alphaB), the

40 small heat shock proteins alphaA- and alphaB-crystallin (alphaA/alphaB(-/-)) develop cataracts.

41 alphaB-Crystallin (alphaB) and HSP27 are the two most widely di

42 sly that the small heat shock protein alphaB-crystallin (alphaB) is exported out of the adult human r

43 The human small heat-shock protein alphaB-crystallin (alphaB) rescues misfolded proteins from irre

44 alphaA-Crystallin (alphaA) and alphaB-crystallin (alphaB), the two prominent members of the sm

45 chanism by which two canonical sHsps, alphaB-crystallin (alphaB-c) and Hsp27, interact with aggregati

46 SPs, the widely expressed human sHSP, alphaB-crystallin ('alphaB'), forms large polydisperse multimer

47 Crystallin-alphaB (CryAB) is a small heat shock protein

48 AlphaB-crystallin (alphaBC) is a small heat shock protein that

49 alphaB-crystallin (alphaBc) or HspB5 is a well-characterized me

50 alphaB-crystallin also prevented the unfolding and nonfibrillar

51 The chaperone proteins, alpha-crystallins, also possess antiapoptotic properties.

52 opose an initial structural model for gammaD-crystallin amyloid fibrils.

53 Here we report that alphaB-crystallin, an antiapoptotic molecular chaperone implica

54 alphaB-crystallin and HSP27 are mammalian intracellular small h

55 eptide (70)KFVIFLDVKHFSPEDLTVK(88) in alphaA-crystallin and the peptide (73)DRFSVNLDVKHFSPEELKVK(92)

56 creases were observed in abundance of betaB2-crystallin and vimentin in 30-day-old lenses of DKO anim

57 olecular mechanisms are applicable for other crystallins and genes highly expressed in terminally dif

58 oligomers (HspB1/Hsp27, HspB3, HspB4/alphaA-crystallin, and HspB5/alphaB-crystallin) are promiscuous

59 morphogenetic protein 4 up-regulated alphaB-crystallin, and its EMT induction was inhibited by knock

60 n vivo and their subsequent interaction with crystallins are responsible, in part, for protein aggreg

61 3, HspB4/alphaA-crystallin, and HspB5/alphaB-crystallin) are promiscuous chaperones, whereas the chap

62 Taken together, our findings point to alphaB-crystallin as a novel regulator of anoikis resistance th

63 Despite its oligomeric nature, Rh of alphaB-crystallin as derived from both NMR methods is found to

64 ptide (73)DRFSVNLDVKHFSPEELKVK(92) in alphaB-crystallin as mini-chaperones.

65 We show here that HSP27 and alphaB-crystallin associated with immunoglobulin-like (Ig) doma

66 ation in Cryba1 (the gene encoding betaA3/A1-crystallin), astrocytes exhibit decreased Notch signalin

67 ised of nine protein spots containing betaB2-crystallin at 10-40-fold higher abundance and three prot

68 When mixed with wt alphaA-crystallin at 1:1 or 1:4 (alphaA(1-162) : wt) ratios to

69 ents on lens tissue show colloidal gels of S-crystallins at all radial positions.

70 signaling up-regulates expression of alphaA-crystallin both directly and indirectly via up-regulatio

71 further enhanced by overexpression of alphaB-crystallin but was inhibited by suppression of alphaB-cr

72 he disorder "solid" carbon nanofibers-->well crystallined carbon nanofibers-->bent graphitic sheets--

73 c of the desmin-related cardiomyopathies and crystallin cardiomyopathic diseases.

74 egates as a result of a mutant CryAB (alphaB-crystallin) causative for human desmin-related cardiomyo

75 The results suggest that the alpha-crystallin chaperone peptides could be used as therapeut

76 Overexpression of alphaB-crystallin could alleviate the deficient exosome release

77 ncogene c-Maf regulates expression of alphaA-crystallin (Cryaa) through binding to its promoter and d

78 ntified a class of molecules that bind alpha-crystallins (cryAA and cryAB) and reversed their aggrega

79 Mutated alphaB-crystallin (CryAB(R120G)), when expressed only in cardio

80 The small heat shock protein alphaB-crystallin (CRYAB) has been implicated in multiple scler

81 ted with increased expression in alpha-basic crystallin (CRYAB), which has previously bound VEGF.

82 cyte-specific expression of a mutated alphaB crystallin, CryAB(R120G).

83 ssion of the schizophrenia-related gene beta crystallin (Crybb1).

84 Here, we identify and validate the mu-crystallin (crym) gene as a high-fidelity marker of the

85 8 kDa protein in DKO lenses, containing beta-crystallin, demonstrating aggregation of beta-crystallin

86 Nanodelivery of alphaB-crystallin-derived mini-chaperone peptide offers an alte

87 as to investigate whether 19 to 20-mer alpha-crystallin-derived mini-chaperone peptides (alpha-crysta

88 ellular uptake of fluorescein-labeled, alpha-crystallin-derived mini-peptides and recombinant full-le

89 e presence of 19 to 20-mer alphaA- or alphaB-crystallin-derived or scrambled peptides.

90 imal while a time-dependent uptake of alphaB-crystallin-derived peptide was observed.

91 Several other crystallin-derived peptides with double basic residues a

92 Wild-type and gC tagged alphaB-crystallin displayed robust CLA.

93 rat, mutation in the gene encoding betaA3/A1-crystallin disrupts both Notch signalling in astrocytes

94 While the alpha-crystallin domain (ACD) dimer of sHSPs is the universal

95 ation reveals that a central conserved alpha-crystallin domain (ACD) forms dimeric building blocks, w

96 also identified a novel C-terminal betagamma-crystallin domain in FgFCO1 devoid of calcium binding mo

97 A betagamma-crystallin domain is formed of two Greek key motifs, acc

98 We show that the alpha-crystallin domain is the elementary Cu(II)-binding unit

99 ts strongly suggest that Hspb8 and its alpha-crystallin domain might act as pleiotropic prosurvival f

100 es not alter the fold of the conserved alpha-crystallin domain nor does it disturb the interface hold

101 so discovered that the truncated form of the crystallin domain of Hspb8 was sufficient to affect cell

102 total, these data imply that the core alpha-crystallin domain of the sHSPs is a platform for flexibl

103 IDM2 encodes an alpha-crystallin domain protein in the nucleus.

104 histone acetyltransferase IDM1 and the alpha-crystallin domain proteins IDM2 and IDM3.

105 but also tethered by contacts with the alpha-crystallin domain shell.

106 hanges its orientation relative to the alpha-crystallin domain which enables alternative packing of d

107 e defined by a conserved beta-sandwich alpha-crystallin domain, flanked by variable N- and C-terminal

108 ction of the N-terminal region and the alpha-crystallin domain.

109 Paralleling the diversity in betagamma-crystallin domains, these motifs also show great diversi

110 Furthermore, inhibition of alphaB-crystallin enhanced monotetraubiquitination of SMAD4, wh

111 Overexpression of alphaB-crystallin enhanced nuclear translocation and accumulati

112 ing motifs are necessary for Ciona betagamma-crystallin expression, and narrow down the likely factor

113 d with SB, altered LECs' morphology and beta-crystallin expression.

114 ell proliferation and uniquely affected beta-crystallin expression.

115 Chemical damage to proteins of the crystallin family, accumulated over a lifetime, leads to

116 y taking advantage of its unique IgE-binding crystallin fold, activates basophils by a novel, cross-l

117 le loop, which is unique to the IPSE/alpha-1 crystallin fold.

118 crystal structure reveals the typical alpha-crystallin fold.

119 , administration of recombinant human alphaB-crystallin for the first week after contusion injury lea

120 he oxidation-mimicking W42Q mutant of gammad-crystallin formed non-native polymers starting from a na

121 These modified alphaB-crystallins formed OC that were larger than wild-type ba

122 will enable in vivo testing of the roles of crystallin fragments in protein aggregation.

123 The accumulation of crystallin fragments in vivo and their subsequent intera

124 Comparison of crystallins from five species: two aquatic and three ter

125 progressive post-synthetic modifications of crystallins from various physical chemical and metabolic

126 Additionally, crystallin-gamma subunits and serotonin-related genes we

127 In the human eye lens, gammaS-crystallin (gammaS-WT) forms a densely packed transparen

128 p300, and recruited a repressor, Sp3 to beta-crystallin gene promoters, to negatively regulate their

129 ver, a direct link between FGF signaling and crystallin gene transcriptional machinery remains to be

130 ctivity for the Ciona intestinalis betagamma-crystallin gene, which drives expression in the lens of

131 ation of Sp1 with the enhancer of the alphaB-crystallin gene.

132 ystem to specifically disrupt the two alphaB-crystallin genes, alphaBa and alphaBb We observed lens a

133 e in abundance after deletion of these alpha-crystallin genes.

134 The alpha-crystallin glass transition could have implications for

135 Overexpression of alphaA-crystallin had no significant effects on the penetrance

136 C-terminal CPP fused crystallins had poor solubility.

137 Therefore, enhanced alphaB-crystallin has an essential role in TSC1/2 complex defic

138 in the human small heat shock protein alphaB-crystallin have been implicated in autosomal cataracts a

139 A number of mutations of lens crystallins have been associated with dominant cataracts

140 The crystallins have relatively high refractive increments c

141 oblot analyses revealed decreases in beta-B1-crystallin, Hsp-90, spectrin and filensin.

142 nefit of the small heat shock protein alphaB-crystallin (HspB5) in animal models of multiple sclerosi

143 with sHsps, including Hsp27 (HspB1), alphaB-crystallin (HspB5), Hsp22 (HspB8), and Hsp20 (HspB6).

144 cross-linking as well as cleavage of gammaS-crystallin in all adult lenses.

145 Here we show that loss of betaA3/A1-crystallin in astrocytes does not impede Notch ligand bi

146 e that mHtt reduces the expression of alphaB-crystallin in astrocytes to decrease exosome secretion i

147 In addition, silencing alphaB-crystallin in metastatic carcinoma cells reduced the num

148 highlight the potent effectiveness of alphaB-crystallin in preventing beta2m aggregation at the vario

149 e uncovered another critical role for alphaB-crystallin in providing stress tolerance to the heart.

150 r work illuminates the involvement of alphaB-crystallin in stress tolerance of the heart presumably t

151 However, the role of alphaB-crystallin in subretinal EMT and fibrosis is unknown.

152 , confocal laser microscopy revealed alpha-B crystallin in subsarcolemmal aggresomes.

153 rystallin, demonstrating aggregation of beta-crystallin in the absence of alpha-crystallins.

154 The core function of gammaS-crystallin in the eye lens may be precisely its capacity

155 ty in vitro, the in vivo functions of alphaB-crystallin in the maintenance of both lens transparency

156 cal role of the chaperone activity of alphaB-crystallin in the maintenance of lens transparency.

157 Overexpression of betaA3/A1-crystallin in those same astrocytes restored V-ATPase ac

158 uction in anoikis, we stably silenced alphaB-crystallin in two different metastatic carcinoma cell li

159 eak affinity to the resident chaperone alpha-crystallin in vitro To better understand the mechanism o

160 dhesion proteins, cytoskeletal proteins, and crystallins in lens opacities caused by the absence of t

161 implications of Ca(2+) binding to betagamma-crystallins in mediating biological processes are yet to

162 Amorphous aggregation of gamma-crystallins in the eye lens causes cataract, a widesprea

163 the accumulation of UV-damaged human gammaD-crystallins in the eye lens.

164 ndent on the stability and solubility of the crystallins in the fiber cells.

165 Strikingly, silencing alphaB-crystallin increased matrix detachment-induced caspase a

166 n induced EMT, whereas suppression of alphaB-crystallin induced a mesenchymal-epithelial transition.

167 In vitro, overexpression of alphaB-crystallin induced EMT, whereas suppression of alphaB-cr

168 is both necessary and sufficient for alphaB-crystallin induction by matrix detachment.

169 onstitutive ERK activation suppresses alphaB-crystallin induction during matrix detachment.

170 xamine the functional consequences of alphaB-crystallin induction in anoikis, we stably silenced alph

171 Silencing of alphaB-crystallin inhibited multiple fibrotic processes, includ

172 ddition of CPP improves the uptake of alphaB-crystallins into HLE B3 cells.

173 ion peptides (CPP) to enhance entry of alpha-crystallins into lens-derived cells.

174 The structural eye lens protein gammaD-crystallin is a major component of cataracts, but its co

175 alpha-Crystallin is a member of the small heat-shock protein (

176 alphaB-Crystallin is a protein chaperone with anti-apoptotic an

177 Human gammaD-crystallin is an eye lens protein that aggregates into a

178 Thus, alphaB-crystallin is an important regulator of EMT, acting as a

179 The small heat shock protein alphaB-crystallin is an oligomeric molecular chaperone that bin

180 The V75D mutant of gammaD-crystallin is associated with congenital cataract in mic

181 We postulate that betaA3/A1-crystallin is essential for normal endolysosomal acidifi

182 ics simulations that the stability of gammaD-crystallin is greatly reduced by the conversion of trypt

183 .e., in the cytosol of astrocytes, betaA3/A1-crystallin is necessary for the phosphorylation of STAT3

184 One of the chaperones, alphaB-crystallin, is primarily found inside cells, while the o

185 king finding was a cohort of lens-associated crystallin isoform mRNAs lost from the eif3ha morphant p

186 of a phenotype previously reported in alphaB-crystallin knock-out mice and suggests that the elevated

187 l retinal pigment epithelium cells in alphaB-crystallin knockout mice compared with wild-type mice.

188 ch is equivalent to a mutant of human alphaB-crystallin linked to cardiomyopathy.

189 higher IgM autoantibodies against alpha beta crystallin, lipopolysaccharide, heat-shock cognate 70, a

190 betagamma-Crystallins make a separate class of Ca(2+)-binding prot

191 t administration of recombinant human alphaB-crystallin may be a good therapeutic approach for treati

192 We show that STAT3 and betaA3/A1-crystallin may co-regulate each other in astrocytes.

193 ated tumorigenesis, and inhibition of alphaB-crystallin may complement the current therapy for TSC.

194 We hypothesize replenishing lens alpha-crystallin may delay or prevent cataract.

195 ransparency, our results suggest that alphaA-crystallin may not be efficient to inhibit aggregation o

196 lins suggesting that the primary sequence of crystallins may be specifically enriched with amino acid

197 We report here that alphaB-crystallin mediates protective effects after spinal cord

198 Oxidation of crystallin methionine and sulfhydryls into sulfoxides wa

199 cantly lower concentrations than free alphaB-crystallin mini-chaperone peptide.

200 ctone (PCL) nanoparticle encapsulated alphaB-crystallin mini-chaperone peptides from H2O2-induced cel

201 PCL nanoparticles containing alphaB-crystallin mini-chaperone were also taken up and protect

202 allin-derived mini-chaperone peptides (alpha-crystallin mini-chaperone) are antiapoptotic, and to ide

203 alphaA- and alphaB-crystallin mini-chaperones offer protection to hfRPE cel

204 xidative stress and either alphaA- or alphaB-crystallin mini-chaperones remained viable and showed ma

205 The entry mechanism in hfRPE cells for alpha-crystallin mini-peptides was investigated.

206 Crystallin modifications and cleavage were quite dramati

207 of alpha-crystallins were observed in alphaB-crystallin modified by the addition of the gC-derived CP

208 ovide evidence that recombinant human alphaB-crystallin modulates the inflammatory response in the in

209 tra collected at various R3Abeta2m to alphaB-crystallin molar subunit ratios, it is concluded that th

210 yproteins containing two neighboring HgammaD-crystallin monomers, we captured an anomalous misfolded

211 f aggregates formed by the P23T human gammaD-crystallin mutant associated with congenital cataracts.

212 cyte-specific expression of a mutant alpha-B-crystallin, mutant CryAB (CryAB(R120G)), which shows imp

213 The alphaB-crystallin mutants exhibited hypersusceptibility to deve

214 we transgenically expressed different gammaD-crystallin mutants in the zebrafish lens and observed a

215 particular interest were gammaB- and gammaD-crystallin mutants linked to dominant cataracts in mouse

216 y the mechanism of aggregation of two gammaD-crystallin mutants, W42R and W42Q: the former a congenit

217 ted formation of amorphous deposits by other crystallin mutants.

218 termine the effects of wt alphaA- and alphaB-crystallins on the degradation of C-terminally truncated

219 uired the downstream expression of the alpha-crystallin ortholog HSP-16.48 Using a combination of pha

220 A scrambled alphaA-crystallin peptide produced no such effects.

221 To achieve this goal, the alphaB-crystallin peptide was re-engineered into a protein poly

222 The alphaA- and alphaB-crystallin peptides inhibited stress-induced aggregation

223 Both the acetyl and native crystallin peptides inhibited stress-induced apoptosis i

224 Whether alphaB-crystallin plays a role in modulating the secondary dama

225 To determine what role this crystallin plays after peripheral nerve damage, we found

226 alphaB-crystallin plays multiple roles in age-related macular d

227 ined the ability to differentiate into gamma-crystallin-positive lentoids by high-dosage bFGF treatme

228 entially under acidic conditions, and alphaB-crystallin prevented this aggregation.

229 iomyocyte stiffness was corrected by alpha-B crystallin probably through relief of titin aggregation.

230 alphaB-crystallins produced by fusing gC or TAT were over-expre

231 Gamma-B crystallins produced from mRNAs with changed codon bias

232 Surprisingly, wild-type gammad-crystallin promoted W42Q polymerization in a catalytic m

233 re, the delivery of recombinant human alphaB-crystallin promotes greater locomotor recovery even when

234 eptide derived from residues 73-92 of alphaB-crystallin protects human retinal pigment epithelial (RP

235 d kinase (ERK) activity and increases alphaB-crystallin protein and messenger RNA (mRNA) levels.

236 imics matrix detachment by increasing alphaB-crystallin protein and mRNA levels, whereas constitutive

237 ynamics of a model calcium-binding betagamma-crystallin protein, Protein S, and elaborate on its inte

238 The multidomain calcium-binding betagamma-crystallin proteins are particularly important because t

239 The human lens is comprised largely of crystallin proteins assembled into a highly ordered, int

240 cts are caused when damage to the major lens crystallin proteins causes their misfolding and aggregat

241 in this fashion by examination of long-lived crystallin proteins extracted from a sheep eye lens.

242 Cataracts are formed by the aggregation of crystallin proteins in the eye lens.

243 lear eye lens brought about by deposition of crystallin proteins in the lens fiber cells.

244 Many in vitro studies have established that crystallin proteins precipitate into aggregates that con

245 For alpha-crystallin proteins, the sites that undergo the greatest

246 from an evolutionary radiation of globular S-crystallin proteins.

247 ntiation characterized by high expression of crystallin proteins.

248 Oligomerization with wt alphaA- or alphaB-crystallins reduces the susceptibility of alphaA(1-162)

249 to regulate the chaperone activity of alphaB-crystallin rendering the NTD a conformational sensor for

250 Our results also suggest that alphaB-crystallin represents a promising molecular target for a

251 Importantly, overexpression of alphaB-crystallin rescues defective exosome release from HD ast

252 gment might exert catalytic activity against crystallins, resulting in the accumulation of distinct L

253 Furthermore, and most importantly, alphaB-crystallin reversibly dissociated beta2m oligomers forme

254 alpha-B crystallin shifted the Fpassive-sarcomere length relatio

255 ts showed that induced expression of corneal crystallins significantly decreased light scattering.

256 e whether the therapeutic activity of alphaB crystallin, small heat shock protein B5 (HspB5), was sha

257 nd analysis show that aqueous eye lens alpha-crystallin solutions exhibit a glass transition at high

258 existence curves for lysozyme and gamma IIIa-crystallin solutions in respective buffers.

259 scattering liquid structure data from alpha-crystallin solutions over an extended range of protein c

260 ilute and concentrated bovine eye lens alpha-crystallin solutions, using small-angle X-ray scattering

261 studies showed that once cleaved from gammaS-crystallin, SPAVQSFRRIVE adopts a markedly different sha

262 These trends are also seen in S-crystallins suggesting that the primary sequence of crys

263 at the same time as Hsp22, Hsp27, or alphaB-crystallin, suggesting that it might physically bring th

264 PSE/alpha-1 is a new member of the betagamma-crystallin superfamily.

265 ion of and refold the model substrate gammad-crystallin, suppress aggregation of mutant huntingtin, a

266 ess under acidic stress, but HSP27 or alphaB-crystallin suppressed this stiffening.

267 Disruption of alphaB-crystallin suppressed Tsc2-null cell proliferation and t

268 Quiescent keratocytes are thought to produce crystallins that match the refractive index of their cyt

269 sides providing new information about gammaD-crystallin, this study demonstrates the complementarity

270 A(1-162) was more susceptible than wt alphaA-crystallin to degradation by the UPP.

271 anged subunits with wt alphaA- or wt alphaB- crystallin to form hetero-oligomers.

272 diators that could be regulated by betaA3/A1-crystallin to modulate both GFAP and VEGF.

273 evaluated by measuring the ability of alpha-crystallins to suppress chemically-induced protein aggre

274 e show that both UTR sequences of a targeted crystallin transcript are necessary but not sufficient f

275 betagamma-Crystallin-type double clamp (N/D)(N/D)XX(S/T)S motif is

276 approach toward a glass transition at alpha-crystallin volume fractions near 58%.

277 The augmented alphaB-crystallin was critical for the migration, invasion and

278 By teenage years, insoluble intact gammaS-crystallin was detected, indicative of protein denaturat

279 -peptides and recombinant full-length alphaB-crystallin was determined in confluent hfRPE.

280 (beta2m) and the molecular chaperone alphaB-crystallin was investigated by thioflavin T fluorescence

281 Uptake of full-length alphaB-crystallin was minimal while a time-dependent uptake of

282 t exchange was observed when gC-fused alphaB-crystallin was mixed with alphaA.

283 alphaB-crystallin was prominently expressed in subretinal fibro

284 alphaB-crystallin was transcriptionally activated by mTOR compl

285 We report here that expression of alphaB-crystallin was upregulated in Tsc1-/- or Tsc2-/- mouse e

286 The Greek key motif in betagamma-crystallins was compared with that in other proteins, us

287 d myofibroblasts expressing human keratocyte crystallins was measured by reflectance confocal microsc

288 nsequently, expression of alphaB- and alphaA-crystallins was not initiated.

289 pression of lens-specific genes such as beta-crystallins, was positively regulated by SUMO1 but negat

290 better define the functional roles of alphaB-crystallin, we generated loss-of-function zebrafish muta

291 To evaluate protein uptake, labeled alpha-crystallins were incubated with HLE B3 cells and monitor

292 ges to the chaperone-like abilities of alpha-crystallins were observed in alphaB-crystallin modified

293 In contrast, N-terminal tagged alphaB-crystallins were soluble.

294 e-related changes to a major protein, gammaS-crystallin, were studied.

295 egment of the amyloid-forming protein alphaB crystallin, which forms an oligomeric complex exhibiting

296 The chaperone crystallin, which is a mild modulator of the lag phase o

297 This holds in particular for human alphaB-crystallin, which is strongly crowded in vivo and inter

298 vely monomeric human eye lens protein gammad-crystallin, whose aggregation leads to cataract disease.

299 Crystallins with Greek keys motifs have significantly hi

300 wo subunits of one multimeric protein, alpha-crystallin, within the ocular lens.